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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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211Complications:Morbidity
Fig. 3.66A–C. Subependymal arterial supply and venous anastomoses (A) rapidly
remodeling after a single subependymal arterial glue deposit (B,C)
3Vein of Galen Aneurysmal Malformation212
Fig. 3.67A–F. Presence of a rich perimesencephalic network (A–C) that did not compromise a satisfactory glue embolization,leading to complete exclusion of the lesion (D–F)
213Complications:Morbidity
Fig. 3.68A–G.Legend see pp.215
3Vein of Galen Aneurysmal Malformation214
Fig. 3.68H–K.Legend see p. 215
215Complications:Morbidity
Fig. 3.68A–N. A 4-month-old child presenting with a well-tolerated VGAM (A–C)
was partially embolized in two sessions over 2 years with nearly complete exclusion
but closure of the falcine sinus and faint subependymal reflux (D–G). Nearly 2 years
later, he presented a sudden intrathalamocapsular and ventricular hemorrhage.
H–K The angiogram demonstrated an angiogenic colonization of the thrombosed venous pouch generating an increased flow into the subependymal vein anastomoses
and their remote rupture away from the VGAM. L–N Further embolization aimed to
reduce the angiogenic field further
3Vein of Galen Aneurysmal Malformation216
Fig. 3.69.A,B. A 7-month-old infant with a well-tolerated VGAM and an early
subependymal venous reflux. The objective of the preventive treatment was first to
make the reflux disappear. Follow-up angiogram 3 months after the first session of
embolization (C)
217Complications:Morbidity
Fig. 3.70.A,B. Catheter glued in place and hanging in the aorta. C, D Follow-up angiogram during an additional session 10 years later.The catheter is now extravascular
and the vertebral artery is patent, allowing for a further microcatheter approach
Fig. 3.71A,B. Droplet of glue remaining at the tip of the catheter when pulled detached in the internal iliac artery to preserve the lower limb arterial patency
new session of embolization of the VGAM. This is to emphasize the need
for a proper pediatric environment when endovascular specialists perform these procedures on babies in an adult hospital (Table 3.11).
We have experienced no limb vascular complications as a result of re-
peated arterial punctures in VGAM patients except in the following case.
In a 3-kg neonate with severe CCF with aortic diastolic steal and poor
peripheral circulation in which the diagnosis of VGAM was uncertain, we
encountered a persistent femoral artery spasm while pulling the 4-F
sheath. As we had decided against treatment, the baby died of systemic
failure 2 days later with an associated severe distal ischemia in his lower
limb.
We have had few venous passages of fragmented glue cast (less than
3%) into the sinuses or further distally; the use of low blood pressure
during glue injection helps in keeping these figures low. However, in case
of bilateral jugular bulb occlusion, a converging and restricted venous
drainage of the VGAM and the brain, any glue passage into the venous
outlet will produce an immediate postembolization hemorrhagic venous
infarction (Fig. 3.73).
If the glue remains in the sinuses,further occlusion of the shunt must
be obtained to avoid the effect of rerouting of the VGAM flow into the
pial venous system. Remodeling over time usually shows satisfactory
recruitment of collateral venous channels. Heparin in these cases will be
needed to preserve the remaining lumen if iatrogenic occlusion is incomplete to allow for that remodeling to take place.
In this same group of treated patients, 2% developed permanent neurological disability.
Children treated by the transvenous route after failure to achieve further embolization by the transarterial approach are at risk of intracerebral
hemorrhage within a few hours after embolization. This occurs when the
3Vein of Galen Aneurysmal Malformation218
Fig. 3.72. Extremity of a Sensé
microcatheter with a drop of
glue that was too big to be withdrawn through the 4F sheath by
the femoral approach.This
4,600-g baby had to be operated
on. The catheter tip was cut
and removed from the abdominal aorta following direct aortotomy. Clinical and morphological follow-up 7 years later
showed excellent results.
