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 Table of Contents  
REVIEW ARTICLE
Year : 2016  |  Volume : 8  |  Issue : 3  |  Page : 176-182

Vascular lesions of head and neck: A literature review


Department of Oral Medicine and Radiology, Institute of Dental Sciences, Jammu, Jammu and Kashmir, India

Date of Web Publication7-Oct-2016

Correspondence Address:
Nazia Masoom Syed
Department of Oral Medicine and Radiology, Institute of Dental Sciences, Sehora, Kunjwani Bisnah Road, Jammu, Jammu and Kashmir
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0976-4003.191726

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  Abstract 

Vascular lesions are among the most common congenital and neonatal abnormalities. These anomalies can occur throughout the whole body, with 60%, however, being located in the head and neck region probably due to its intricate vascular anatomy of region. There is a significant confusion in the literature because of the use of confusing descriptive terminology for the same vascular entity and eponyms. Correct naming of lesion, appropriate classification, and clinical appearance of vascular lesions have a direct impact on understanding of etiologies of these complex lesions, diagnosis, and in treating patients. Thus, the aim of this article is to provide comprehensive knowledge about classifications and to have an insight of various important vascular lesions affecting head and neck region based on its pathogenesis, clinical presentation, and management.

Keywords: Arteriovenous malformation, capillary malformation, hemangioma, lymphatic malformation, venous malformation


How to cite this article:
Syed NM. Vascular lesions of head and neck: A literature review. Indian J Dent Sci 2016;8:176-82

How to cite this URL:
Syed NM. Vascular lesions of head and neck: A literature review. Indian J Dent Sci [serial online] 2016 [cited 2019 May 20];8:176-82. Available from: http://www.ijds.in/text.asp?2016/8/3/176/191726


  Introduction Top


Vascular lesions are localized structural defects of the vasculature. The clinical presentation of vascular anomalies is confusing because all lesions appear in the color spectrum of blue, pink, and red. Unfortunately, the same word has been used to describe the entirely different vascular lesions. For example, “hemangioma” has been a generic term for various vascular lesions with distinctive natural histories and differing etiologies. Port-wine stain, a lesion that never regresses, has also been classified as a “capillary hemangioma.” This has led to improper diagnosis, illogical treatment, and misdirected research.[1] The purpose of this article is to summarize classifications, and to point out the differences between various important vascular lesions affecting head and neck region based on its etiology, clinical presentation, and treatment modalities.


  Classification Top


The first classification of vascular lesions was developed by Virchow (1863) and his student Wegener (1877). Based on the microscopic appearance of vascular lesions, they separated all vascular tumors into angiomas and lymphangiomas, which were then characterized as “simplex,” “cavernosum,” and “racemosum.” After this, many different classifications were presented that use anatomical labels or descriptive terms without regard to the biological behavior of the various vascular tumors present. This led to the misconception that most of these lesions spontaneously disappear within the 1st year of life. As a consequence, congenital vascular malformations were often misdiagnosed and left untreated.[2] Mulliken and Glowacki, in 1982, introduced a simple classification based on the clinical, histochemical, and cellular criteria to distinguish various vascular anomalies which provided framework for the proper identification of these lesions and was later on adopted in 1996, as an official frame by the International Society for the Study of Vascular Anomalies (ISSVA).[3],[4] They described two distinct entities - hemangiomas and vascular malformations.[3] They classified the different types of vascular malformations according to the type of involved vessels present. These may be single vessel forms (capillary, arterial, lymphatic, or venous) or a combination.[3],[4] The subsequent modification was carried out in 1999 to classify the vascular lesions based on depth of the lesion, predominant vessel type, and characteristics of the flow of lesion.[5] This classification was proved to be clinically useful and correlated well with the pathological and radiological data.[5] Malformations with an arterial component are rheologically fast-flowing lesions while others are slow-flowing lesions.[5] The ISSVA society further modified the biological classification in their continuing workshop and divided vascular lesions into vascular tumors and vascular malformations [6] [Table 1].
Table 1: Classification of Vascular lesions

