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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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5.5.2 Dural Sinus High Flow
Similar clinical and imaging findings that occur in primary high-flow
dural AVSs, can also be encountered in high-flow pial lesions (Fig. 5.16),
provided that the same dural conditions are present (Scheme 5.1B).These
hydrodynamic disorders are specific to very young children,prior to the
maturation of the Pacchionian granulations.
All the events described in infancy involving hydrodynamic failure
(see Chaps. 2 and 3,this volume) can occur, including tonsillar prolapse,
hydrocephalus, and melting-brain syndrome as soon as venous ischemia
starts to develop (see Chap.2, this volume). Rapid brain destruction can
be observed,but this occurs most rapidly at the end of the neonatal period (Fig. 5.17).
Careful attention should therefore be paid to any early warning symptoms. Convulsion, which in CAVM indicates a local insult,should lead to
urgent management, regardless of the good clinical tolerance. Multiple
convulsive episodes often accompany obvious cerebral damage and indicate a melting-brain phenomenon;morphological exclusion of the lesion
at this stage will not prevent severe disability.
5Cerebral Arteriovenous Malformations312
Scheme 5.1a. Ve nous high-flow angiopathy in cerebral arteriovenous malformations
(AVM) in children. AV s h unt,arteriovenous shunt. Asterisk,Water retention is found
in infants
3135.5.2 Dural Sinus High Flow
Scheme 5.1b. Ve nous high-flow angiopathy in cerebral arteriovenous malformations
(AVM) in children. AV s h unt,arteriovenous shunt. Asterisk,Water retention is found
in infants.
Fig. 5.16A,B. Neonate presenting at birth with acute cardiac failure. Loud intracranial bruit could be heard.Angiography demonstrates a large posterior fossa AVM
5Cerebral Arteriovenous Malformations314
Fig. 5.17A–D. Neonate presenting with moderate to severe heart failure demonstrates on nonenhanced CT (A) and enhanced CT (B) severe focal cortical atrophy involving the left temporal/occipital/parietal lobe with abnormal enhancement caused
by cerebral arteriovenous malformation (CAVM). One year later following partial
embolization that corrected the congestive heart failure (CHF), MRI T1W1 (C, D)
showed severe focal cerebral atrophy as well as diffuse ventricular enlargement. The
child had persistent neurological deficits and developmental delay
5.5.3 Venous Ischemia and Thrombosis
All possible degrees of venous ischemia can be observed with the severest expression resulting in melting-brain syndrome, which occurs at the
end of the neonatal period and during infancy. Subacute brain loss can
often be noted in retrospect, as focal ischemia in infants may produce
seizures or deficits that can remain limited or can regress if the lesion is
quickly managed or if the venous impairment is limited or compensated
(Fig. 5.18). The new equilibrium that results from progressive changes in
the venous drainage or from successive adaptations to subacute episodes
may eventually fail. Under such circumstances, usually in early childhood, hemorrhagic venous infarction will occur. The related deficit depends on the extent of the hemorrhagic infarct, but regression is seldom
complete because of the underlying ischemia. Depending on where the
thrombosis is located,the infarction may be closely related to the malfor-
may be multifocal,remote,and bilateral if the thrombosis affects the dural sinuses (Scheme 5.1C).
315Ve n o us Ischemia and Thrombosis
Fig. 5.18A,B. A young girl presented at the age of 9 years with generalized seizures,
cerebellar syndrome, and nystagmus.Slight exophthalmia was also detected. Note the
focal atrophy
5.5.4 Venous Hemorrhage
Ve n o us thrombosis or any other obstacle may also lead to venous rupture, which may be located at some distance from the nidus. In such cases, a false aneurysm of venous origin can sometimes be demonstrated.
