vascular lesions

1. DR.DAVIS NADAKKAVUKARAN M.D.S.
SENIOR LECTURER
DEPT. OF ORAL & MAXILLOFACIAL
SURGERY
MALABAR DENTAL COLLEGE MANOOR
Vascular Lesions
of Head & Neck

2. Content
 INTRODUCTION
 CLASSIFICATION
 EMBRYOLOGY
 HEMANGIOMA
 VASCULAR MALFORMATIONS
 COMPLICATIONS
 TREATMENT
 CONCLUSION
 REFERENCES

3. CLASSIFICATION
Anatomicopathological
Classification:Virchow-1863
 Angioma Simplex
 Angioma Cavernosum
 Angioma Racemosum
Wegner (1876-1877)

4.  Bilogical Classification :Mulliken &
Glowacki 1982
 Hemangiomas
Proliferating
Involuting
 Malformations
Capillary
Lymphatic
Venous
Arterial
Combined

5.  International Society For The Study Of
Vascular Anomalies ;1996
Tumors
•Juvenile hemangioma
•Rapidly involuting congenital hemangioma
•Non involuting congenital hemangioma
•Kaposiform hemangioendothelioma
•Tufted angioma
Vascular malformations
•High-flow Arteriovenous malformation
•Low-flow Venous malformation
•Lymphatic malformation
•Lymphatic-venous malformation
•Capillary (or venular) malformation (portwine stain)

6. Haemangiomas And Vascular Malformations Of The Maxillofacial Region-
a Review.
Bjoms2005;2291-2300
Haemangiomas
Superficial
Deep
Compound
Vascular Malformations
Simple Lesions-
•Lowflow
•High Flow
Combined Lesions
•AVM
•LVM
•Other Combinations

7. Hemangiomas Malformations
Benign tumour Congenital abnormality
30% visible at birth, 70% during first few
weeks of life
Present at birth, may not be evident until
months & years
Female predilectopn 3:1 No gender predilection
Rapid post natal growth followed by slow
involution
Slow steady growth, with no involution
Endothelial cell hyperplasia Normal turnover
Increased mast cells Normal
Multilaminated basement membrane Normal thin basement membrane
No coagulation abnormalities Primary stasis, localized consumptive
coagulopathy
Mass effect on adjacent bone-infrequent Hypertrophy, bone destruction
80-90% respond to steroids No response
Seminars in Pediatric Surgery (2006) 15,124-

8. PRESENT AT BIRTH
YES-VM
NO-H
RAPID
PROLIFERATION
YES-H
NO-VM
INVOLUTION
YES-H
NO-VM
PRESENT IN
ADULTHOOD
RESIDUAL
HAEMANGIOMA
VASCULAR
MALFORMATION
WANER &SUEN
DIAGNOSITIC APPROACH
Haemangiomas And Vascular Malformations Of The Maxillofacial Region-a Review.
Bjoms2005;2291-2300

9. HEMANGIOMA

10. Epidemiology
 It is the most common tumor
of infancy.
 However in premature infants
with low birth wgt it occur
more frequently during first
year of life.
 80% solitary,
head/ face most
common site
 F:M =3:1

11. FIRST SIGN
 Fully grown hemangioma is seen at birth.
 The initial sign is is either erythematous macular
patch,a blanched spot,or localised telangiectasia.
 It will grow as single localized tumor or simultaneously
in multiple sites anywhere in the body.
 The hallmark of hemangioma is rapid neonatal growth

12. Clinical differential dignosis
 Patient history
 Hemangioma grows rapidly,beginning in the first week
affter birth,at a rate beyond that of infant.
 Vascular malformation may or may not be noted at
birth.once detected they expand commensurately with
the child.
 Palpation is also helpful-
Hemangioma -firm and rubbery,and blood contained
within tumor cannot be evacuated by pressure
Vascular malformation-soft,easily compressible and
rapidly emptied of blood by digital pressure

13. Differential diagnosis
Portwine stains
 Present since birth & stay flat
Spider angiomas
 Tiny on face & hands
Pyogenic granulomas
Occur in >1 year old & bleed