Click here to view



  Vascular Tumors Top


Hemangioma

Hemangioma is a benign lesion of a hamartomatous growth of capillaries with a high proliferation index. Hemangiomas are categorized into infantile hemangioma (IH) and congenital hemangioma (CH). IH is subcategorized depending on the site of its occurrence as focal, segmental, and indeterminate, and also depending on the depth of the lesion from the skin surface as superficial (previously called capillary hemangioma), deep (previously called cavernous hemangioma), and mixed (capillary cavernous hemangioma). CH is further subcategorized into rapidly involuting CH (RICH) and noninvoluting CHs (NICHs).[5],[7]

Infantile hemangioma

IH is not present at birth and arises during the first 8 weeks of life. IH is a true benign neoplasm of endothelial cells (ECs) with a unique biological behavior of high proliferative phase for 6–12 months followed by a gradual involution phase and a spontaneous regression by the age of 5–9 years.[7] The incidence in the general newborn population is between 1.1% and 2.6%, but increases up to 12% by 1 year of age.[7] It occurs more often in females compared to males and is also more prevalent in premature infants.[8]

Pathogenesis

Various theories suggest that the pathogenesis of IH is related to an intrinsic defect of hemangioma ECs (hemECs): Clonality of hemECs, somatic mutation of single progenitor cell, and loss of heterozygosity to chromosome 5q. Other theories suggest that hemECs' response to extrinsic defects is presented in the local environment. A balance between intrinsic and extrinsic factors and between stimulators and inhibitors of angiogenesis factors might account for the rapid growth and slow involution of IH. A number of stimulator factors that act on ECs include local tissue environment hypoxia or acidity, vascular endothelial growth factor (VEGF), basic fibroblast growth factor, matrix metalloproteinases-9, intercellular adhesion molecule-3, monocytes chemoattractant protein-1, E-selectin and angiogenesis inhibitors that act on ECs that include proteins such as angiostatin, platelet factor-4, thrombospondin-1, interferon-α (IFN-α), tissue inhibitor of metalloproteinases, and plasminogen activator inhibitors.[7],[8],[9]

Clinical features

Initially, the lesion clinically appears as circumscribed area of discoloration or telangiectasia of facial skin. IH may clinically show scaring, wrinkling, telangiectasia, or loose fibro-fatty tissue at the site of their clinical appearance. Focal IH is the most common variant, appearing as localized raised tumor-like lesion that tends to occur at the area of embryological fusion. Segmental IH is flat plaque-like larger lesion that shows a geographic segmental distribution, and indeterminate IH shows the characteristics of both focal and segmental IH. Color of the IH varies with the depth of the lesion and they can be bright red (superficial), purple, blue, or normal skin color (deep).[7]

Histopathologic features

Histologically proliferating IH is characterized by nonencapsulated masses and dense cords of mitotically active plump ECs with pericytes whereas involuting IH is characterized by enlarged vascular lumina with flattened ECs. Involuted phase of IH has more dilated vascular spaces with adipocytes, fibrous deposits, and with few remaining vessels.[10]

Complications

Depending on the size and location of the hemangioma, many serious problems can ensue. Eyelid IH can cause deprivation amblyopia, a subglottic IH can compromise the airway, and extremely large IH can cause high-output congestive heart failure.[7],[8] Some IH ulcerate and bleed, which then requires transfusion and/or surgery. Infants with large segmental facial hemangiomas are at a risk of having PHACE syndrome. PHACE refers to posterior fossa brain abnormalities, hemangiomas, arterial malformations, coarctation of the aorta and other cardiac defects, as well as eye abnormalities. Ectopic expression of type 3 iodothyronine deiodinase in IH has been shown to inactivate thyroid hormone systemically and cause hypothyroidism.[7],[8]

Congenital hemangioma

CHs have been recognized for years. More recently, these lesions have been found to be biologically distinct from the IH. IHs appear more common (70%) than CH (30%).

