Vascular malformation

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) 15,124-132

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 1 st -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 L ymphangioma )

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. Staging of arterio -venous malformations 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

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

41. 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.

42. ( 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 .

43. 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

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

45. 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

46. 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

47. 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.

48. 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.

49. 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 .

50. 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.

51. 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 )

52. 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

53. HISTORY OF TREATMENT 55 1. LIGATION AND EXCISION In 1714, Turner favoured surgical resection , ligation and caustics for vascular birthmarks During 19 th 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 20 th century, surgical excision continued to be a primary mode of therapy.

54. 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 CO 2 crayon techniques were once commonly employed

55. 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.

56. 58 4. SCLEROSANT THERAPY Injection of “stimulating solutions” for treatment of hemangiomas had its shadowy beginnings in 19 th century : Ergot (Hammond,1876), Tannic acid , Carbonic acid (Bradley, 1876), Iron perchloride and 95% alcohol ( Holgate, 1889) In 20 th 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 )

57. 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.

58. 60 6. COMPRESSION Compression therapy can be traced to the early 19 th 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.

59. CURRENT MANAGEMENT 61 1. PRIMUM NON NOCERE Description of spontaneous involution of hemangioma can be found scattered throughout 19 th 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 5 th year of life”.

60. 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.

61. 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% .

62. 64 Systemic steroid should be used only in selected infants with hemangioma those with Cervicofacial lesion causing distortion of features Large lesion especially with recurrent bleeding,Ulceration , infection Lesion interferes with physiological function. Lesion complicated by high output cardiac failure Lesion complicated by platelet depletion coagulopathy Prednisone is given 2-3 mg /kg/day for 2-3 weeks

63. 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.

64. 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.

65. 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.

66. 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

67. 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.

68. Sclerotherapy 70 Sclerosants : 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

69. LYMPHATIC MALFORMATIONS 71 Several agents have been utilized for lymphatic malformations including ethanol, bleomycin , and doxycycline . Several authors say L Ms 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.

70. 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 .

71. 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.

72. 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 replantati on ( 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

73. 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.

74. 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 Observe Observe YES NO

75. 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.

76. 78 THANK you

77. 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