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MANAGMENT OF VASCULAR MALFORMATIONS

MANAGMENT OF VASCULAR MALFORMATIONS. RIADH ABID Imaging Departement Elfarabi Sfax Tunisie . INTRODUCTION. Vast / varied clinical /  evolutionary / prognosis : variability Subiquitous : Multiple specialistis Nomenclature and classification. CLASSIFICATIONS.

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MANAGMENT OF VASCULAR MALFORMATIONS

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  1. MANAGMENT OF VASCULAR MALFORMATIONS RIADH ABID Imaging DepartementElfarabi Sfax Tunisie

  2. INTRODUCTION • Vast / varied • clinical / evolutionary/ prognosis: variability • Subiquitous: Multiple specialistis • Nomenclature and classification

  3. CLASSIFICATIONS • Merland J.J: Ann.Chir.Plast: 1980, 2, 105. • Muliken J.B : Plast Recons. S: 1982, 69, 412 • Hambourg classification: 1988/1989 • Iternationnal Society for the Study of VascularAnomamlies (ISSVA Rome 1996) • The IAN Jackson classification 1993 • The orbital society classification J Rootman

  4. VASCULAR ANOMALIES VASCULAR TUMOURS ADULT VASCULAR TUMOURS INFANT VASCULAR MALFORMATIONS LOW FLOW Capillary malformations CM Venous malformations VM CMV Lymphatic malformations LM HIGH FLOW Arteriovenousfistula AVF Arteriovenous malformations AVM HEMANGIOMA RCIH NCIH

  5. HEMANGIOMA

  6. HEMANGIOMA • transienterror of vascular morphogenesis • proliferation of endothelial cells identical to the parenchyma angioformateur • endothelial marker, GLUT-1: +

  7. HEMANGIOMA / CLINICAL • threeclinical types: Tuberous subcutaneous Mixed

  8. HEMANGIOMA / EVOLUTION Evolution triphasic spontaneouslyresolvent • Is mostly not presentatbirth • Is discoveredafter a few weeks • Growsdisproportionallyuntil 6 or 9 months • Still stable until 18 month • Involuteslowly in 3 or 5 years

  9. HEMANGIOMA / HOW TO BEHAVE • Imaging : not required • mainlyecho Doppler • seldom MRI • How to behave • Abstention in 90% of cases(monotoring) • therapeutic intervention in 10% of cases • Corticotherapy local or general • Avlocardyl • surgeryrepararatrice

  10. VASCULAR MALFORMATIONS

  11. LOW FLOW VASCULAR MALFORMATIONS

  12. CAPILLARY MALFORMATIONPORT- WINE STAIN (PWS) • Capillary dilatation • Macularerythemawhichispresentatbirth and persiststhroughout life • Localized or extended • Clinicaldiagnosis • Mostlyaestheticproblem LASER PULSE DYE IS THE TREATMENT OF CHOICE

  13. PWS INDICATOR OF COMPLEX SYNDROMA • false PWS: management seeavm • PWS cutaneous marker of systematized  vascular malformation  • Sturge Weber Krabbe • KlippelTrenaunay • Parkes Weber

  14. CAPILLARY-VENOUS MALFORMATIONCVM

  15. CVM • gradual expansion of the sector venular immediately post  capillary with or without  agenesis of  draining veins swelling • particular ability to invade without cleavage plane of neighboring structures difficultsurgerybleedingrecurrence

  16. CMV / CLINICAL • Compressible blueswelling • No thrill • Local normal temperature • Outbreakspainful and inflammatory

  17. FUNDAMENTALCHARACTERISTIC change in size  depending on the  position

  18. CMV / IMAGING • Plain X – ray: phleboliths • Echo- Doppler: venous signal • IRM / TDM: depth extension / bone extension • direct opacification: beforesclerotherapy

  19. CMV / DIRECT OPACIFACATION • diagnostic confirmation • number of compartments • appreciation of the venous return

  20. CVM / THERAPEUTIC MEANS • MedicalTreatment • elasticstockings • Low doses of aspirin seem to minimize phlebothromboses • Surgery : • incompleteresection • bleeding • recurrence • Sclerotherpy • Sclerotherpy + Surgery

  21. VENOUS SCEROSING AGENTS • Sodium tetradecylsulphate 3% et 1% • Alcohol / Asolute Ethanol • Ethibloc • Polidocanol /Asclera  and Aethoxysklerolcauses fibrosis inside varicose veins, occluding the lumen of the vessel, and reducing the appearance of the varicosity. • Ethanolamine oleate : Ethamolin a sclerosing agent. It works by creating scar tissue inside a swollen or dilated (wider than normal) vein to prevent bleeding.