14. 14
 Life cycle consists of 2 phases :
Proliferation stage
Involution stage

15. Phases
1. Proliferation : 1-10 months
 Most rapid 1-4 months
 Complications occur in
this phase

16. Clinical Features- proliferative phase
16
 Most manifest during 1st-4 weeks of life.
 Initial sign is either an erythematous
macular patch, a blanched spot, or
localized talengiectasia surrounded by a
pale halo.
 May grow as a single localized tumor or may
simultaneously proliferate in multiple sites
anywhere in body.
 The hallmark of hemangioma is rapid
neonatal growth.
• If cellular proliferation is in superficial dermis, the skin becomes
raised and bosselated with a vivid crimson colour.
• Most superficial hemangiomas can be diagnosed by clinical examination
and a detailed and accurate history.

17. Proliferation
17

18. 2. Involution: After 6-10 months
 Soften, grey surface
 50% involution by age 5
 90% involution by age 9
Involution

19. Clinical Features- Involution phase
19 After a period of rapid growth, hemangioma
stabilize with time, growing at same rate as the
child.
 First sign of regression is fading of the shiny
crimson surface to a dull purple hue.
 Lesion is less tense to palpation.
 When child cries lesion does not swell.
 By age of 5 years last traces of color are fading.

20. 20

21. Complications
 Ulceration
 Infection
 Visual impairment
 Airway obstruction
 Congestive heart failure
 Kasabach -Merritt syndrome
 Posterior fossa defects
 Skeletal distortion

22. Ulceration
 It is more common in the lips
and the anogenital area.
 Secondary infection invariably
accompanies ulceration.
 Topical antibiotics
 Oral antibiotics; analgesics
 Pulsed dye laser
 Oral prednisone (2mg/kg)

23. Visual impairement
 Obstruction of the visual axis
causing deprivation amblyopia and
failure to develop binocular vision
is the best known example of a
hemangioma impinging on a critical
anatomic location.
 Oral prednisone
 Intralesional steroids
 Pulsed dye laser if early
 Elliptical surgical excision
 Referral to ophthalmology
 Late complication of the periorbital
hemangioma include globe
proptosis ,asymmetric refractive
error,and optic atrophy

24. Airway obstruction
 Hemangioma growing within the
nasal tip may block the vestibular
passages during the first three
month of the life when the infant is
an obligatory nose breather.
 Hemangiomatous proliferation in
the subglottic airway is insidious
and potentially life threatening.
 Infants are asymptomatic at birth
but within 6 mnth thy develop
stridor and respiratory distress
 Direct laryngoscopy for stridor
 Surgical excision

25. Auditory
 Hemangioma of the parotid region may obstruct the
external auditory canal,causing mild to moderate
conductive hearing loss.
 The blockage is relieved with regression of the
tumor.
 This is the potential problem if there is bilateral
obstruction ,persisting beyond 1 year of age,when
auditory conduction is necessary for normal speech
and development.

26. Posterior fossa defects
PHACE
 Posterior fossa
malformation
 Hemangioma
(segmental)
 Arterial anomalies
 Cardiac anomalies
 Eye defects

27. Vascular Malformations
27
 Vascular malformations are present at birth and unlike
hemangiomas, do not go through a a “rapid proliferative phase” and
they do not “involute”.
They grow commensurately with the patient.
 Approximately 31% of these malformations are found in the
head and neck region.
 Vascular malformations are thought to “result when there is
interruption at a particular stage of development of a vessel”.
 The type of vascular malformation that results depends on the
stage at which normal morphogenesis is interrupted.

28. Development of Vascular Malformations
28
 Blood vessels form as the result of series of steps.
 First stage: ENDOTHELIAL stage, multiple endothelium lined lakes are
formed.
 Second stage: RETIFORM stage, capillary communication develops
between these lakes.
 Some of these interconnecting channels have muscular sheaths and
others do not.
 Final stage: MATURATION stage, channels that have muscular lining
differentiate to become arteries and those without muscle become
veins.
 Abnormal development of either arterial or the venous side
of vascular network during this phase of development may
result in vascular malformation.

29. 29
 Trauma, infection, and hormonal fluctuation
(pregnancy or puberty) may stimulate increased
growth of the vascular malformation.

