2. Anatomicopathologic Classification
The earliest attempt at classification of vascular lesions was made by
Virchow(1863) a) angioma
b) lymphangioma
1.Angioma simplex: system composed of capillaries.
2.Angioma cavernosum: a replacement of normal vasculature with
large chanels.
3.Angioma racemosum: tissue consisted of markedly dilated
interconnected vessels.
Vascular malformations are developmental abnormalities of the
vascular system.
2
3. Biologic Classification
Mulliken and Glowacki, (1982).
• On basis of cell kinetics, there are two major
types of vascular anomalies:
• Hemangiomas : lesions demonstrating
endothelial hyperplasia.
• Vascular Malformations : lesions with normal
endothelial turnover.
3
5. • In 1996 this classification was modified by ISSVA( International
society for the study of vascular anomalies)
• Presently ISSVA differntiates vascular tumors from vascular
malformations.
VASCULAR TUMORS VASCULAR MALFORMATIONS
1) Benign tumors 1) Slow/low flow
Infantile Hemangioma Venular
Congenital Hemangioma venous
lymphatic
2) Intermediate tumors 2) Fast /high flow
Kaposiform hemangioendothelioma AVM
Spindle cell hemangioendothelioma AVF
5
6. Hemangiomas
• The word "hemangioma" comes from the Greek haema-, "blood";
angeio , "vessel"; -oma , "tumor".
• A hemangioma is a benign and usually self-involuting tumor of the endothelial
cells that line blood vessels, and is characterised by increased number of
normal or abnormal vessels filled with blood.
• Exhibits rapid early growth until 6-8 months of age, followed by regression by 5-9 years
of age.
Capillary Hemangioma: (occur in superficial
layer of skin) This is the most common type
of hemangioma. It is made up of small
capillaries that are normal in size and
diameter, but high in number.
Because of their proximity to the surface of
the skin, capillary hemangiomas are
typically brighter red in color
Cavernous Hemangioma In contrast with a
capillary hemangioma, a cavernous
hemangioma is made up of larger blood
vessels that are dilated. The blood vessels are
not as closely packed as in a capillary
hemangioma, and the spaces (or "caverns")
between them are filled with blood.
6
8. PATHOGENESIS of Hemangioma
• Various theories:
1. Virchow speculated that mechanism was a progressive
irritation of tissue, likely to occur about the margins of fetal
clefts that are well supplied by blood vessels.
2. Malan (1974) proposed that “dormant angioblasts” become
activated to form hemangiomas- a delayed expression of
genetically programmed growth and involution of embryonic
capillary network.
3. Kaplan (1983) stated that hemangioma is a failure of normal
morphogenesis from the embryonic stage of
undifferentiated capillary network.
8
9. • Life cycle consists of 2 phases : Proliferation stage
Involution stage
• Hemangiomas initially noticed as an erythematous, macular
patch, progressing through a rapid proliferative phase whereby
it changes/deepens its color and grows faster than the growth
of the child.
• Following proliferation,hemangiomas enter a slower or no
growth phase, known as plateau phase. This phase
typically lasts from 9 to 12 months of age
• At 12 months of age most hemangiomas have shown signs of
involution.
• The process of involution is normally slow and completes by the
age of 5 to 9 years.
9
10. Proliferation
• Hallmark of the immature hemangioma is
proliferation of endothelial cells, forming synctial
masses, with and without lumen.
• Mature hemangioma is organized into lobular
compartments, separated by fibrous septa that
contain large caliber feeding and draining vessels.
• Role of mast cells in evolution of hemangioma not
fully understood.
10
11. • 30-40 times increase in number of mast cells compared
with normal tissues.
• In vitro studies have shown Mast cells produce heparin
which stimulates migration of cultured capillary
endothelium and potentiates the proliferation of
endothelium by endothelial cell growth factor.
• Various studies also confirmed that the number of mast
cells is highest during the involuting phase, lower in the
involuted phase, and lowest in the proliferating phase.
11
12. Clinical Features- proliferative phase
• 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.
12
14. Involution
• Proliferation and involution occur concurrently after the first
year. i.e., even when involution is well under way there are
scattered proliferative foci. (Mulliken and Glowacki, 1982).
• Progressive deposition of perivascular, inter and intralobular
fibrous tissue.
• Within electron microscope: tissues from involuting
hemangioma reveals signs of endothelial discontinuity and
vessel degradation. Lumens contain endothelial debris.
• End stage involuted hemangioma is composed of thin walled
vessels that resemble normal capillaries.
• There are islands of fat and dense collagen deposited in the
perivascular areas (Dethlfsen, Mulliken and Glowacki,
1986).
