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




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
INFANT
VASCULAR
MALFORMATIONS
V
A
S
C
U
L
A
R
T
U
M
O
U
R
S
HEMANGIOMA
LOW FLOW
HIGH FLOW
Capillary malformations CM
Arteriovenous fistula AVF
Venous malformations VM CMV
RCIH
NCIH
Lymphatic malformations LM
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 cutaneous
Mixed
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 MALFORMATION
PORT- 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
 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
CVM
CMV / CLINICAL
 Compressible blue swelling
 No thrill
 Local normal temperature
 Outbreaks painful and infla
mmatory
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


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.
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
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 technique
low pressure sclerotherapy
K.R.HAMZA CIRSE 2011
ALEX. 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

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
Bleeding
Ischemia 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 QUIESCENT:
abstention
AVM EVOLUTIONARY
therapeutic intervention
embolisation
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
 Plastic surgeon
 Pediatricia
 Dermatologist
Interventional
radiologist
 Vascular surgeon
 Orthopedic surgeon
 Pathologist
 Nursing staff
 Maxillo facial surgeon
 Pédiatric surgeon
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, S159S171.