30. Venous Malformations - Low-flow
lesions
 Venous malformations are bluish, soft and easily
compressible, and auscultation reveals no bruits.
 The clinical absence of “pulsations or a thrill”
generally indicates a low flow Venous vascular
malformation
 Most of the VeM that are sequestered from the main
vessel undergoes a spontaneous continuous cycle of
thrombosis and thrombolysis, and these thrombus
may undergo calcifications to form phleboliths that
become painful on palpation and could be a radiologic
marker for these type of malformations
30

31. Venous Malformations – Phleboliths
31
.
Phleboliths that may be noted on radiographic examination are
found only in low flow lesions.

32. Capillary Malformations ( portwine stain)
32
appear as reddish-pink macules over facial dermatomes may be smooth initially but
become more “ pebble – like” as the patient grows.
In older classifications these malformations are denominated as Capillary
Malformations, while in 1999 Waner and Suen based on their identification of the
anomalies of these lesions in the post-capillary venules (rather than in the
capillaries) re-categorized them as Venular Malformations

33. Lymphatic Malformations - Low- flow
lesions
33
 Obstruction or sequestration of the primitive lymphatic
vessels during embryogenesis produce ectopic
lymphatic systems, and the resulting failure of drainage
from these areas lead to increase in intravascular
pressure and LMs.
 Within the oral cavity the LMs are more commonly
found on the anterior 2/3 of tongue, followed by
palate,gingiva, and oral mucosa.
 Predilection for head and neck and the axilla, where
embryonic lymph sacs are located.

34. Lymphatic Malformations
34
In the oral cavity appear as multiple
translucent non-compressible cysts or
vesicles of <2 cm.
containing viscous clear fluid,
producing a
pebbly or warty surface resembling
“frog
spawn” or “tapioca pudding”.
MICROCYSTIC LM ( Outdated
term Lymphangioma)

35. Lymphatic Malformations
35
Macrocystic LMs (outdated terms include lymphangioma
cavernosum,cystic hygroma, lymphangioma cysticum)
usually presents as multiple cysts of >2 cm
and are commonly found in the supra-clavicular fossa of the
posterior triangle of the neck, and in the cervical area just below
the angle of the mandible.
They clinically appear as localized painless non-pulsatile swelling
with
no bruit or thrill, having a rubbery
compressible consistency, and covered by
normal appearing skin unless hemorrhage or
communication with venous malformations
produce a blue discolouration.

36. Arterial / Arteriovenous Malformations (AVM) “High-flow
lesions”( outdated terms - cirsoid aneurysm,arteriovenous aneurysm)
36
 They represent a group of congenital malformations that
create a direct communication between the arterial and
venous systems.
 AVM is present at birth, but become clinically apparent
only during the 4-5th decade of life and is often
misdiagnosed due to delay in clinical presentation.
 The most common site for AVM is the brain, followed by
the head, neck, limbs, trunk, and viscera.
 The majority of the head and neck lesions occur on the
cheek, followed by the ear, nose, forehead and upper lip.

37. Arterial / Arteriovenous Malformations
 They appear as purple-blue raised painful macule, are
pulsatile with thrill and bruit, warm to touch,
 do not empty fully on compression, and refill quickly on
reliving digital pressure.
 They are associated with embolism, pain, bleeding,
ulceration, and congestive cardiac failure due to increased
cardiac load.
37

38. 38
 Often a patient presents with severe bleeding as the
first sign that a high flow-lesion is present. They may
also complain of recurrent gingival bleeding and loose
or depressible teeth.

39. Schobinger Staging of AVM
39
 Stage 1(Quiescence) : A blue-skin blush
 Stage2 (Expansion) : A mass associated with a
bruit and a thrill
 Stage 3 (Destruction) :A mass associated with
ulceration, bleeding and pain
 Stage 4 (Decompensation) :lesions producing
heart failure

42. Associated syndromes:
42
 Rendu-osler-weber syndrome
 Sturge-weber syndrome
 Kasabach-merritt syndrome
 Maffucci syndrome
 Klippel-Trenaunay –Weber syndrome

43. HEREDITARY HEMORRHAGIC TELANGIECTASIA
(Rendu Osler Weber disease)
43
 Congenital hereditary disease
 Skin lesion are discrete,spider like,bright
red maculopapules,usually 1-4 mm in
diameter and typically located on face,
tongue ,lips,nasal and oral mucous
membrane.
 Telangiectatic skin lesion may appear in
early childhood but more commonly they
become apparent after puberty and increses
with advancing age.
 Bleeding from telangiectasia in brain and
spinal cord can produce neurological
symptoms.

