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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 Shunts412
Fig. 7.14A–C. Neonatal diagnosis of dural arteriovenous shunt
in which MRI suggested A torcular and B left-sided DSM.
Macrocrania and ventricular dilatation led to ventricular
shunting. C At 7 months, the child presented with a large,
right-sided hematoma. Note the secondary thrombosis with
tonsillar prolapse and a slow-flow signal in the midline and
left-sided sinus
at this already eloquent phase,then melting-brain syndrome will eventually occur (Fig. 7.15), usually remote from the DSM site, where the venous
constraints are maximum (see Chap.2, this volume).
These lesions are often seen in utero,and therefore early correction of
the AVS and preservation of the remaining venous outlets seems to be a
logical immediate goal.Yet similar to VGAMs and CAVMs, early delivery
is not recommended,as we will then face an even more immature vascular system in a patient who needs emergency treatment.It appears that the
413Fetal and Postnatal Changes of Sinuses
Fig. 7.15A–D. A 1-month-old boy presenting with mild cardiac overload that was not
treated and progressive macrocrania with a large ventricle. Magnetic resonance imaging (A) and angiography (B, C) confirmed the DSM with bilateral thrombosis of the
sigmoid sinus. Persistence of occipital and marginal sinus offered insufficient venous
outlet. Note the melting-brain syndrome (D)
therapeutic window following the first symptoms for these technically
challenging lesions is quite narrow.In some instances, the delay between
the first symptom and referral is such that irreversible brain damage has
already occurred. In others, the impact of the malformation is such that
the thrombosis has compromised the only remaining cerebral drainage.
In these situations, regardless of the techniques available, the child will
develop cerebral hemorrhagic infarction. In some of the less extensive
forms of the malformation, we have successfully occluded the associated
AV S in an emergency procedure, despite minimal or even absent symptoms (Fig. 7.16).Heparin treatment following the AVS occlusion has been
used to keep the only patent jugular vein open.In other cases,the demonstration of alternative draining pathways for the brain may allow the
transvenous exclusion of the venous lake or in such rare and favorable
situations, the AVS and the DSM lake may thrombose spontaneously
(Fig. 7.17). These children grow normally and have a normal neurocognitive status for their age.
The key angioarchitectural features that will influence the natural history and therefore prompt immediate endovascular preventive or corrective measures are the following (Barbosa et al. 2003) (Scheme 7.2):
DSM involving the torcular: noted in 14 patients (46.6%) (Table 7.2;
Figs. 7.16–7.19; Scheme 7.3).
Pial, straight, and superior sagittal sinus reflux: present in 15 patients
(50.0%) (Table 7.3; Scheme 7.4).
Dysmaturation of the jugular bulb (postnatal occlusion of the jugular
bulb and retrograde thrombosis of the sigmoid sinus) demonstrated
in 16 patients (56.0%) (Table7.4); persistence of a medial occipital
sinus by-passing the occluded jugular bulb must be looked for
(Schemes 7.5,7.6).
To tal bilateral cavernous sinus capture (drainage of deep and superfi-
cial sylvian veins in the cavernous plexus) seen in 14 patients (46.7%).
Partial cavernous sinus capture present in eight patients (26.7%).
No cavernous sinus capture was noted in eight patients (26.7%)
(Table 7.5).
The treatment includes endovascular techniques (transarterial or trans-
venous), often associated with medical management with heparin.
The choice of embolization material is either glue or coils and in some
cases both. Some neonates or young infants are not embolized due to
either preexisting brain damage or a low Bicêtre admission score at
the time of consultation. The therapeutic options depend on the individual case’s angioarchitecture and state of the maturation or dysmaturation process. When there is partial or no cavernous capture and no
pial reflux, there is an option of treating with heparin and embolizing
the shunts with glue, with the expectation that cavernous capture will
take place with minimal or no consequences for the hydrovenous equilibrium of the maturing brain and granulations. If there is significant
AV shunting causing pial reflux or adding to restricted outlets, embolization is necessary to prevent venous hypertension and cerebral ischemic
damage. The goal is to reduce to pial reflux, realizing that the shunts
may preserve the patency of the sinuses.If the dural AVSs are completely
7Dural Arteriovenous Shunts414
415Fetal and Postnatal Changes of Sinuses
Fig. 7.16A–H. Neonatal diagnosis of left-sided capillary hemangioma of the face.
