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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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7Dural Arteriovenous Shunts402
Fig. 7.7A–D. Legend see p.403
403Fetal and Postnatal Changes of Sinuses
Fig. 7.7A–F. A 5-year-old boy who presented with a failure to thrive, an objective intense bruit of which he did not complain, moderate macrocephaly, dyspnea with
effort, and poor school performance. A Chest X-ray shows moderate enlargement of
the cardiac silhouette.B Intravenous digital angiography demonstrates a large supra-
tentorial venous lake derived from the left lateral sinus. C Coronal enhanced CT. Se-
lective injections in the left internal carotid (D) and maxillary artery (E) demonstrate
the multiple feeders to the pouch (supratentorial) (arrow and double arrow); infratentorial, transosseous,and vessels on the right side supplied the lesion (not shown).The
shunt was well controlled by incomplete embolization and the systemic effects of the
shunt on growth and school performance abated within 1 year.F Follow-up showed a
moderate decrease in the size of the venous mass and the presence of an underlying
cerebellar DVA
▲
7Dural Arteriovenous Shunts404
Fig. 7.8A–C. A 6-month-old girl presenting with a calvarial hemangioma (A). MR
and angio-MR demonstrated an underlying DSM as well as a possible communication between both lesions (B, C).D,E see p. 405
Among the six patients with brain damage, five died and one was lost
to follow-up.The cause of death was ICH in two, IVH in one, and uncontrollable high ICT with tonsillar prolapse in the remaining two.In
four patients who presented without brain damage, diagnostic angiography showed no cavernous capture with involvement of torcular; the progression was poor in three (two died) and good in one.
The patient with good progression did not have satisfactory delayed
venous phase imaging to evaluate the cavernous capture; however,
alternate pathways were likely sufficient. In this group of patients, the
absence of cavernous capture and the involvement of torcular gave
rise to an unfavorable neurological progression related to spontaneous thrombosis of the torcular.
Under these circumstances, timely diagnosis and treatment is crucial, in order to avoid early torcular thrombosis before the cavernous
sinus capture occurs.
405Fetal and Postnatal Changes of Sinuses
Fig. 7.8. (continued) A 6-month-old girl presenting with a calvarial hemangioma (A).
MR and angio-MR demonstrated an underlying DSM as well as a possible communication between both lesions (B, C).Angiography confirmed the DSM and showed the
so-called hemangioma to correspond to an emissary venous communication for the
superior sagittal sinus mimicking a sinus pericranii (D, E )
7Dural Arteriovenous Shunts406
Fig. 7.9A–D. Large middle cranial fossa (epi)dural sinus malformation
following the path of the embryonic tentorial sinus.The lesion was
incidentally discovered in view of hemangiomatous lesions on the
ipsilateral face and skull (E).Spontaneous thrombosis occurred
without significant clinical expression (F–I). However,careful analysis
of the cerebral venous drainage showed severe pseudo-phlebitic
remodeling (J, K), constituting a potential risk for seizures in the
future. F–K see p. 407
▲
407Fetal and Postnatal Changes of Sinuses
Fig. 7.9F–K. Legend see p. 406
Seven patients presented without brain damage, with partial or no
cavernous capture, and the DSM was located some distance from the
torcular. The follow-up showed six patients with good progression
(six cured) and one with poor progression.The patient with the poor
progression showed a progressive increase in the size of her malformation for 9 months and later died from intracranial hemorrhage due
to associated cavernomas. Another patient presented without brain
damage, bilateral cavernous capture, jugular bulb dysmaturation, but
no pial, straight sinus, or SSS reflux. This patient had his mural AVS
embolized with good progression in time. Five patients presented
without brain damage, bilateral cavernous capture, jugular bulb dysmaturation and reflux into pial veins, straight sinus, or SSS. These patients were embolized transarterially for their arteriovenous shunt
(AVS) and transvenously by coils to disconnect the pial vein openings.
Four patients had good subsequent progression.One of them had stable progression for 18months and later presented with an intraventricular hemorrhage due to persisting pial reflux.
7Dural Arteriovenous Shunts408
Fig. 7.10A–D. A 2-year-old child (A) presenting with ipsilateral DSM (B,C) and facial
soft tissue lesion much larger than the small AVM demonstrated on the angiogram
(D)
409Fetal and Postnatal Changes of Sinuses
Fig. 7.11A–C. A 3-month-old child presenting with macrocrania
and a subgaleal mass. Clinical examination demonstrated a
large pulsatile mass and intracranial bruit.Angio-MRI showed a
large, partially thrombosed superior sagittal sinus,torcular,
and straight sinus DSM. There was a large meningeal supply
converging to the various pouches
7Dural Arteriovenous Shunts410
Fig. 7.12A–C. A 4-month-old boy presenting with an intracranial bruit. MRI performed at 7months of age showed a
complex malformation of the superior sagittal sinus initially
demonstrated with a decrease in the intralesional flow and
a partial thrombosis (A). No therapeutic decision was taken.
The child presented at 8months with a bilateral venous
infarction with hemorrhage and ventricular rupture (B, C)
The other patients with better progression had lateralization of the
DSM or a location away from the torcular on the SSS, allowing the
brain to drain through the contralateral sinus or via the Labbé veins
downstream from the DSM.In three patients from this group,a spontaneous cure with remodeling of the sinuses was observed.
The clinical problem created by the dural sinus malformation is determining to which extent the venous outlets of the brain have been diminished and the additional overload into the sinus by the AVS.
The endothelial properties of the malformed portion of the dural sinuses are also altered.Spontaneous thrombosis is common and spreads rapidly in certain forms (midline giant lakes associated with DVAs opening into
the malformed sinus; Fig. 7.12).It may lead to complete occlusion of all venous outlets and sometimes coagulation factor consumption syndromes
(Fig. 7.13).Bilateral venous infarctions are usually seen when spontaneous
occlusion of the entire pouch occurs and can sometimes be promoted by
endovascular embolization of the associated AVS. In one case, a venous
stroke was demonstrated unilaterally on MRI but was still clinically asymptomatic (Fig. 7.12).In other situations, the available venous outlets remain
sufficient for a while,and the manifestations will mostly be subacute,associated with convulsive episodes or focal intracerebral (Fig. 7.14) or subdural hemorrhages. If the lesion is still not recognized and properly managed
411Fetal and Postnatal Changes of Sinuses
Fig. 7.13A,B. Neonatal diagnosis of lateralized DSM preserving part of the torcular
and one lateral and sigmoid sinus.Symptoms included intracranial bruit and macrocrania. A coagulation disorder (Kasabach-Meritt-like syndrome) was noted in this
particular patient.Lymphatic malformation of the cranial cervical region was also diagnosed. (Courtesy of G.Wilms)
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