44. (Sturge-Weber syndrome) encephalotrigeminal
angiomatosis
44
 It is characterized by a congenital facial birthmark
and neurological abnormalities.
 This stain is a birthmark caused by an
overabundance of capillaries near the surface of the
skin
 It consists of congenital Hamartomatous
Malformations that may affect the eye, the skin,
and the central nervous system at different times.
Klippel-Trenaunay –Weber syndrome
Triad of cappilary malformations, bone
hypertrophy and venous malformations.

45. Kasabach – Merritt Syndrome
 Severe thrombocytopenia & hemorrhage
because of platelet trapping within the tumour
 Not associated with the common hemangioma of
infancy
 The overlying skin is deep red-purple in colour,
tense & shiny
 Ecchymosis appears over & around the tumour,
& there are generalised petechiae
 potentially fatal complication of rapidly growing
vascular lesions in infants

46. DIAGNOSIS
46
 History
 Clinical examination
 MRI
 Doppler Ultrasound
 CT
 Arteriography

47. 47
 Magnetic resonance images (MRI) may differentiate low-flow from high flow
lesions. The presence of fatty deposits, venous lakes, phleboliths in the MRI
are all indicative of low- flow lesions.
 CT scans document a lesion’s extension into the surrounding soft tissue.
 Doppler imaging can also distinguish high flow lesion from low flow lesions .
 If the lesion involves bone, then a “soap bubble” or a “honeycomb
appearance” is the usual radiographic finding.
 Contrast enhanced MRI and computed angiography are the
commonly used modality forevaluating vascular lesions

48. 48
MRI showing the extent of the high
flow lesion in temporalis muscle
Axial MRI shows arterio-venous malformation as
lobulated, high-signal-intensity mass (arrows)
Axial CT mandible shows arterio-venous malformation showing thinning of cortical
plates

49. DOPPLER ULTRASOUND
49
A Doppler ultrasound is a test that uses high frequency
sound waves (ultrasound) to measure the amount of
blood flow through arteries and veins. Vascular flow
studies, also known as blood flow studies, can detect
abnormal flow within an artery or blood vessel.
The ‘chaotic’ or turbulent flow results from the area being filled with numerous individual velocity
vectors randomly occurring in all directions.

50.  During Doppler ultrasound , a handheld device is
passed lightly over the skin above a blood vessel. The
device is called a transducer. It sends and receives
sound waves that are amplified through a
microphone. The sound waves bounce off solid
objects, including blood cells. The movement
of blood cells causes a change in the pitch of the
reflected sound waves. This is called the Doppler
effect. If there is no blood flow, the pitch does not
change.

51. ARTERIOGRAPHY
51
 An invasive diagnostic test that
uses x-rays to take pictures of
blood vessels.
 A long flexible catheter is inserted
through the femoral artery to
deliver dye (Iodine & Barium
compounds) into the arteries
making them visible on the x-ray.
 This test can help diagnose an
arteriovenous malformation,
tumor, clots, and arterial stenosis.

52. 52
 The catheter is advanced from
the femoral artery to one of
four arteries in the neck that
lead to lesion and tissues.
 80-90 ml of Contrast is
injected into the bloodstream
to make the blood vessels
visible on the monitor. The
result is a kind of roadmap of
the arteries.