Scale is in centimeters
219Complications:Morbidity
Ta b l e 3 .11. VGAM Therapeutic results 1981–2002a:complications in the patients
receiving embolization (193 surviving children)
Tr ansient neurological complications 3 1.55%
Permanent neurological complications 4 2%
Non-neurological complications 13 6.7%
Hemorrhage after embolization 11 5.7%
a
Death: 23/216 patients (10.6%); angiography no embolization = 4 (one technical
failure, three angiograms only); after embolization = 14 (death related to
embolization); between sessions = 4; after embolization and surgery = 1.
Fig. 3.73. A A 6-month-old boy
in whom macrocrania revealed
a VGAM.Progressive occlusion
in the jugular bulb produced
a significant congestion on the
cerebral veins. The superior
petrosal sinus on the left side
drained the malformation into
the ophthalmic vein.Prior to
admission, the child presented
with a generalized seizure that
required antiepileptic medication. He had proptosis on the
left side and facial collateral
circulation,but had a score of 4.
He was embolized three times
with significant improvement
in the facial circulation.
B, C Following erratic venous
embolic material during the
final session, a large lethal
venous infarct in the left
hemisphere resulted from the
occlusion of the ipsilateral
cavernous sinus,and immediate
extension to all its converging
venous afferents
occlusion of the venous outlet to the pouch is complete and the remaining
flow into the VGAM insufficiently reduced toward subependymal anastomoses. Hemorrhages have been reported in the literature but they refer to
unrecognized VGAD treated with the transvenous approach. A total of
5.7% of hemorrhages (including the ones mentioned in Sect. 3.12) have
been noted mostly caused by arterial perforation in the vicinity of the
shunt with small arterial feeders and using a microguidewire. Immediate
gluing of that feeder led mostly to minor and transient manifestations.
We have never seen the so-called perfusion break-through phenomenon in the many acute closures of high-flow fistulas that we have performed (see Chap.4, this volume), nor have we seen a VGAM increase in
size following thrombosis,as our experience has shown that shrinkage of
the mass occurs rapidly after significant transarterial embolization. Furthermore, we have not observed in any patients a consumption of coagulation factors type of syndrome induced by thrombosis in the large venous pouches. In one patient, a giant VGAM progressively thrombosed
after embolization, and the infant awoke a few days after sedation was
discontinued.All clinical and EEG parameters corresponded to those of a
sleeping child, and it was demonstrated that the pouch behaved like a
reservoir and was still releasing drugs. The child woke up 5 days after
embolization with his VGAM completely excluded and had a score of
5at the age of 13.
3.15.4 Overall Mortality
In our series, and after applying our selection criteria, treatment was withheld in 18% of children. The mortality rate in our group of embolized children was 10.6% (23/216 patients).Many of these were early cases which today would be scored below 8 and would thus be included into the nontreatment group. They belong to the „death despite treatment group“ at
the beginning of our experience or to the newly recognized group of irreversible suprasystemic pulmonary hypertension resistant to NO.
The proportion of patients with a rapidly fatal form still remains lower than the quoted mortality rate in comparable series with different selection criteria or different therapeutic techniques (Casasco et al. 1991;
Ciricillo et al. 1990; Dowd et al. 1990; Merland et al. 1987; Mickle and
Peters 1993; Hoffman et al. 1982; Johnston et al. 1987; Raimondi 1987;
Yasargil et al. 1976). In most cases where fatal outcome occurred even
though the individual procedures were successful, the timing and
sequence of the interventions resulted in the accumulation of secondary
effects eventually causing death.
Sudden death occurred in one infant, probably due to transtentorial
herniation, following ventricular shunting in the presence of bilateral
subdural effusions. Complete embolization of a large VGAM was performed 3 days later.The baby was not kept asleep and was sent back to the
ward, where he remained clinically intact till he collapsed 24 days after
embolization.
The overall management (decision not to treat and treatment-related)
of VGAM in our series carried a 23.7% mortality rate.
3Vein of Galen Aneurysmal Malformation220
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