A, B Clinical examination led to diagnosis of large dural malformation involving the
left sigmoid and lateral sinus and reaching the left side of the torcular. C,D A highflow fistula into the sinus from the middle meningeal artery was embolized at
6months.Considering the already existing venous restriction (tonsillar prolapse),the
contralateral jugular vein narrowing, and the restriction in the cortical vein drainage,
the child was treated with low-molecular-weight heparin for 5 months.At 16months
of follow-up,the hemangioma was stable, the occlusion of the fistula was confirmed,
and the child was normal on neurocognitive evaluation.Left-sided hyperemia persisted, corresponding to a large hemangiomatous phenomenon with no dural sinus communication, but the tonsillar prolapse subsided (E,F). G, H Associated cutaneous le-
sions.E–H see p. 416
7Dural Arteriovenous Shunts416
Fig. 7.16E–H. Legend see see p. 415
417Fetal and Postnatal Changes of Sinuses
Fig. 7.17A–C. A 2-month-old boy presented with macrocrania. A, B Early MRI
already demonstrated tonsillar prolapse related to posterior fossa venous congestion
secondary to superior sagittal sinus dural malformation, partially thrombosed, but
remote from the torcular.Conservative treatment was chosen.Spontaneous thrombosis of the lesion occurred 12 months later and produced a significant reduction in the
size of the lesion. C The superior sagittal sinus distal to the lesion reduced in size.The
torcular remained patent, as did the sigmoid sinus bilaterally.The tonsillar prolapse
resolved
7Dural Arteriovenous Shunts418
Scheme 7.2. Effect of the spontaneous or induced thrombosis of dural sinus malformation according to type and occurrence of maturation processes
Ta ble 7.2. Location of the dural sinus malformation (Barbosa et al. 2003)
To rcular involvement No torcular involvement
Favorable progression 4 (28.6%) 13 (81.25%)
Unfavorable progression 10 (71.4%) 2 (12.5%)
No follow-up 0 1 (6.3%)
To tal no. of patients 14 (46.6%) 16 (53.3%)
419Fetal and Postnatal Changes of Sinuses
Fig. 7.18A–F. Legend see p. 420
7Dural Arteriovenous Shunts420
Fig. 7.18A–I. At the age of 9 and 11 months, this child was medically treated for leftsided seizures.At 1.5 years,the child sustained a cranial trauma and was submitted to
surgery for drainage of a right temporo-occipital subdural hematoma. A–C Digital
subtraction angiography (DSA) showed a dural arteriovenous fistula (DAVF) in the
left sigmoid/transversus sinus. D Angiography and embolization using the venous
approach; E–G 4.35 m of 38 guidewire was delivered into the left lateral and sigmoid
sinus. H–I Six months later, angiographic control showed no arteriovenous (AV)
shunts.The child is currently still well and without complications. Note the patency of
one sinus and the quality of central drainage (Courtesy of R. Piske)
421Fetal and Postnatal Changes of Sinuses
Fig. 7.19A–C. A 1-month-old girl presented with a generalized seizure and macrocrania. A MRI shows mild ventriculomegaly with large subarachnoid spaces. There
was evidence of a right-sided subdural hematoma. B Angiography demonstrated lateralized dural sinus malformation with a venous lake and adjacent arteriovenous
shunting. C Several patent venous outlets remained; however,minimal tonsillar prolapse was already evident. The baby was partially embolized and low-molecular heparin was administered
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