53. 53
 The X-ray images taken may either be still images,
displayed on a image intensifier or film, or motion
images.
 The images are usually taken using a technique called
digital subtraction angiography (DSA).
 This technique "subtracts" the bones and other organs
so only the vessels filled with contrast agent can be
seen.
 Dyes used are –
Iohexol (Omnipaque 350)
Iopromide (Ultravist 370)
Iodixanol (Visipaque 320)
Diatrizoate (Hypaque 50)
Metrizoate (Isopaque 370)
Ioxaglate(Hexabrix)

54. 54
Digital subtraction
carotid angiogram showing an
arteriovenous malformation of the tongue
involving the lingual artery.
Arteriovenous malformation of the
tongue
Hemangiomas could be distinguished from vascular
malformations by the presence of a well circumscribed
mass demonstrating intense tissue staining, usually
organized in a lobular pattern

55. HISTORY OF TREATMENT
551. LIGATION AND EXCISION
 In 1714, Turner favoured surgical resection, ligation and
caustics for vascular birthmarks
 During 19th century, surgeons devised ingenious methods of
interrupting the vascular supply to a hemangioma using figure-
of-eight, spiral or inter-locking subcutaneous sutures
of catgut,wire or silk.
 Untill the natural involution of hemangiomas was fully
appreciated in 20th century, surgical excision continued to be a
primary mode of therapy.

56. 56
2. ARTIFICIAL ULCERATION
 The old observation that a hemangioma that ulcerates
goes on to heal, leaving skin of pale color, suggested that
artificially induced ulceration would work as well.
 A variety of astringents and caustics have been applied
to superficial hemangiomas – potash and lime, fuming
nitric acid, liquid arsenical, croton oil
 Efforts to freeze hemangiomas became popular
early in 19th century
 Carbon dioxide slush or solid CO2 crayon techniques
were once commonly employed

57. 57
3. ELECTROLYSIS AND THERMOCAUTERY
 A hot wire of silver or platinium were placed on
the hemangioma, or needles were inserted
subcutaneously prior to activation of a number of
batteries to adjust the voltage .
 Modern thermocautery units, with a needlepoint
attachment, were used to puncture deep hemangiomas
is called Endothermy Coagulation or to cause
surface coagulation .This modality is the antecedent of
today’s sophisticated laser technology.

58. 58
4. SCLEROSANT THERAPY
 Injection of “stimulating solutions” for treatment of
hemangiomas had its shadowy beginnings in 19th century :
Ergot (Hammond,1876), Tannic acid, Carbonic acid
(Bradley, 1876), Iron perchloride and 95% alcohol (
Holgate, 1889)
 In 20th century, sclerosant therapy continued with 5% sodium
morrhuate( Watson & McCarthy,1940) Quinine
hydrochloride, hypertonic saline(Andrews & Kelly, 1932),
Ethamolin (Mathews,1954) and Sodium Tetradecyl sulfate
( Walsh and Tompkins,1956)

59. 59
5. RADIATION
 Radiation for hemangiomas was remarkably successful
in 1930 to 1950 era.
 Several modalities were used :Interstitial gamma
irradiation and external beam radiation.
 Difficult to correct the late skin changes – atrophy,
contracture, pigmentation.
 The advent of the steroid therapy now limits the need
for radiation therapy.

60. 60
6. COMPRESSION
 Compression therapy can be traced to the early 19th
century.
 Pressure also was advocated by Forster (1860); for an
infant with a scalp hemangioma, he used a lead plate,
Plaster of Paris and Elastic bands applied for 6-8
weeks.
 There are contemporary reports of success from use of
compressive elastic garments for hemangiomas of
extremities (Moore 1964).
 Difficult to document the efficacy of any proposed remedy.

61. CURRENT MANAGEMENT
61
1. PRIMUM NON NOCERE
 Description of spontaneous involution of
hemangioma can be found scattered throughout
19th century medical literature.
 Lister (1938) published his prospective study, in
which he observed hemangioma in 77 children
and concluded: “No exception has been found to
rule out that naevi which grow rapidly during the
early months of life subsequently retrogress and
disappear of their own accord, on the average
about 5th year of life”.

62. 62
 Photographs and measurements should be taken during the initial visit to
document the subsequent changes.
 Monitor the growth and reassure the parents.
 By 6-8 months of age, when growth begins to plateau and early signs of
regression are seen and compared with earlier measurements and pictures.