14
15. Clinical Features- Involution phase
• 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.
• In time surface assumes a mottled grayish mantle that
spreads centrifugally toward periphery of the lesion.
• Lesion is less tense to palpation.
• When child cries lesion does not swell.
• By age of 5 years last traces of color are fading.
15
18. Incidence
-most common tumor of infancy.
-frequency in new born infants, in first few days of life
is 1.1-2.6% (Pratt 1967; Jacobs & Walton 1976).
-at 1 year of age frequncy of appearance: 10-12%
(Jacobs).
Female-male ratio- 3:1 (Mulliken 1983).
18
19. Vascular Malformations
• 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.
19
20. Development of Vascular Malformations
• 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.
20
21. • Trauma, infection, and hormonal fluctuation (pregnancy or
puberty) may stimulate increased growth of the vascular
malformation.
• The mechanism of growth is not increased endothelial
proliferation - which is within a normal range in these
lesions, as is the number of mast cells – “but alteration in
the flow dynamics within and around the lesion”.
• This results in recruitment of “collateral vessels” and
dilatation of involved vessels.
21
22. 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
22
23. Venous Malformations – Phleboliths
.
Phleboliths that may be noted on radiographic examination are found
only in low flow lesions.
23
24. Capillary Malformations ( portwine stain)
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
24
25. Lymphatic Malformations - Low- flow lesions
• 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.
25
26. Lymphatic Malformations
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)
26
27. Lymphatic Malformations
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.
27
28. Arterial / Arteriovenous Malformations (AVM) “High-flow
lesions”( outdated terms - cirsoid aneurysm,arteriovenous aneurysm)
• They represent a group of congenital malformations that create
a direct communication between the arterial and venous
systems, through a nidus formed by arteriovenous shunts, along
with hypertrophy of the afferent arterial and efferent venous
system.
• 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.
28
29. 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.
29
30. • 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.
30
31. Staging of arterio-venous malformations
Schobinger Staging of AVM
• 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
31
32. Clinical Differences
Hemangioma
• A hemangioma may or may not be
present at birth.
• They involute spontaneously with
age.
• Rapid postnatal growth and very
slow involution.
• Females are more commonly
affected; 3:1 (Mulliken and
Glowacki, 1982).
.
• They are true benign neoplasm of
endothelial cells.
Vascular malformation
• Vascular malformations are always
present at birth.
• They donot involute usually.
• A vascular malformation grows
proportionately with the child.
• Vascular malformations have no
gender predilection.
• Are localized defects of vascular
morphogenesis that results in
formation of abnormal, tortuous
and enlarged vascular channels
32
33. Cellular Differences.
Hemangioma
• The rapidly growing
hemangioma is composed
of rapidly dividing
endothelial cells.
• In addition, mast cells,
known to play a role in
neoangiogenesis, increase
during the proliferating
phase
• The mast cells fall to normal
levels as involution is
concluded.
Vascular malformation
• No evidence of cellular
hyperplasia but rather
progressive ectasia of
structurally abnormal
vessels.
• The malformed chanels are
lined by flat, quiescent
endothelium, lying on a
thin basal lamina.
• No increase in mast cells.
33
34. Radiographic differences
Hemangioma
• Angiographic study shows
hemangioma as a well
circumscribed mass with
intense, prolonged tissue
staining that is usually
organized in a lobular
pattern.
• Feeding arteries may form
an equatorial network at the
periphery of the tumor.
Vascular malformation
• Vascular malformations are
diffuse lesions consisting
entirely of vessels without
intervening parenchymal
staining.
• The angiographic pattern
depends on the
predominant chanel type,
i.e., capillary, venous,
arterial or a combination.
34
35. Skeletal Differences
Hemangioma
• Proliferating hemangioma
rarely causes bony/
cartilagenous distortion or
hypertrophy.
• Maxillary or mandibular
overgrowth may occur
secondary to increased
blood flow during
proliferation.
• May produce mass effect,
e.g depression of the outer
calvaria, shift of nasal
skeleton, or secondary
enlargement of orbit.
Vascular malformation
• Low flow vascular
malformations are
frequently associated with
diffuse skeletal hypertrophy,
distortion or elongation.
• High flow arteriovenous
malformations often cause
destructive intraosseous
changes.
35
37. HEREDITARY HEMORRHAGIC TELANGIECTASIA
(Rendu Osler Weber disease)
• Congenital hereditary disease
• Numerous telangiectatic or angiomatous areas.
• Triad of telangiectasia, recurrent epistaxis,
and a positive family history.