Clinical features

CH clinically presents as fully developed lesions at birth which either rapidly involutes during the 1st year of life or may never show involution. These lesions do not exhibit a proliferative phase and usually do not grow after birth. RICHs are present at birth either as red-purple color plaques with coarse telangiectasia, as flat violaceous lesions, or as a grayish tumor surrounded by a pale halo with multiple tiny telangiectasias. RICH undergoes a rapid regression phase and completely disappears by 12–18 months of age. NICHs are present at birth as pink or purple-colored plaque-like lesions with prominent overlying coarse telangiectasia and peripheral blanching. NICH does not show a regression phase, may grow proportionately with the growth of the child, and can be mistaken for vascular malformations.[7],[11],[12]

Histopathologic features

RICH is characterized by small-to-large lobules of capillaries with moderately plump ECs and pericytes. NICH and IH have similar appearances histologically. Tissue-specific immunohistochemical markers such as glucose transporter-1 (GLUT-1), merosin, Fc-gamma-RII, and Lewis Y antigens are positive for IH and thus aid in differentiating IHs from other vascular tumors or malformations.[10],[11]

Kaposiform hemangioendothelioma

Kaposiform hemangioendothelioma (KHE) is a distinctive vascular neoplasm of childhood associated with profound thrombocytopenia, petechia, and bleeding, known as Kasabach–Merritt syndrome. The tumor is generally present at birth, although it can also appear postnatally. The sexes are equally affected. They are unifocal and commonly involve the trunk, shoulder girdle, thigh, perineum or retroperitoneum, and less commonly, the head and neck region.[13],[14]

Pathogenesis of KHE is not inherited, researchers are still studying the cause of these rare tumors.

Clinical features

Clinically, it usually appears as deep, reddish-purple, firm, and warm to touch. The skin is often shiny and tense. There may be tiny purple or red spots and a bruise-like discoloration near or around the lesion. In rare cases, KHE can present without thrombocytopenia or coagulopathy.[13],[14]

Histopathologic features

KHE's histopathologic picture shows both vascular and lymphatic components consisting of irregular infiltrating nodules of compressed vessels.[10],[13]

Pyogenic granuloma

Pyogenic granuloma is a common vascular tumor that appears either spontaneously or after trauma. Pyogenic granulomas are commonly seen on the gingiva, where they are presumably caused by calculus or foreign material within the gingival crevice. Hormonal changes of puberty and pregnancy may modify the gingival reparative response to injury, producing what was once called a “pregnancy tumor.”

Clinical features

These lesions clinically are red, pedunculated nodules that frequently bleed spontaneously.[13],[14]

Histopathologic features

Histologically, it is similar to IH, however, in general, with smaller dimensions.[10],[13]

Angiofibroma

Angiofibromas are uncommon and constitute <1% of all head and neck tumors. They occur exclusively in young males between 10 and 25 years of age. The site of origin of this tumor is thought to arise from nasopharynx or take origin in the pterygopalatine fossa in the recess behind the sphenopalatine ganglion, at the exit aperture of pterygoid canal. The pathogenesis of this lesion remains uncertain and unclear. The predilection of juvenile angiofibroma (JA) for young adolescent males led to a suggested interrelationship between hormones and JA.[13],[15]

Clinical features

Clinically, it usually presents with unilateral nasal obstruction, epistaxis, and nasopharyngeal mass.[13],[15]

Histological features

Histologically, it is characterized by the presence of a collagenized vascular stroma containing numerous, irregularly shaped blood vessels lacking elastic fibers in their wall.[10],[13]


  Vascular Malformations Top


Vascular malformations arise from an error in morphogenesis in any combination of arterial, venous, and lymphatic vascular networks. These vascular anomalies present at birth, grow proportionally to the size of the child, and do not exhibit any tendency to involute spontaneously. Trauma, puberty, and pregnancy can also cause accelerated growth. The great majority of congenital vascular malformations are recognizable in childhood.[7] Their incidence is 1.5%, approximately two-thirds are predominantly venous, and they are evenly distributed according to sex and race.[7] They are considered diffuse or localized defects in embryonic development and have been traditionally attributed to sporadic mutations. However, recent evidence points to a possible familial hereditary component.[7]

Capillary malformation

(previously called port-wine stain, capillary hemangioma) capillary malformations (CMs) have an equal sex distribution; the birth prevalence is reported to be 0.3%, the cutaneous discoloration is often, but not always, evident at birth.[5],[16] Facial CMs often occur in a dermatomal distribution. Forty-five percent of facial port-wine stains are restricted to one of the three trigeminal dermatomes, while 55% of the facial CMs overlap sensory dermatomes, cross the midline, or occur bilaterally.[17]

