managment of vascular malformations
DESCRIPTION
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. - PowerPoint PPT PresentationTRANSCRIPT
MANAGMENT OF VASCULAR MALFORMATIONS
RIADH ABIDImaging Departement Elfarabi Sfax Tunisie
INTRODUCTION Vast / varied
clinical / evolutionary/ prognosis: variability
Subiquitous: Multiple specialistis
Nomenclature and classification
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 Vascular
Anomamlies (ISSVA Rome 1996) The IAN Jackson classification 1993 The orbital society classification J Rootman
VASCULAR ANOMALIES
VASCULAR TUMOURS ADULT
VASCULAR TUMOURS
INFANT
HEMANGIOMA
RCIHNCIH
VASCULAR MALFORMATIONS
LOW FLOW
Capillary malformations CM
Venous malformations VM CMV
Lymphatic malformations LM
HIGH FLOW
Arteriovenous fistula AVF
Arteriovenous malformations AVM
HEMANGIOMA
HEMANGIOMA transient error of vascular
morphogenesis
proliferation of endothelial cells identical to the parenchyma angioformateur
endothelial marker, GLUT-1: +
HEMANGIOMA / CLINICAL three clinical types:
Tuberous sub cutaneousMixed
HEMANGIOMA / EVOLUTION
Evolution triphasic spontaneously resolvent Is mostly not present at birth Is discovered after a few weeks Grows disproportionally until 6
or 9 months Still stable until 18 month Involute slowly in 3 or 5 years
HEMANGIOMA / HOW TO BEHAVE Imaging : not required
mainly echo Doppler seldom MRI
How to behave Abstention in 90% of cases( monotoring) therapeutic intervention in 10% of cases
Corticotherapy local or general
Avlocardyl surgery repararatrice
VASCULAR
MALFORMATIONS
LOW FLOW
VASCULAR MALFORMATIONS
CAPILLARY MALFORMATIONPORT- WINE STAIN (PWS)
Capillary dilatation
Macular erythema which is present at birth and persists throughout life
Localized or extended Clinical diagnosis Mostly aesthetic problem
LASER PULSE DYE IS THE TREATMENT OF CHOICE
PWS INDICATOR OF COMPLEX SYNDROMA
false PWS: management see avm
PWS cutaneous marker of systematized vascular malformation Sturge Weber Krabbe Klippel Trenaunay Parkes Weber
CAPILLARY-VENOUS MALFORMATION
CVM
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
difficult surgery bleeding recurrence
CMV / CLINICAL Compressible blue
swelling
No thrill Local normal temperature
Outbreaks painful and inflammatory
FUNDAMENTAL CHARACTERISTIC
change in size
depending on the position
CMV / IMAGING Plain X – ray: phleboliths
Echo- Doppler: venous signal
IRM / TDM: depth extension / bone extension
direct opacification: before sclerotherapy
CMV / DIRECT OPACIFACATION diagnostic
confirmation number of
compartments appreciation of the
venous return
CVM / THERAPEUTIC MEANS Medical Treatment
elastic stockings Low doses of aspirin seem to
minimize phlebothromboses Surgery :
incomplete resection bleeding recurrence
Sclerotherpy Sclerotherpy + Surgery
VENOUS SCEROSING AGENTS Sodium tetradecyl sulphate 3% et 1% Alcohol / Asolute Ethanol Ethibloc Polidocanol / Asclera and
Aethoxysklerol causes 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.
