Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3733_Библиотеки_им_академика_М_И_Перельмана.pdf
be additionally supplemented with tantalum particles to enhance radiopacity.
Given that NBCA precipitates nearly immediately upon contact with ionic
solutes in blood, the delivery microcatheter has to be prerinsed with
dextrose–water before administration. The flow rate and eventual penetration
potential of the embolic agent as it emerges from the delivery catheter can be
modulated by adjusting final viscosity based on concentration of Ethiodol as
well as by adjusting the intensity and pace of the hand injection through the
microcatheter. Given the significant adhesive properties of NBCA, it is
imperative that the delivery catheter be removed immediately following
delivery of agent as failure to do so can result in significant vascular injury as
removal of a stuck microcatheter is attempted in a delicate intracranial
vascular tree. Onyx is a newer liquid embolic agent that does not instantly
precipitate, thereby theoretically allowing for greater downstream
penetration. Furthermore, a developing Onyx cast does not demonstrate
adhesion to the delivery catheter. As such, although it remains important to
not allow excessive reflux along the microcatheter of Onyx precipitate, it is
possible to build a small Onyx plug along the distal-most end of the
microcatheter. This allows for enhanced proximal occlusion of the
microcatheterized feeding pedicle, creating a “back pressure” that then
permits subsequent Onyx injections to penetrate deep into downstream
nidus.
23,24
Although a treatment session with Onyx can take significantly
longer as compared to when using NBCA, in our experience, it allows for
more controlled and targeted delivery of embolic agent.
Patient Preparation
The initial aspects of patient preparation include a detailed discussion with
the patient and/or family regarding the goals of treatment. As discussed
earlier, it is our recommendation that all patients being considered for
treatment be initially evaluated with a digital subtraction cervicocerebral
diagnostic angiogram. Review of the data provided by this study and
correlation of the findings with each patient’s specific clinical situation will
allow the practitioner to formulate and present a comprehensive rationale for
treatment. Following this, all patients should undergo an appropriate
preoperative medical workup, including assessments of their medical
comorbidities. The presence of significant medical conditions can
significantly affect prognosis, and this should factor into discussions
regarding the risks and benefits of therapy. Finally, renal function should be
assessed as endovascular therapy of these lesions will often require a
significant contrast load and those with impaired renal function should
undergo appropriate preprocedure hydration. Following these steps, patients
are brought to the angiography suite and placed under general anesthesia.
Appropriate blood pressure monitoring in the form of invasive arterial
transduction is established to allow for close blood pressure monitoring and
titration.
Endovascular Treatment Platform
Arterial access for endovascular therapy is typically obtained via the
transfemoral route and a 6-Fr short sheath. Alternative access can be
established via a transradial route (if the aortic arch is significantly diseased
or if a tortuous vertebral artery with unfavorable proximal anatomy is to be
accessed). A longer sheath with its tip in the common carotid artery can be
used if additional support is desired in the setting of a capacious descending
aorta or aortic arch. In the absence of any recent intracranial hemorrhage, a
loading bolus of 3,000 to 5,000 International Units of intravenous (IV)
heparin is given and an activated clotting time goal of 200 to 260 seconds is
set. If planning to use Onyx for embolization, it is imperative to use a
DMSO-compatible microcatheter. Our current catheter of choice is the
Marathon flow-directed catheter (Covidien, Irvine, California). Given the
supple nature of this embolic delivery catheter, it is imperative to use an
intermediate coaxial catheter system that will allow for distal navigation of
the delivery microcatheter. For this purpose, we generally use a 6-Fr guide
catheter (Neuron 0.70 in [Penumbra, Alameda, California] or Envoy MPD
0.70 in [DePuy Orthopaedics, Inc., Warsaw, Indiana]) along with a distal
access catheter (DAC 0.38 in [Concentric Medical, Hertogenbosch, the
Netherlands]). For the anterior cerebral circulation, the DAC is typically
delivered into the proximal middle cerebral artery (MCA) or anterior cerebral
artery (ACA), whereas for the posterior circulation, it is typically taken up to
the level of the distal vertebral artery. Following this, the Marathon
microcatheter is typically navigated over a 0.10-in microwire into a feeding
arterial pedicle from which point onward the microwire is withdrawn into the
microcatheter and the catheter tip is flow-directed to a point just proximal to
entry into the nidus. The ability to navigate as close as possible to the nidus
will allow for optimal penetration of delivered embolic material into the
AVM nidus. This is critically important as embolization of feeding pedicles
alone will not result in adequate treatment of the lesion as deafferented nidus
will re-recruit additional arterial supply over time. Penetration of embolic
material with resulting obliteration of the nidal lumen is critical for effective
treatment of these lesions. It is therefore imperative that adequate effort be
undertaken to navigate the microcatheter tip into as optimal a position as
possible. The use of intermediate coaxial guide and delivery catheters (as
detailed earlier) serves to assist with distal delivery of the microcatheter tip,
particularly in the setting of tortuous vascular anatomy.
