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Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3644_Библиотеки_им_академика_М_И_Перельмана
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experience gained with vein of Galen malformation, we have seen the
benefit of the progressive staged obliteration of these lesions, allowing
the vasculature and the maturing brain to adapt to the new hemodynamic circumstances.
In the Bicêtre series, 48 of 49 pediatric patients with CAVFs were treated by embolization alone and one with embolization and radiosurgery;
91% of the supratentorial CAVFs were treated with glue alone, 6% with a
combination of coils and glue, and 3% with coils alone. A single embolization session was performed in 34%, two or three sessions in 49%,
and four or five sessions in six cases (17%).These data were approximately the same for the endovascular approach to posterior fossa CAVFs: 79%
were treated with glue alone, 14% with a combination of coils and glue,
and 7% with coils alone.Although it is known that an AVF can be cured if
the occlusion is achieved distal to the last normal arterial branch and
proximal to the first normal opening vein, this is often more simply
achieved by the transarterial approach. No retrograde transvenous
approaches were performed.
It is not our intention to describe the techniques used in detail, as its
practice takes time and requires appropriate guidance (see Vol. 2.2,
Chap. 14 for various techniques of high-flow fistula occlusions).It should
be clearly understood that injections into high-flow fistulas with pure
glue require experience. While the endovascular occlusion of a single
channel representing the AVF is in most cases technically feasible and
safe, many of the AVFs actually have multiple arterial feeders converging
on to a single draining vein and closure of such angioarchitecture may
benefit from a staged or a multidisciplinary approach in order to achieve
the desired clinical outcome at the lowest risk.
The results of endovascular or surgical therapy needs to be assessed
with the clinical outcome in mind.Curative treatment performed without
recognizing that it is contraindicated will necessarily lead to poor clinical
outcome (Fig. 4.23). On the other hand, partial and staged treatment that
is well targeted and performed for the proper reasons may result in stabilization of the hemodynamic equilibrium with clear improvement over
the anticipated natural history.
Following endovascular management of the supratentorial CAVFs,
89% were asymptomatic, improved, or clinically stabilized in Weon’s
series; 74.3% of the patients were neurologically normal and 14.3% continued to have minor neurological symptoms, which were unchanged
from their status at the time of the original referral. Treatment was considered complete following a maximum of three embolization sessions in
78% of patients, which also included the treatment of multifocal lesions.
The average number of sessions was 2.3 per child, with each intervention
lasting between 30 and 90 min per session.Follow-up since the last intervention ranges from 6 months to 7 years (mean, 4.2 years).
Complications of endovascular therapy of high-flow AVFs might be related to the inadvertent distal embolization of the embolic material (glue
or coils) or the proximal occlusion of the parent vasculature (Fig. 4.30).
Proper analysis of the angioarchitecture and the choice and sequence of
the embolic materials to be used will avoid many of these pitfalls.
281Management
4Cerebral Arteriovenous Fistulas282
Fig. 4.30A–D. A neonate female presented with moderate to severe heart failure and
showed at MRI T2 W coronal (A) and sagittal (B) views to have prominent flow voids
along high-convexity left hemisphere (long arrow) and near the vein of Galen region
(short arrow). Left ICA angiogram on AP view (C) and oblique view (D) demonstrated a high-flow AVF (short arrow) arising from the left posterior cerebral artery and
draining toward the vein of Galen as well as a second AVF (long arrow) fed by the left
middle cerebral artery. Staged embolizations were performed at 2 weeks and
2months ofage, and a neurological deficit occurred following inadvertent deposition
of a small droplet of glue into the M1 segment upon withdrawal of the microcatheter
following embolization of the MCA AVF.E–I see p.283
283Management
Fig. 4.30E–I. (continued)
Postembolization carotid
angiogram in lateral view (E)
demonstrated near complete
occlusion of the PCA AVF,while
CT scan (F, G ) showed evidence
of embolic material within the
MCA trunk (long arrow) and
early ischemia (short arrow).
Eighteen months later after a
mild transient hemiparesis,
the child was neurologically
normal, the MCA was fully
patent,and the left parietal
AVF was occluded. The large
posterior AVF has significantly
decreased its flow,as shown
by the dramatic change of the
vein of Galen size; however,
spectacular angiectasia has
taken place in the vicinity of the
previous fistulous point (H, I)
4Cerebral Arteriovenous Fistulas284
Fig. 4.31A–C. A 10-year-old
boy with a family history of
HHT was known to have a
history of intermittent
epistaxis. He then presented
with a generalized seizure
caused by an intracranial
hemorrhage. T1 W MRI sagittal
view (A) revealed prominent
flow voids along the medial
aspect of the posterior left
frontal lobe cortex as well as
along the right parietal lobe
region adjacent to the recent
hemorrhage, as shown on T2 W
axial view (B). Left ICA
angiogram on lateral view (C)
showed a parasagittal AVF fed
by the anterior cerebral system.