Pathogenesis

The pathogenesis of the CMs is thought to be at least part of an abnormal neural regulation process. It is suggested that defect lies in the maturation of the cutaneous sympathetic innervations causing vasodilatation. Mutation of RASA1 gene which regulates Ras/MAP kinase pathway involved in vascular development and cellular apoptosis is also a suggested cause of this malformation.[18]

Clinical features

Early stains are usually flat and pink. As the child matures, as the vasculature dilates, the CM may evolve into a raised, thickened plaque. The CM becomes deep red to purple. Lesions may become studded with vascular papules, imparting a cobblestone-like appearance. The area of skin affected grows in proportion to general growth.[5],[7]

This malformation is often associated with Sturge– Weber syndrome More Details. This syndrome consists of a facial CM with eye disease (choroidal vascular malformation, glaucoma buphthalmos) and neurologic disease (leptomeningeal venous malformations [VMs], seizures, hemiparesis, etc.).[19],[20]

Histopathologic features

Histologically, there are numerous dilated capillary or venule size structures present in the dermis.[6],[13]

Venous malformations

VMs are the most common type of vascular malformation, previously termed as cavernous hemangioma. They are composed of thin-walled, dilated, sponge-like channels of variable size and mural thickness with normal endothelial lining and deficient smooth muscle. Venous anomalies are common in the skin and subcutaneous tissue of the head and neck region, particularly in the lips and cheeks.[5],[8]

Pathogenesis

The pathogenesis of this malformation is due to mutation in angiopoietin receptor (TEK). These mutations lead to loss of function of TIE2 receptor (tyrosine kinase receptor).[21]

Clinical features

It is a soft, compressible nonpulsatile mass with rapid refilling. Expansion will occur on compression of the jugular vein or Valsalva maneuver or with the head in a dependent position. These lesions grow proportionately with the child and tend to expand following puberty, trauma, or attempted subtotal excision. Sluggish flow and stasis lead to phlebothrombosis, which presents clinically as recurrent pain and tenderness.[5],[7] VMs can occasionally be completely intraosseous and the mandible is the most common bone involved, although maxillary, nasal, and frontal lesions have also been reported. It is thought that most lesions that are described as “intraosseous hemangiomas” are in fact VMs.[5]

Histological features

Histologically, VMs are characterized by enlarged vein-like channels of variable size with thin walls because of the lack of smooth muscles.[6],[13]

Lymphatic malformation

Lymphatic malformations (LMs) are rare, slow-flow, congenital vascular malformations comprising malformed lymphatic channels that are forming cysts. LM can be macrocystic, previously termed as cystic hygroma; microcystic, previously termed as lymphangioma; or mixed.[5],[7],[22] The head and neck area is the most common site of LMs. LMs usually enlarge slowly over time, but abrupt enlargement may occur in cases of infection or internal hemorrhage.[5],[7],[23]

Pathogenesis

The etiology of LM is not exactly known, but presumably involves the failure of embryonic lymphatic systems to adequately separate from or to connect to the venous system. The mutation in the vascular endothelial growth receptor 3 as well as TIE2/TEK (tyrosine kinase receptor) has also been implicated in LM.[23],[24]

Clinical features

The clinical appearance of these lesions varies according to the size, depth, and site of the lesion. Often, multiple translucent vesicles containing a viscous fluid are present at the level of the skin or mucosa, which resembles “frog spawn.” The surrounding skin is normal, sometimes with a bluish hue. The surface lesions are connected to deeper cisternae for lymph fluid lying in the subcutaneous or submucosal tissue. Microcystic lesion is characterized by comparatively firm lesions with poorly defined edges and massive generalized edema, mostly affecting floor of mouth, jugal mucosa, and tongue.[23] Macrocystic lesion is commonly found in the supraclavicular fossa of the posterior triangle of the neck and in the cervical area just below the angle of the mandible. These lesions are painless, nonpulsatile masses with rubbery consistency that are covered by normal-colored skin.[23] The complications include infection, bleeding, obstruction of the airway, disturbances of speech, and abnormal facial growth. Hypertrophy of both soft tissue and skeleton is common and occurs in up to 83% of the cases.[5]

Histological features

Histologically, it is characterized by thin-walled vessels and cysts with lumina that appear empty.[6],[13]

Arteriovenous malformations

Arteriovenous malformations (AVMs) are localized, extensive high-flow malformations. Intracranial AVM is the most common, followed by extracranial head and neck, extremity, truncal, and visceral site.[7],[19] Although AVMs are present at birth, clinical presentation is usually delayed and lesions may present in the second, third, or even fifth decade.