Embolization Technique
Once microcatheter delivery to an optimal location has been achieved, it is
critical to study the relevant angiographic runs carefully before commencing
embolization. These should consist first of an overall angiographic image of
the vascular architecture of the relevant part of the brain, which is typically
obtained by contrast injection into an upstream guide catheter. This should
allow for complete visualization of the nidus and delineate all significant
feeding arterial pedicles, draining veins, and blood flow patterns to the
surrounding brain. Second, a microinjection through the microcatheter should
be performed, and this will provide a focused overview of the angiographic
anatomy downstream of the microcatheter tip.23 Particular attention should be
paid to the nidal penetration of injected contrast material, the presence of any
en passage arterial supply to normal brain, and the location and timing of
venous outflow. Only upon obtaining a clear understanding of the anatomy
and flow dynamics of the lesion should embolization be undertaken. In
preparation for use of Onyx, the microcatheter is prerinsed in situ with an
appropriate volume of DMSO. This volume will be equivalent to the
microcatheter dead space volume, which is available in the microcatheter
package. It is imperative that the catheter be purged of ionic contents before
Onyx injection as failure to do so will result in Onyx precipitation within the
catheter itself. However, it is also important to note that DMSO injection into
the catheter should be performed very slowly as this solvent is caustic and
can induce vasospasm and angionecrosis in downstream vasculature. Once
this has been performed, Onyx liquid embolic is gently injected under direct
fluoroscopic visualization, and careful modulation of the hand injection
intensity and pace is used to allow the injected stream to gradually progress
down the catheterized arterial pedicle and into the nidus. It is essential that
Onyx penetration into the draining venous system be avoided as venous
compromise significantly increases the risk of hemorrhage and must be
avoided. As the Onyx cast builds up proximally to the catheter tip, the initial
injection is halted and the intravascular embolic cast is allowed to solidify.
Subsequent injections are modulated very carefully to maximize distal
penetration of embolic material and minimize proximal reflux. Although a
small degree of Onyx reflux along the distal catheter can be tolerated, a
significant cast should not be created along the microcatheter as this will
impede its removal. Even though Onyx is not adhesive, its cohesive
properties can cause microcatheters to get lodged, and attempted removal can
result in significant traction on the intracranial vascular tree, significantly
increasing the risk of hemorrhagic complications.
25,26
Once embolization
through the pedicle of choice is completed, the microcatheter is gently
disengaged from the Onyx cast. This will frequently require the progressive
building of tension on the microcatheter tip. As this tension is built, the
intermediate DAC catheter that was previously parked in the proximal
vasculature can be brought into the proximal portion of the feeding pedicle,
allowing for more direct force transmission to the microcatheter tip and less
distortion of the intracranial vascular anatomy. Upon successful
disengagement, the microcatheter is removed. Follow-up angiography is
performed to assess the results of the embolization (Fig. 13.2). At this point,
it is critical to look specifically for any signs of untoward occurrence
including compromise of venous outflow, presence of embolic material in
unintended locations, or any extravasation indicative of hemorrhage. In the
absence of these conditions, a new microcatheter can then be navigated into
the vascular tree for purposes of microcatheterizing additional feeding arterial
pedicles if desired. Although there is debate regarding how much of the nidus
can be safely embolized in a single treatment setting, in our practice, we
generally limit ourselves to approximately one-third of the lesion.