63. 63
2. STEROID THERAPY
 In 1963 Serendipitous discovery was made, when a
large facial hemangioma began to shrink coincidently
with steroid administration for thrombocytopenia.
 Subsequently investigators confirmed that
Prednislone may hasten the onset and involution of
hemangioma.
 The response is reported to be in range of 30-90% .

64. 64
 Systemic steroid should be used only in selected infants
with hemangioma those with
a. Cervicofacial lesion causing distortion of features
b. Large lesion especially with recurrent bleeding,Ulceration, infection
c. Lesion interferes with physiological function.
d. Lesion complicated by high output cardiac failure
e. Lesion complicated by platelet depletion coagulopathy
 Prednisone is given 2-3 mg /kg/day for 2-3 weeks

65. 65
 Sensitive hemangioma shows results in 10 days.
 If steroid is responsive thn the dose should be
lowered to 1/kg/day or the infants given alternate
day regimen of the dose to 0.75mg/kg/day
 Usually ,prednisone is given for a cycle of 4-6 wks
followed by rest period.
 Rebound growth may occur due to reduced steroid
dosage in proliferating phase lesions, an additional
2-3 wk cycle of prednisone may be started at a
dosage of 1mg /kg/day or on alternate days.

66. 66
 Complication such as
 Decreased appetite
 Temporary retardation of growth
 Depress the T cell function and cause immunological abnormalities
 Otitis media
 Pneumonia
Thus it is advisable to use the lowest effective dose of
prednisone for the shortest time until the hemangioma
begins to regress.

67. 4. INTERFERON THERAPY
 Giant hemangiomas that have been unresponsive to
corticosteroid therapy have been successfully treated
using interferon therapy.
 Interferon therapy, which inhibits angiogenesis,
could be considered for life-threatening hemangiomas
due to its high success rate, although it is expensive,
burdensome, and possibly toxic. It is administered
subcutaneously and daily.
 Ezekowitz et al demonstrated 50% reduction in lesion
size in cases which were refractory to corticosteroid
therapy.

68. 4. LASER THERAPY
 Apfelberg (1981) & Hobby(1983) advocated the use of
Argon Laser treatment for hemangiomas in
proliferative phase.
 Argon Laser penetrates the skin, and the blue-green
light is absorbed by red cells within the hemangioma
and normal vessels in the papillary dermis. The
absorbed light energy is transformed into heat, causing
thrombosis or destruction of the vascular channels and
perivascular tissue.
Disadvantages – Thermal damage within the skin may
cause ulceration of the superficial portion of the
hemangioma; the end result is scar.
 persistence of deep hemangioma because currently available
argon lasers donot penetrate deeper than 1.5mm into the skin.
 Laser is useful in treating capillary dermal malformations

69. 5. OPERATIVE THERAPY
 If every hemangioma began as a localized nest of cells, the
ideal would logically be early excision before the tumor
extended into the surrounding dermis ( Modlin,1955; Andrews
et al,1957)
 It is usually best to wait untill the child is 8-12 years of age
before trimming the residual that exists after regression.
 There is usually sufficient extra skin remnant after involution
for linear closure.

70. Sclerotherapy
70Sclerosants : Boiling water , Alcohol, Sodium Morrhuate, Quinine, Silver
Nitrate and Iron or Zinc Chloride.
 A more appealing stratagem is direct injection of a Sclerosing solution into
the epicentre of the venous anomaly during occlusion of arterial inflow and
venous outflow.
 A liquid vegetable protein, Ethibloc has been used extensively; particularly
effective in obliterating AV and pure venous malformations.
 Other agents are – Sodium tetradecyl sufate, ethanol, hypertonic saline,
Surgical resection
 Total excision is the definitive treatment for a venous malformation.
 Resection is indicated to reduce bulk and improve contour and function.
VENOUS MALFOMATIONS

71. LYMPHATIC MALFORMATIONS
71 Several agents have been utilized for lymphatic malformations including
ethanol, bleomycin, and doxycycline.
 Several authors say LMs donot respond well to sclerosing agents, pressure
therapy, almost all are either tolerated well by the patient or treated
surgically.
 Infection should be treated aggressively with antibiotics , when indicated is
Surgical Excision.
 A well-localized cystic lymphatic anomaly can be dissected from surrounding
tissue.
 A lymphatic anomaly is not neoplastic. But it invades adjacent tissue,such as
muscle of lip or tongue.
 Surgery risks deformity or functional loss, nerve injury.
 It is not uncommon to excise a LM in 2/3 stages.