Pathogenesis

The etiology of AVM is because of the failure of regression of arteriovenous channels in the primitive retiform plexus. AVMs may grow, usually secondary to the development of collateral channels for blood flow. Sporadic and familial genetic mutations have been also implicated in AVM.[21],[25]

Clinical feature

The clinical presentation depends on the extent and size of the lesion and can range from an asymptomatic birthmark to congestive heart failure. Oral lesions are more common on the gingiva, causing mobility of teeth and profuse periodontal bleeding.[26] Lesions close to the surface may produce a palpable thrill or pulsation. They are firmer than VMs and do not empty readily when they are compressed. Schobinger divided the development of AVM into four stages: (i) Quiescence: characterized by pink violaceous macule and arteriovenous shunt detectable by echo-Doppler ultrasound; (ii) expansion: As in stage I, and pulsatile red macule with obvious presence of tortuous vessels; (iii) destruction: As in stage II, dystrophic skin changes, ulceration, bleeding, continuous pain; (iv) decompensation: As in stage III, heart failure.[19],[26],[27]

Histological features

Histologically, it is characterized by dysplastic arteries that drain into arterialized veins forming a vascular nidus in AVMs by passing capillary bed.[6],[13]


  Investigations Top


Diagnosis of most vascular lesions is made by the use of accurate terminology of lesion, detailed clinical history (time of appearance, presence of precursor lesion, growth pattern, and involution) and physical examination of lesion. Special investigations such as imaging modalities in the form of Color Doppler-ultrasound, magnetic resonance imaging (MRI), computerized tomography (CT), phlebography, nuclear imaging studies, single photon emission CT, and multiplanar computed angiography help diagnose and distinguish vascular lesions.[5],[7],[27],[28] MRI is the investigation of choice as it provides accurate information about the extent of the lesion, better contrast between the lesion and surrounding tissues, and has multiplanar capabilities. It can also help distinguish between the different types of vascular anomalies. It provides anatomic and physiologic information noninvasively with the use of nonionizing radiation from the radiofrequency band of the electromagnetic spectrum. MRI depends on the properties of nucleus. MRI is commonly performed without a gradient echo sequence (GRE) or without the intravenous administration of contrast material. Fat-suppressed T2-weighted images are mainly used to evaluate the extent of the abnormality; GRE images are used to identify the hemodynamic nature of the condition (high vs. low flow lesion), and contrast-enhanced images are used to determine the extent of the malformation and to distinguish slow-flow vascular anomalies (VM vs. LM)[6],[7],[27],[28] [Table 2]. Contrast-enhanced CT has a role in evaluating intraosseous lesions and the bony margins of extensive lesions that are under consideration for resection, but this modality is ill-advised in children owing to radiation risk. Gray-scale ultrasound and color Doppler analysis are useful in defining whether the lesion is solid or cystic and to establish the presence or absence of high-flow vessels [5],[7],[27],[28] [Table 2]. Angiography is usually reserved for therapeutic endovascular interventions. Angiography includes arteriography, venography, and direct intralesional contrast agent injection. Arteriography is used for the evaluation of high-flow vascular lesions. Arteriography has no diagnostic value in the assessment of low-flow lesions.[5],[7],[26],[27] Nuclear imaging techniques can be used for the study of congenital vascular malformations.[7] This technique provides functional information of the lesion.[7] Immunohistohemical studies after scapel biopsy also help in distinguishing vascular malformations from hemangiomas. This technique have shown that IH is Glucose transporter (GLUT) -1 positive while CH, Vascular Malformations are negative for GLUT -1 protein. In contrast to hemangiomas, vascular malformations do not express proliferating cell nuclear antigen, VEGF, fibroblast growth factor (FGF), type IV collagenase, and urokinase.[2],[4],[11]
Table 2: Key imaging features of most common vascular lesions of head and neck