Embolizations that are more aggressive than this carry with them the risk of
increasing hemorrhagic complications resulting from significantly increased
transient flow through the remaining nonembolized nidus.
25,27
Therefore, it is
important to emphasize tight blood pressure control following embolization.
If there is inadvertent embolization of a significantly larger portion of nidus
than was initially intended or any untoward sign concerning for venous
outflow compromise, then strong consideration should be given to urgent
same-day surgical resection of the remaining lesion. In case staged
embolizations are deemed suitable, the patient is brought back for another
embolization session 2 to 3 weeks after the previous session.
POSTOPERATIVE MANAGEMENT
Upon completion of embolization and successful withdrawal of the
microcatheter/DAC construct, a final set of angiographic images is obtained
to assess the final results of the procedure. Specific attention is directed
toward assessing the extent of final nidus embolization and ensuring that
venous outflow patterns remain preserved. Additionally, the remaining
hemispheric vasculature must be inspected carefully to ensure that there are
no vascular cutoffs secondary to inadvertent distal embolization of embolic
material or thromboembolism. The guide catheter should be withdrawn
carefully from the cervical segment of the internal carotid or vertebral artery
and a final cervical angiogram performed to confirm absence of inadvertent
injury to the cervical segment. Finally, these terminal angiographic images
can be closely scrutinized at the end of the case to determine the need (if any)
for further staged embolization procedures and the potential vascular access
route to be used if further endovascular intervention is to be pursued.
TIPS AND TRICKS
REFERENCES
1. Achrol AS, Guzman R, Varga M, et al. Pathogenesis and radiobiology
of brain arteriovenous malformations: implications for risk stratification
in natural history and posttreatment course. Neurosurg Focus.
2009;26(5):E9.
2. Fullerton HJ, Achrol AS, Johnston SC, et al. Long-term hemorrhage risk
in children versus adults with brain arteriovenous malformations. Stroke.
2005;36(10):2099–2104.
3. Brown RD Jr, Wiebers DO, Forbes G, et al. The natural history of
unruptured intracranial arteriovenous malformations. J Neurosurg.
1988;68(3):352–357.
4. Buis DR, Van Den Berg R, Lagerwaard FJ, et al. Brain arteriovenous
malformations: from diagnosis to treatment. J Neurosurg Sci.
2011;55(1):39–56.
5. Deruty R, Pelissou-Guyotat I, Morel C, et al. Reflections on the
management of cerebral arteriovenous malformations. Surg Neurol.
1998;50(3):245–255.
6. Niazi TN, Klimo P Jr, Anderson RCE, et al. Diagnosis and management
of arteriovenous malformations in children. Neurosurg Clin N Am.
2010;21(3):443–456.
7. Barr JC, Ogilvy CS. Selection of treatment modalities or observation of
arteriovenous malformations. Neurosurg Clin N Am. 2012;23(1):63–75.
8. Monaco EA III, Niranjan A, Kano H, et al. Management of adverse
radiation effects after radiosurgery for arteriovenous malformations.
Prog Neurol Surg. 2013;27:107–118.
9. Reig AS, Rajaram R, Simon S, et al. Complete angiographic obliteration
of intracranial AVMs with endovascular embolization: incomplete
embolic nidal opacification is associated with AVM recurrence. J
Neurointerv Surg. 2010;2(3):202–207.
10. Consoli A, Scarpini G, Rosi A, et al. Endovascular treatment of
unruptured and ruptured brain arteriovenous malformations with
Onyx18: a monocentric series of 84 patients [published online ahead of
print October 14, 2013]. J Neurointerv Surg.