72. ARTERIOVENOUS MALFORMATIONS
72
EMBOLIZATION
Also known as Embolotherapy or Endovascular therapy.
 This procedure involves the injection of glue or other
non-reactive liquid adhesive material into the AVM in order
to block it off.
 For this purpose, a small catheter is passed through a groin
vessel all the way up into the blood vessels supplying the
AVM.
 Access is gained through a retrograde femoral approach.
Digital subtraction is used and the catheter is guided by
fluoroscopy.
 Embolization materials used are ethanol, Gelform, Steel coils
and wisps of cotton, polyvinyl alcohol, and isobutyl
cyanoacrylate.

73. 73
 Percutaneous embolization has been described using a 20-guaze
Seldinger needle inserted directly into the lesion through the
skin and thinned bone.
 Not all AVMs can be treated with embolization. AVMs are
carefully studied at the time of a preliminary angiogram by
highly skilled radiologists to determine if catheters can be
passed up into the AVM without any complications before they
are considered for embolization.
 COMPLICATIONS:
Arterial spasm, vessel rupture, necrosis, inadvertant
embolization of internal carotid artery, production of pulmonary
emboli due to escape of material through the lesion.

74. 74
 The goals of surgery are to completely remove the lesion while maintaining control
of hemorrhage, and to reconstruct the defect to functional and aesthetic level.
 An extraoral incision is preferable when the lesion extends proximally into the angle
or ramus; a transoral approach does not allow good visibility and rapid control of
haemorrhage.
 Smaller lesions can be unroofed and packed as removal is carried out.
RESECTION with immediate replantation( EXTRACORPOREAL
APPROACH)
 Resection of the mandible containing the lesion, and extracorporeal curretage and
extarction of teeth .
 An osteotomy can be made distal to the lesion, and the involved segment can then be
rotated laterally to allow direct visualization of lingual surface of mandible.
 The resected mandible can be modified to form an autologous tray for the bone graft.
 The hollowed mandible is packed with cancellous bone. The reimplanted mandible
and bone grafts are stabilized with plates.
 IMF is placed to assist in maintaining proper jaw position and for immobilization
during healing
SURGERY

75. 75
OPG Showing moth eaten
radiolocency (AVM) in left
mandibular parasymphysis region
Resected mandibular segment containing
focal lesion
Extracorporeal removal of teeth and
curretage of lesion
Reimplantation of mandibular
segmenr and stabilization with mini
plates.

76. History and
examination
Vascular
malformation
Hemangioma
MRI. Doppler,
Arteriogram
High flow Low flow
Embolize
Ablative
surgery
Observe
Excision ,
Laser,
Sclerosing
agents
Observe
Proliferation phase
Life threatening or
visual disturbance
Steroids
Control
Observe
Fail to
control
Interferon
Observe
Parent
education
Observe
Involution complete
No
residual
lesion
Residual
lesion
Excision ,
Laser,
Sclerosing
agents
ObserveObserve
YES NO

77. CONCLUSION
 Vascular malformations are a challenging
group of entities that can be successfully managed with
interventional techniques.
 It is important for the physicians who treat these complex
patients to be familiar with the different approaches,
techniques, and sclerosing and embolic agents that can be
used, so that these patients can be offered the best available
treatment for each specific case.

78. 78
THANK you

79. References
 Plastic Surgery; McCarthy
 Maxillofacial Surgery; Peter Ward Booth
 Oral & Maxillofacial Pathology; Robert E. Marx
 Ethunandan M., Mellor Timorthy K. Haemangiomas and vascular
malformations of the maxillofacial region-A review. British Journal Of Oral and
Maxillofacial Surgery 2005;2291-2300
 Lam Samuel M., Williams Edwin F. Vascular anomalies: review and current
therapy. Current opinion in Otolaryngology & Head and Neck Surgery
2002;10:309-315
 Seminars in Pediatric Surgery (2006) 15,124-132