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  Treatment Top


Treatment of vascular lesions is often very complex, and consensus should be reached among a broad group of specialists. There are various treatment modalities and guidelines for the management of hemangiomas and vascular malformations depending on the stage and type of lesions; each has its pros and cons and is under incessant renewal.[29] Most hemangiomas do not require any treatment and only need close observation to ensure that complications do not arise.[24] Corticosteroids are the first line of treatment for alarming or potentially endangering hemangiomas and may be administered systemically, intralesionally, or topically.[2],[19],[29],[30] The response rates may vary and correlate with the proliferative rate of the lesion as well as anatomic site. Normal starting dose begin at 2–3 mg/kg/day of prednisolone followed by the tapering of dose gradually once the adequate response is obtained.[31] If the lesion does not respond to corticosteroids, vincristine or IFN-α-2b can be used as a second line of treatment.[2],[29],[30] Laser therapies are also effective for treating superficial and deep hemangiomas. These lasers cause vessel wall damage through destruction of hemoglobin while minimizing injury to adjacent structures. Superficial lesions with small and intermediate size vessels can be treated successfully with pulse dye laser whereas larger vessels with deep hemangiomas can be treated with neodymium:yttrium aluminum garnet laser. Tissue necrosis and scarring are often observed by uncritical use of lasers. Surgical excision of lesion should be considered when there is threat to life or function, complicated course, failure of pharmacotherapy, cosmetic revision of scars after lesion involution, atypical growth, or emotional burden.[2],[5],[7],[29] Treatment of other vascular lesions such as KHE is treated first by systemic corticosteroids followed by vincristine or IFN. All these therapies are less effective in treating KHE than hemangioma.[19] The treatment of pyogenic granuloma is curettage, shave excision and laser phototherapy, or full-thickness excision.[19]

The current management techniques of CM are cosmetic camouflage, laser therapy followed by excision, and grafting, and for VMs, they are elastic compression, sclerotherapy, and surgical resection or a combined approach.[5],[19],[28],[29] Sclerotherapy is used to reduce the size of lesion or preoperatively as a support to surgery. There are many types of sclerosing agents used to destroy the vascular endothelium through different mechanisms: chemical agents (iodine or alcohol), osmotic agents (salicylates or hypertonic saline), detergents (morrhuate sodium, sodium tetradecyl sulfate, polidocanol, and diatrizoate sodium), and anti-cancer drugs, which change the surface tension of the cell, producing tissue maceration.[29],[32] Sclerotherapy induces inflammation and thrombosis of the lesion, leading to fibrosis and shrinkage of lesion. Ethanol is recognized as the most effective sclerosing agent in the treatment of VM. Surgery is indicated in well-circumscribed malformations of moderate size, in which possibilities of anatomic and functional restoration are maximal. Surgical treatment of more extensive lesions can often lead to loss of motor function, nerve damage, and massive bleeding.[29],[32] Embolization and surgery are the treatment choice for AVMs. Goal of surgery in AVMs is to completely remove the lesion while maintaining control of hemorrhage and to reconstruct the defect to a functional and esthetic level.[5],[19],[27],[29] The treatment options for LMs include surgery, sclerotherapy, and laser therapy. Surgery remains the mainstay or even the only treatment choice and still remains the first choice in the hands of many surgeons.[5],[19],[29] Macrocystic lesions, on the other hand, are more localized and respect tissue planes and are more easily excised compared to microcystic lesion. Diffuse microcystic lesions are more difficult and may require multiple operations. Superficial oral mucosal microcystic LMs can be treated with laser therapy. Sclerotherapy may be an effective treatment for macrocystic lesions.[5],[19],[29]

Each vascular lesion case should be managed on its merits after careful discussion and counseling. An individualized treatment protocol should be made based on the condition of the patient and the technical availability. Most often, application of a multidisciplinary approach will achieve the best results when planned well and implemented.[29]


  Conclusion Top


Vascular lesions are thus the disorders of aberrant angiogenesis, vasculogenesis, or lymphangiogenesis.[31] It is utmost important that academicians/clinicians should have knowledge regarding outdated term, confusing terminologies, and clinical appearance of various vascular lesions to diagnose them accurately as each vascular lesions require different treatment modalities.[2],[5],[6],[7],[33] Although a great deal of progress has been achieved in this regard, there remains much to be accomplished to understand regarding its pathogenesis and target-specific therapy of these lesions to improve the quality of life.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
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    Tables

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  In this article
Abstract
Introduction
Classification
Vascular Tumors
Vascular Malform...
Investigations
Treatment
Conclusion
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