11. Fiehler J, Stapf C. ARUBA—beating natural history in unruptured brain
AVMs by intervention. Neuroradiology. 2008;50(6):465–467.
12. Mohr JP, Moskowitz AJ, Parides M, et al. Hull down on the horizon: A
Randomized Trial of Unruptured Brain Arteriovenous Malformations
(ARUBA) trial. Stroke. 2012;43(7):1744–1745.
13. Stapf C. The rationale behind “A Randomized Trial of Unruptured Brain
AVMs” (ARUBA). Acta Neurochir Suppl. 2010;107:83–85.
14. National Institute of Neurological Disorders and Stroke. A Randomized
Trial of Unruptured Brain Arteriovenous Malformations (ARUBA).
National Institute of Neurological Disorders and Stroke Web site.
http://www.ninds.nih.gov/news_and_events/news_articles/ARUBA_trial_results.htm
Updated January 29, 214. Accessed October 31, 2013.
15. Ondra SL, Troupp H, George ED, et al. The natural history of
symptomatic arteriovenous malformations of the brain: a 24-year
follow-up assessment. J Neurosurg. 1990;73(3):387–391.
16. Englot DJ, Young WL, Han SJ, et al. Seizure predictors and control
after microsurgical resection of supratentorial arteriovenous
malformations in 440 patients. Neurosurgery. 2012;71(3):572–580;
discussion 580.
17. Elhammady MS, Aziz-Sultan MA, Heros RC. The management of
cerebral arteriovenous malformations associated with aneurysms. World
Neurosurg. 2013;80:e123–e129.
18. Ezura M, Takahashi A, Jokura H, et al. Endovascular treatment of
aneurysms associated with cerebral arteriovenous malformations:
experiences after the introduction of Guglielmi detachable coils. J Clin
Neurosci. 2000;7(suppl 1):14–18.
19. Deruty R, Mottolese C, Soustiel JF, et al. Association of cerebral
arteriovenous malformation and cerebral aneurysm: diagnosis and
management. Acta Neurochir (Wien). 1990;107(3–4):133–139.
20. Bristol RE, Albuquerque FC, McDougall CG. The evolution of
endovascular treatment for intracranial arteriovenous malformations.
Neurosurg Focus. 2006;20(6):E6.
21. Rodríguez-Boto G, Gutiérrez-González R, Gil A, et al. Combined staged
therapy of complex arteriovenous malformations: initial experience.
Acta Neurol Scand. 2013;127(4):260–267.
22. Kano H, Kondziolka D, Flickinger JC, et al. Stereotactic radiosurgery
for arteriovenous malformations after embolization: a case-control
study. J Neurosurg. 2012;117(2):265–275.
23. Weber W, Kis B, Siekmann R, et al. Endovascular treatment of
intracranial arteriovenous malformations with onyx: technical aspects.
AJNR Am J Neuroradiol. 2007;28(2):371–377.
24. Saatci I, Geyik S, Yavuz K, et al. Endovascular treatment of brain
arteriovenous malformations with prolonged intranidal Onyx injection
technique: long-term results in 350 consecutive patients with completed
endovascular treatment course. J Neurosurg. 2011;115(1):78–88.
25. Ledezma CJ, Hoh BL, Carter BS, et al. Complications of cerebral
arteriovenous malformation embolization: multivariate analysis of
predictive factors. Neurosurgery. 2006;58(4):602–611; discussion 602–
611.
26. Sun Y, Lv X, Li Y, et al. Complications caused by cerebral
arteriovenous malformation embolization. Neuroradiol J.
2012;25(5):541–547.
27. Biondi A, Le Jean L, Capelle L, et al C. Fatal hemorrhagic complication
following endovascular treatment of a cerebral arteriovenous
malformation: case report and review of the literature. J Neuroradiol.
2006;33(2):96–104.