  22. SCLEROTHERAPY Sclerotherapy induces an inflammatory reaction that will worsen the symptoms during the week following intervention. Analgesics and anti-inflammatory agents (nonsteroidal anti-inflammatory agents or corticoids) must be given to minimize the symptoms. There should be a time delay of 1–3 months between each sclerotherapy session

  23. MECHANISM OF ACTION • scerosant agent causes irritation and inflammation of bloodvesselwalls that will worsen the symptoms during the week following intervention. • Analgesics and anti-inflammatory agents must be given to minimize the symptoms. • healing of this inflammation leads to fibrosis and sclerosis with collapse of cubicles • There should be a time delay of 2–4 months between each sclerotherapy session

  24. Towneedles techniquelow pressure sclerotherapy K.R.HAMZA CIRSE 2011 ALEX. BERNACLE CIRSE 2011

  25. LYMPHATIC MALFORMATION LM

  26. LYMPHATIC MALFORMATION /LM • Vesiculeswithlymphaticfuidwithout flux  • Presentatbirth bat canbecameevidentlater /Never regress • Expandwithinflamation

  27. LYMPHATIC MALFORMATION /LM • Clincal: Cystic , Tissue, Mixed • Diagnosis: clinical  / ultrasound • Extension : sometimes TDM / IRM • Tretment: • Surgery: recurrence • sclerotherapy

  28. HIHG FLOW MALFORMATIONARTERIOVENOUS MALFORMATION

  29. AVM /DEFINITION • Anatomically : abnormal communication without an interposed  normal capillary  network between artery and a vein • Haemodynamic:  • high flow • Active • the most severe vascular malformation and the most difficult to handle Arterycapillaryvein

  30. HIGH FLOW MALFORMATIONS • AVFistulas: a single point of communication betweenfeedingartery and drainingvein • AVMalformations: niduswithseveralarteriel feeders and one severeldrainingveins

  31. AVM / NIDUS It consist of arteriel feeders (alimenteur)and enlargeddrainingveins

  32. AVM / CLINICAL / DIAGNOSIS • Hot mass or swelling red or purplish  throbbing with thrill souflante • Bleedingepisodes

  33. AVM / EVOLUTION UNPREDICTABLE • Presentatbirth but maybecameevidentlaiter • Neverr regress • May remain quiescent • Can become evolutionary • Spontaneously • hormonal changes: pregnancypuberty • punctureincompletesurgicalbiopsy

  34. AVM / COMPLICATION Evolutionary AVM Bleeding Ischemianecrosis Cardiacfailure

  35. AVM / /MONITORING • Initial assessment • echo Doppler / • angio CT / MRI • Angiography:  subclinical  stigma of scalability • Monitoring: regulirement or if Scalability

  36. AVM /CLASSIFICATION / SCHROBINGER • Stage1: lesion-pink-bluish, stain warm, Doppler US- AV shunting (quiescent phase) • Stage 2: lesion –pulsation, thrill, bruit (  expansion phase ) • Stage 3: dystrophic skin changes, bleeding, ulceration, pain (destruction phase) • Stage 4: high output cardiac failure

  37. THERAPEUTIC  / MEANS • abstention • Syrgery : • ofteninadequate • Amountbleeding • incompleteresectionwithrecurrence • proximal ligation of the artery should be avoided • ineffective by a develloppement of a network  arteriolar • can causes a flare evolutionary • closes the door to the embolization

  38. AVM / THERAPEUTIC MEANS • Embolizationarterialpercutaneousvenous • Combination: arteriel / percutaneous / venous • Multiples sessions

  39. AVM /ANGIO ARCHITECTURE • Uterstanding the anatomy of the various of AV communications is the most important factor to traitingtheseslesions by embolization. • Arterio- venous • Arteriolo-venous • More thanthreefeeding vesselscommunicating • with an identifiable venous sac • Arteriolo-venulous

  40. THERAPEUTIC AGENTS • N-Butylcyano acrylate • Alcohol • Onyx • PVA / Embospheres • Coils • ……

  41. GOALS OF TREATMENT • Control /Prevention of complications / bleeding • Stabilization / control of growth • aesthetic aspects • Curative • Preoperative

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