SCLEROTHERAPYSclerotherapy 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
MECHANISM OF ACTION scerosant agent causes irritation and
inflammation of blood vessel walls 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
Tow needles techniquelow pressure sclerotherapy
K.R.HAMZA CIRSE 2011ALEX. BERNACLE CIRSE 2011
LYMPHATIC MALFORMATION
LM
LYMPHATIC MALFORMATION /LM
Vesicules with lymphatic fuid without flux
Present at birth bat can became evident later /Never regress
Expand with inflamation
LYMPHATIC MALFORMATION /LM Clincal: Cystic , Tissue, Mixed
Diagnosis: clinical / ultrasound
Extension : sometimes TDM / IRM
Tretment: Surgery: recurrence sclero therapy
HIHG FLOW MALFORMATION
ARTERIOVENOUS MALFORMATION
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
Artery capillary vein
HIGH FLOW MALFORMATIONS AVFistulas:
a single point of communication between feeding artery and draining vein
AVMalformations: nidus with several arteriel feeders and one severel draining veins
AVM / NIDUS
It consist of arteriel feeders (alimenteur)and enlarged draining veins
AVM / CLINICAL / DIAGNOSIS Hot mass or
swelling red or purplish throbbing with thrill souflante
Bleeding episodes
AVM / EVOLUTION UNPREDICTABLE Present at birth but may
became evident laiter Neverr regress May remain quiescent Can become evolutionary
Spontaneously hormonal changes: pregnancy
puberty puncture incomplete surgical biopsy
AVM / COMPLICATION
Evolutionary AVM
BleedingIschemia necrosis
Cardiac failure
AVM / /MONITORING
Initial assessment echo Doppler / angio CT / MRI Angiography: subclinical stigma of scalability
Monitoring: regulirement or if Scalability
AVM /CLASSIFICATION / SCHROBINGER Stage 1: 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
THERAPEUTIC / MEANS abstention Syrgery :
often inadequate Amount bleeding incomplete resection with recurrence
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
AVM / THERAPEUTIC MEANS Embolization
arterial percutaneous venous
Combination: arteriel / percutaneous / venous
Multiples sessions
AVM /ANGIO ARCHITECTURE Uterstanding the anatomy of the various of AV
communications is the most important factor to traiting theses lesions by embolization.
Arterio- venous
Arteriolo-venous More than three feeding vessels communicating with an identifiable venous sac
Arteriolo-venulous
THERAPEUTIC AGENTS
N-Butyl cyano acrylate Alcohol Onyx PVA / Embospheres Coils ……
GOALS OF TREATMENT Control /Prevention of complications / bleeding
Stabilization / control of growth
aesthetic aspects Curative Preoperative
PURPOSE OF TREATMENT
EXCLUDE
THE
NIDUS
Treatment of AVM Simple vascular malformation
percutaneous sclerotherapy
Treatment of AVM Vascular malformation
with several feeding arteries and drainage veins.
begins with a flow-control procedure (the drainage vein)
Additional sclerotherapy to the nidus is then performed.
Treatment of AVM vascular malformation
with several drainage veins and feeding arteries, one of which was embolized.
This is an ineffective procedure that makes the latent feeding arteries apparent.
Without ablation of the nidus, a good outcome cannot be expected.
HEMANGIOMA / TAKE HOME MESSAGES
Diagnosis: clinical appearance triphasic evolution
Imaging : not required mainly echo Doppler
How to behave Abstention in 90% of cases( monotoring) therapeutic intervention in 10% of cases
Local or general corticotherapy surgery repararatrice
CVM / TAKE HOME MESSAGES
Diagnosis : clinical Therapeutic managment
Sclerotherpy percutaneous Sclerosis constutie the treatment of choice and first-line. She can avoid a difficult surgery and often incomlete
In other cases it allows the preparation of the deed operative avoiding mutilating and iterative surgery
AVM / TAKE HOME MESSAGES Definition : abnormal communication
between A and V
Diagnosis : clinical
Iitial assessment and regular monitoring
Evolution : unpredictable
Therapeutic management
AVM /THERAPEUTIC MANAGEMENT A MULTIDISCILINARY DECISION
REGULAR MONITORING
AVM EVOLUTIONARY
therapeutic intervention
embolisation
AVM QUIESCENT: abstention
CONCLUSION Vascular malformations are varied and
ubiquitous classification distinguishes vascular
malformations according to the affected area (artery, vein, capillary, lymphatic) and according to the flow (high and low flow)
The clinical directed imaging, therapeutic prognosis
Vascular malformations require multidisciplinary management
MANAGMENTS OF VASCULAR MALFORMATIONS
Pediatricia
Dermatologist
Pathologist
Nursing staff
Plastic surgeon
Vascular surgeon
Orthopedic surgeon
Maxillo facial surgeon
Pédiatric surgeon
Interventional
radiologist
FLOW RELATED CLASSIFICATION AND RECOMMENTED TREATMENT
Slow flow lesion SCLERTHERAPY
Intermediate flow lesion SCLEROTHERAPY+/-
EMBOLIZATION
High flow lesion EMBOLIZATION +/-
SCEROTHERAPY
Merland J.J: Ann.Chir.Plast: 1980, 2, 105. Muliken J.B : Plast Recons. S: 1982, 69, 412 Goleria - 2012 - Medical - 222 pages The ian Jackson classification (1993) J.Dubois Nov 2001 , RadioGraph 21, 1519-1531 L.Flors and all sep 2011 RadioGraph, 31, 1321-
1340. H Hideki October 2005 RadioGraphics, 25,
S159-S171.