37
Hemolytic anaemia , thrombocytopenia and
coagulopathy.
KASABACK – MERRITT SYNDROME
38. (Sturge-Weber syndrome) encephalotrigeminal angiomatosis
It consists of congenital Hamartomatous
Malformations that may affect the eye, the skin, and
the central nervous system at different times.
38
Klippel-Trenaunay –Weber syndrome
Triad of cappilary malformations, bone
hypertrophy and venous malformations.
40. • 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
40
41. 41
Coronal 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
42. DOPPLER ULTRASOUND
DOPPLER EFFECT
• The variation of the apparent frequency of sound waves,
with change in distance between the source and the
receiver.
DOPPLER ULTRASOUND is an adaptation of ultrasound
technology. Depends on the frequency shift of ultrasound
reflected from moving red cells being proportional to the
velocity of flow.
42
The ‘chaotic’ or turbulent flow results from the area being filled with numerous individual velocity vectors
randomly occurring in all directions.
43. ARTERIOGRAPHY
• 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.
43
44. • The catheter is advanced from
the femoral artery to one of four
arteries in the neck that lead to
lesion and tissues.
• While viewing an x-ray monitor,
called a fluoroscope, the doctor
steers the catheter through the
blood vessels.
• 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.
44
45. • 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)
45
46. Digital subtraction carotid angiogram showing
an arteriovenous malformation of the tongue
involving the lingual artery.
Arteriovenous malformation of the tongue
46
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
47. HISTORY OF TREATMENT
1. 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 ( Davis and Wilgis,1934; Matthews,1954; Modlin 1955).
47
48. 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 ( Gross, 1859; Kingston,1862;
Blair,1884)
• Efforts to freeze hemangiomas became popular early in
19th century (Pusey,1907; Bunch 1911)
• Carbon dioxide slush or solid CO2 crayon techniques were
once commonly employed ( Semon, 1934; MacCollum,
1935)
48
49. 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 (Knott,1875; Coombs,1881).
• Endothermy Coagulation - Modern thermocautery units,
with a needlepoint attachment, were used to puncture
deep hemangiomas or to cause surface coagulation
(MacCollum, 1935). This modality is the antecedent of
today’s sophisticated laser technology.
49
50. 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)
50
51. 5. RADIATION
• Radiation for hemangiomas was remarkably successful in
1930 to 1950 era.
• Several modalities were used : Thorium-X varnish,
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.
51
52. 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.
52
53. CURRENT MANAGEMENT
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”.
53
54. • 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.
54
55. 2. STEROID THERAPY
• Serendipitous discovery, 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 (Fost &
Esterly,1968; Brown,Neerhout & Fonkalsrud,1972).
• The response is reported to be in range of 30-90%
(Edgerton 1976).
55
56. 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.
57. 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 with in 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 with in 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
58. 5. OPERATIVE THERAPY
• If every hemangioma began as a localized nest of cells, the ideal t/t
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.
Beta blockers(propranolol)
A recent use of beta blockers is under investigation but appears
promising.
59. Sclerotherapy
venous malformations have been treated with irradiation, electrocoagulation
(Figi,1948), Freezing techniques (Goldwyn & Rosoff, 1969; Jarzab, 1975),
Intravascular Magnetic needles (Martin & Papp,1981) and Sclerosants : Boiling
water (Wyeth,1903), Alcohol, Sodium Morrhuate, Quinine, Silver Nitrate and Iron
or Zinc Chloride(Boman,1940)
• 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.
59
VENOUS MALFOMATIONS
60. LYMPHATIC MALFORMATIONS
• Several agents have been utilized for lymphatic malformations including
ethanol, bleomycin, OK-432, 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 and the mainstay of
therapy, 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.
60
61. ARTERIOVENOUS MALFORMATIONS
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. In
some cases, occlusion of the proximal vasculature or tortuosity of
feeding vessel results in failure of conventional embolization
technique. 61
62. • 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
interventional 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.
62
63. • 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
63
SURGERY
64. 64
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.
65. Immunohistochemical studies
A scalpel-biopsy may help distinguish VMs from
hemangiomas, and have shown that H are Glucose
Transporter (GLUT)-1 positive while VMs do not express
GLUT-1 protein.
In contrast to hemangiomas, VMs do not express
proliferating cell nuclear antigen (PCNA),
vascular endothelial growth factor (VEGF),
fibroblast growth factor (FBF),
type IV collagenase, and urokinase.
65
66. History and
examination
Vascular
malformation
Hemangioma
MRI. Doppler US,
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
Observe
Observe
YES NO
