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3]

Review Article

Vascular Lesions of Head and Neck: A Literature Review

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

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.

Key words: Arteriovenous malformation, capillary malformation, hemangioma, lymphatic malformation, venous malformation

Introduction tumors present. This led to the misconception that most of these
lesions spontaneously disappear within the 1st year of life. As
Vascular lesions are localized structural defects of the
a consequence, congenital vascular malformations were often
vasculature. The clinical presentation of vascular anomalies is
misdiagnosed and left untreated.[2] Mulliken and Glowacki, in
confusing because all lesions appear in the color spectrum of
1982, introduced a simple classification based on the clinical,
blue, pink, and red. Unfortunately, the same word has been used
histochemical, and cellular criteria to distinguish various
to describe the entirely different vascular lesions. For example,
vascular anomalies which provided framework for the proper
“hemangioma” has been a generic term for various vascular
identification of these lesions and was later on adopted in
lesions with distinctive natural histories and differing etiologies.
1996, as an official frame by the International Society for the
Port‑wine stain, a lesion that never regresses, has also been
Study of Vascular Anomalies (ISSVA).[3,4] They described two
classified as a “capillary hemangioma.” This has led to improper
distinct entities ‑ hemangiomas and vascular malformations.[3]
diagnosis, illogical treatment, and misdirected research.[1] The
They classified the different types of vascular malformations
purpose of this article is to summarize classifications, and to
according to the type of involved vessels present. These may
point out the differences between various important vascular
be single vessel forms (capillary, arterial, lymphatic, or venous)
lesions affecting head and neck region based on its etiology,
or a combination.[3,4] The subsequent modification was carried
clinical presentation, and treatment modalities.
out in 1999 to classify the vascular lesions based on depth
of the lesion, predominant vessel type, and characteristics
Classification of the flow of lesion.[5] This classification was proved to be
The first classification of vascular lesions was developed by clinically useful and correlated well with the pathological and
Virchow (1863) and his student Wegener (1877). Based on the radiological data.[5] Malformations with an arterial component
microscopic appearance of vascular lesions, they separated all are rheologically fast‑flowing lesions while others are
vascular tumors into angiomas and lymphangiomas, which
were then characterized as “simplex,” “cavernosum,” and Address for correspondence: Dr. Nazia Masoom Syed,
Department of Oral Medicine and Radiology, Institute of Dental Sciences,
“racemosum.” After this, many different classifications were
Sehora, Kunjwani Bisnah Road, Jammu, Jammu and Kashmir, India.
presented that use anatomical labels or descriptive terms E‑Mail: dr.syednaziamasoom@gmail.com
without regard to the biological behavior of the various vascular

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DOI: How to cite this article: Syed NM. Vascular lesions of head and neck:
10.4103/0976-4003.191726
A literature review. Indian J Dent Sci 2016;8:176-82.

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Syed: Vascular Lesions of Head and Neck

