MANAGMENT OF VASCULAR MALFORMATIONS

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.