A–C see p. 285
In Yoshida’s series, there was no significant morbidity and no mortality immediately related to the endovascular procedures in the 23 AVFs
treated at the posterior fossa level. However, two patients developed a
transient and one patient a permanent neurological deficit among 35 patients treated for supratentorial CAVFs.Delayed hemorrhage occurred in
two patients who were undergoing staged endovascular treatment several months after partial treatment (Figs. 4.31,4.32).
Staging is therefore an important element of our ability to anticipate
the natural history of these lesions, their multifocal character, or the impossibility of further embolizing a lesion located in an eloquent area, potential limiting factors. Thorough knowledge of the brain maturation
processes, as well as the arterial and venous anatomy, are necessary to
properly apply the agents or combinations of agents available today
in a timely manner. The transarterial route still remains the optimal
approach at this time in our experience.Yet several cases have had their
venous sector embolized through the arterial feeders (Figs. 4.33,4.34).
285Management
Fig. 4.31D,E. (continued) The RIC angiogram on lateral views (D, E ) showed a right
parietal AVF,confirming the multiplicity of the AVFs. Fatal hemorrhage occurred several months after staged partial embolizations
4Cerebral Arteriovenous Fistulas286
Fig. 4.32A–F.Legend see p. 287
287Management
Fig. 4.32A–H. Fig. 4.32A–H. A 20-month old baby presented with macrocrania and
arymptomatic moderate cardiomegaly Sine age of 12 month. MRI (A,B) and angiography (C,D,E) demonstrate two AVFs in the porterior fona. Four senious and 6 arteri-
al feeders reduced the lesions by over 50% as seen on angiography (F).A significant
amount of glue was delivered (G).The treatment was spread over 2 years period.After the last MRI (H) he was well and scheduled for further session 6 month later. He
died suddenly from brain strem hemorrhage while diving in a swimming pool.
▲
4Cerebral Arteriovenous Fistulas288
Fig. 4.33A–G. A 3-year-old boy presented with speech difficulties.Axial MRI (A) an-
giogram showed a high-flow fistula with short feeders in an eloquent area (B–D).The
embolization was therefore performed with coils transarterially in one session into
the venous chamber of the fistula. At 6 months, the nearly complete exclusion immediately after coil deposit was completed (E–G). The child is neurologically normal
289Management
Fig. 4.34A–E. A 4-year-old child presenting with single hole AVF on the frontal lobe
(A, B).The short arterial feeder to the fistula’s chamber led to the use of coils deposited on the venous side after transarterial catheterization across the fistula. Follow-up
angiogram 5 months after the treatment (C,D); the child is clinically normal
5.1 General Remarks 292
5.2 Angioarchitecture of Cerebral Arteriovenous Malformations 298
5.2.1 Single Nidus Versus Multifocal Niduses 298
5.3 Conditions Associated with CAVMs 302
5.4 Conditions Mimicking CAVMs 306
5.4.1 False Pial Arteriovenous Malformations Including
Proliferative Angiopathies 306
5.4.2 Perinidal Angiogenesis 306
5.4.3 Postischemic Luxury Perfusion 306
5.4.4 Proliferative Angiopathy 306
5.4.5 Induced Pial AV Shunts Secondary
to Dural Sinus High-Flow Lesions 309
5.5 Angioarchitectural Progression of CAVMs in Children 311
5.5.1 Venous Angiopathy 311
5.5.2 Dural Sinus High Flow 312
5.5.3 Venous Ischemia and Thrombosis 315
5.5.4 Venous Hemorrhage 316
5.5.5 Venous Enlargement 321
5.5.6 Arterial Angiopathy 324
5.5.7 Spontaneous Thrombosis of Arteriovenous Malformations 330
5.6 Objectives of Treatment 330
5.6.1 Complete Exclusion 330
5.6.2 Partial Treatment 336
5.6.3 Neonates and Infants 340
5.6.3.1 Hydrodynamic Disorders 341
5.6.3.2 Multiple Arteriovenous Malformations 342
5.6.4 Children 342
5.6.5 Rebleeding 344
5.7 Technical Management 345
5.7.1 General Remarks 345
5.7.2 Other Techniques 345
5.7.2.1 Surgery 345
5.7.2.2 Radiation Therapy 352
5Cerebral Arteriovenous Malformations
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