slow‑flowing lesions.[5] The ISSVA society further modified theories suggest that hemECs’ response to extrinsic defects
the biological classification in their continuing workshop and is presented in the local environment. A balance between
divided vascular lesions into vascular tumors and vascular intrinsic and extrinsic factors and between stimulators and
malformations[6] [Table 1]. inhibitors of angiogenesis factors might account for the rapid
growth and slow involution of IH. A  number of stimulator
Vascular Tumors factors that act on ECs include local tissue environment
hypoxia or acidity, vascular endothelial growth factor (VEGF),
Hemangioma basic fibroblast growth factor, matrix metalloproteinases‑9,
Hemangioma is a benign lesion of a hamartomatous growth
intercellular adhesion molecule‑3, monocytes chemoattractant
of capillaries with a high proliferation index. Hemangiomas
protein‑1, E‑selectin and angiogenesis inhibitors that act on
are categorized into infantile hemangioma (IH) and congenital
ECs that include proteins such as angiostatin, platelet factor‑4,
hemangioma (CH). IH is subcategorized depending on the site
thrombospondin‑1, interferon‑α  (IFN‑α), tissue inhibitor of
of its occurrence as focal, segmental, and indeterminate, and
metalloproteinases, and plasminogen activator inhibitors.[7‑9]
also depending on the depth of the lesion from the skin surface
as superficial (previously called capillary hemangioma), Clinical features
deep (previously called cavernous hemangioma), and Initially, the lesion clinically appears as circumscribed area of
mixed (capillary cavernous hemangioma). CH is further discoloration or telangiectasia of facial skin. IH may clinically
subcategorized into rapidly involuting CH  (RICH) and show scaring, wrinkling, telangiectasia, or loose fibro‑fatty
noninvoluting CHs (NICHs).[5,7] tissue at the site of their clinical appearance. Focal IH is the
Infantile hemangioma most common variant, appearing as localized raised tumor‑like
IH is not present at birth and arises during the first 8 weeks of lesion that tends to occur at the area of embryological fusion.
life. IH is a true benign neoplasm of endothelial cells (ECs) Segmental IH is flat plaque‑like larger lesion that shows a
with a unique biological behavior of high proliferative phase geographic segmental distribution, and indeterminate IH shows
for 6–12 months followed by a gradual involution phase the characteristics of both focal and segmental IH. Color of the
and a spontaneous regression by the age of 5–9 years.[7] The IH varies with the depth of the lesion and they can be bright
incidence in the general newborn population is between 1.1% red (superficial), purple, blue, or normal skin color (deep).[7]
and 2.6%, but increases up to 12% by 1 year of age.[7] It occurs Histopathologic features
more often in females compared to males and is also more Histologically proliferating IH is characterized by
prevalent in premature infants.[8] nonencapsulated masses and dense cords of mitotically
Pathogenesis active plump ECs with pericytes whereas involuting IH is
Various theories suggest that the pathogenesis of IH is characterized by enlarged vascular lumina with flattened ECs.
related to an intrinsic defect of hemangioma ECs (hemECs): Involuted phase of IH has more dilated vascular spaces with
Clonality of hemECs, somatic mutation of single progenitor adipocytes, fibrous deposits, and with few remaining vessels.[10]
cell, and loss of heterozygosity to chromosome 5q. Other
Complications
Depending on the size and location of the hemangioma, many
Table 1: Classification of Vascular lesions serious problems can ensue. Eyelid IH can cause deprivation
amblyopia, a subglottic IH can compromise the airway, and
Vascular tumors Vascular malformations
extremely large IH can cause high‑output congestive heart
IH Slow (low) flow
CH
failure.[7,8] Some IH ulcerate and bleed, which then requires
RICH CM
transfusion and/or surgery. Infants with large segmental facial
NICH VM hemangiomas are at a risk of having PHACE syndrome. PHACE
KHE LM refers to posterior fossa brain abnormalities, hemangiomas,
Angiofibroma Fast (high) flow arterial malformations, coarctation of the aorta and other cardiac
Spindle cell hemangioendothelioma. AVMs defects, as well as eye abnormalities. Ectopic expression of type 3
Tufted angioma Arteriovenous fistula iodothyronine deiodinase in IH has been shown to inactivate
Pyogenic granuloma and other Arterial malformations thyroid hormone systemically and cause hypothyroidism.[7,8]
dermatologic‑acquired tumors
Others, rare hemangioendothelioma Complex/combined Congenital hemangioma
(epithelioid, composite, retiform, malformations (various CHs have been recognized for years. More recently, these
polymorphous, Dabska tumor, combinations of the above) lesions have been found to be biologically distinct from the
lymphangioendotheliomatosis, etc.)
IH. IHs appear more common (70%) than CH (30%).
RICH: Rapidly involuting congenital hemangioma, NICH: Noninvoluting
congenital hemangioma, Capillary malformation, VM: Venous
malformation, LM: Lymphatic malformations, IH: Infantile hemangioma,
Clinical features
CH: Congenital hemangioma, KHE: Kaposiform hemangioendothelioma, CH clinically presents as fully developed lesions at birth
AVMs: Arteriovenous malformations which either rapidly involutes during the 1st year of life or

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Syed: Vascular Lesions of Head and Neck
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]
178
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
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
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Syed: Vascular Lesions of Head and Neck
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. 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,
Indian Journal of Dental Sciences  ¦  2016  ¦  Volume 8  ¦  Issue 3
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
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Syed: Vascular Lesions of Head and Neck
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
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
180
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]
Treatment
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
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Syed: Vascular Lesions of Head and Neck
Table 2: Key imaging features of most common vascular lesions of head and neck
US with CDUS
IH Hyperechoic or hypoechoic
Hypervascular on CDUS
RICH Central, nonenhancing, hypodense, hypoechoic, more
robust feeding vessels with larger diameter than IH
NICH Almost similar to IH
VMs Solid echogenic mass with phleboliths, often multispacial
and compressible. Low flow or monophasic or no flow
on CDUS
LM Variable multicystic, multispacial masses, with or without
fluid and debris levels. No flow pattern on CDUS
AVM Clusters of vessels with no intervening well‑defined
mass. High flow (arterial flow) on CDUS. Arterial
and venous signals from vessels in the lesions with
arterializations of venous structure
US: Ultrasound, CDUS: Color Doppler ultrasound, MRI: Magnetic resonance imaging, T1W: T1‑weighted, T2W: T2‑weighted, IH: Infantile hemangioma,
RICH: Rapidly involuting congenital hemangiomas, NICH: Noninvoluting congenital hemangiomas, VMs: Venous malformations, LM: Lymphatic
malformation, AVM: Arteriovenous malformation
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
Vascular lesions are thus the disorders of aberrant angiogenesis,
vasculogenesis, or lymphangiogenesis. [31] It is utmost
Indian Journal of Dental Sciences  ¦  2016  ¦  Volume 8  ¦  Issue 3
MRI
Iso‑to‑intermediate signal on T1W, bright signal on T2W, high
intensity flow enhancement on gradient echo, internal flow voids,
vigorous enhancement after contrast administration
T2W hyperintense component is quite prominent
Almost similar to IH
T1W heterogeneous intermediate signal, no flow voids, T2 fast
spin echo fat‑saturated or short T1 inversion recovery high‑signal
intensity, T1W spin echo postgadolinium enhancement
T1W low to intermediate signal intensity, T2W high‑signal intensity,
T1W postgadolinium: no enhancement except with in septa
T1W and T2W sequences show serpiginous signal voids without a
focal mass
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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Indian Journal of Dental Sciences  ¦  2016  ¦  Volume 8  ¦  Issue 3