When extravascular blood is shown, it can point to the exact site of the
rupture (Figs. 5.19–5.21).The size of the hematoma is unpredictable, and
there is no relationship between the size of the hematoma and the size of
the AVM. Since the rupture is venous, in our experience, subarachnoid
bleeding under these circumstances is rarely seen alone and subdural
hemorrhage can be seen, particularly in infants. The course of such false
aneurysms usually involves their partial integration into the venous
drainage of the malformation. The hemorrhage usually provokes an isolated seizure, and its repetition can be indicative of an early recurrence,
which is not rare in early childhood. The deficit caused by the hematoma
tends to resolve without residual neurological impairment. Some permanent sequelae may be seen in very eloquent areas in older children
(Scheme 5.1D).
5Cerebral Arteriovenous Malformations316
Scheme 5.1c. Ve nous high-flow angiopathy in cerebral arteriovenous malformations
(AVM) in children. AV s h unt,arteriovenous shunt. Asterisk,Water retention is found
in infants
317Ve n o us Hemorrhage
Fig. 5.19A–D. Neonate presented at the age of 3 days right partial sensory-motor
epilepsy. MR examination disclosed a rolandic region arteriovenous malformation
that was confirmed by angiography (A, B).An embolization was planned but before
the procedure could be performed, the child had an intracranial hemorrhage due to
rupture of the lesion (C,D)
5Cerebral Arteriovenous Malformations318
Fig. 5.20A–D. A 9-year-old girl presented with intracerebral hemorrhage and neurological deficit. On MRI T2W1 axial (A) and coronal view (B), it was demonstrated that
she had increased signal surrounding a well-defined area of mixed signal (arrows),
which at left internal carotid angiography frontal views (C,D) proved to be caused by
venous pseudoaneurysm (arrow)
319Ve n o us Hemorrhage
Fig. 5.21A–D. Unenhanced CT (A, B) demonstrates evidence of recent right cerebellar hemorrhage with defined area of slightly lower hyperdensity (arrow) in a 5-yearold girl. MRI at that time demonstrated the same lesion on T2WI (C) to have a mixed
signal but showed homogeneous enhancement (arrow) with contrast (D). E,F see p.
320
5Cerebral Arteriovenous Malformations320
Fig. 5.21E,F. (continued) Vertebral angiogram in frontal views (E, F) showed this
lesion to be venous pseudoaneurysm (arrows)
Scheme 5.1d. Ve nous high-flow angiopathy in cerebral arteriovenous malformations
(AVM) in children. AV s h unt,arteriovenous shunt. Asterisk,Water retention is found
in infants
5.5.5 Venous Enlargement
Ve n o us pouches are very frequent in children, since thrombosis and high
flow are often present.They are characteristic of CAVFs seen in HHT children (see Chap.4, this volume). These pouches behave like any large pulsatile mass and may have neurological manifestations,although the ability of the infant’s head to enlarge often allows giant pouches to be diagnosed with almost no mass-related symptoms.Adaptation of the adjacent
brain makes these huge pouches rarely directly responsible for symptoms
in children.Some subtle deficits can be noted,as well as seizure activity.In
our experience, the latter is nearly always associated with a spontaneous
partial thrombosis of the pouch.MRI at this point demonstrates an area of
signal hyperintensity in the brain surrounding the pouch (Berenstein
1992a). It is of interest to note that the thrombosis of similar pouches induced by embolization does not produce the same perilesional changes,
nor does it produce deficit or seizures. Increasing size of these pouches
can be observed over time subsequent to the development of restriction of
the downstream outlets; it can be difficult to distinguish a giant arterial
pouch from a giant venous pouch when located within a nidus (Fig. 5.22).
Spontaneous thrombosis of a false sac and the secondary possibilities of
angiogenesis within the thrombosed pouch should not be underestimated
and therefore followed up (Fig. 5.13; Scheme5.1E).
321Ve nous Enlargement
Scheme 5.1e. Ve nous high-flow angiopathy in cerebral arteriovenous malformations
(AVM) in children. AV s h unt,arteriovenous shunt. Asterisk,Water retention is found
in infants
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