Procedure-Related Complications: AVMs




Abstract


Endovascular embolization of central nervous system arteriovenous malformations is a powerful adjunct to other therapeutic modalities, including microsurgical resection and stereotactic radiosurgery. Occasionally, arteriovenous malformations can be cured safely using endovascular techniques alone. Embolization, however, may also be perilous and can have permanent deleterious effects if employed carelessly. Here we review the major complications associated with endovascular embolization of central nervous system arteriovenous malformations, with special emphasis on their avoidance.




Keywords

arteriovenous malformation, endovascular embolization, complication avoidance

 




Highlights





  • Endovascular therapy for brain arteriovenous malformations is one piece of a multidisciplinary therapeutic approach.



  • Neurologic complications from AVM embolization are often devastating and only occasionally can be managed endovascularly.



  • Complication management must be focused on prevention.





Background


Cerebral arteriovenous malformations (AVMs) are rare lesions that are best addressed using a combination of complementary technologies and medical subspecialists, including neurosurgeons, neurologists, radiologists, and radiation therapy specialists, such as radiation oncologists or surgeons with specialized training in stereotactic radiosurgery. These lesions harbor a significant risk of rupture—in general, about 2% to 3% per year—with high rates of resultant neurologic disability or death. The ARUBA (A Randomized Trial of Unruptured Brain Arteriovenous Malformation) study raised important questions about the safety and necessity of therapies undertaken to prevent morbidity and mortality associated with these lesions. Endovascular approaches have evolved over several decades and now represent powerful adjunctive therapies aiding in the surgical treatment of AVMs; in some cases, endovascular therapies can serve as stand-alone cures.


Many specialized catheters and embolization agents have been developed since the inception of endovascular AVM embolization, but the most frequently encountered complications remain the same. The most common complication resulting from AVM embolization is hemorrhage—either from inadvertent vessel perforation, venous hypertension after venous outflow occlusion, or normal perfusion pressure breakthrough after extensive or complete embolizations. Ischemic complications are similarly common, resulting from either reflux into or direct embolization of vessels supplying normal brain tissue. Complications directly attributable to catheter technologies and malfunctions are also more commonly seen as endovascular interventions gain widespread implementation. In this chapter, we will review the sources of these complications and discuss strategies for their avoidance.




Anatomic Considerations


Cerebral AVMs are an anatomically diverse group of lesions. In general, a brain AVM consists of one or more feeding arteries that drain directly into one or more draining veins without any intervening capillary bed ( Fig. 41.1 ). Unlike most arteriovenous fistulae, in an AVM there is a complex nidus of small arteries and arterialized veins at the site of the arteriovenous communication. There may be varying amounts of brain matter insinuated between vessels within the nidus, but this brain is invariably gliotic due to vascular steal away from normal capillary beds. There may be loss of cerebral vascular autoregulation globally in the affected brain region, which predisposes to hemorrhagic complications and edema after treatment, as we will discuss later.




Fig. 41.1


Anatomy of a Spetzler-Martin grade 2 arteriovenous malformation of the right frontal lobe fed by branches of the left anterior cerebral artery (ACA), draining via an enlarged cortical vein. Note the enlarged ACA branches feeding the nidus, consistent with a fistula according to the criteria of Yuki. A1, First segment, right anterior cerebral artery; A2, second segment, right anterior cerebral artery; ACoA, anterior communicating artery; CmA, callosomarginal artery; DV, draining vein; N, nidus; PcA, pericallosal artery.


In terms of natural history risk of hemorrhage, it appears that deep venous drainage pattern increases the 5-year risk of rupture for all-comers with the diagnosis of brain AVM from 21% to 34% and increases the 20-year risk from 39% to 52%. Size >5 cm increases the 20-year risk of rupture to 52% as well. Other anatomic considerations that impact the risk associated with brain AVM include the presence of prenidal or intranidal aneurysms, infratentorial location, and previous rupture.


The most commonly used classification schema for characterizing the surgical risk of AVMs is the Spetzler-Martin (SM) grading scale. This scale assigns points on the basis of AVM nidus diameter (1 point for <3 cm, 2 points for 3–6 cm, and 3 points for >6 cm), eloquence of the brain surrounding the lesion (0 points for noneloquent, 1 point for eloquent), and pattern of venous drainage (0 points for cortical/superficial, 1 point for deep venous drainage). Spetzler’s own case series, presented with the description of his eponymous classification system, demonstrated dramatically increased surgical morbidity and mortality when attempting to surgically excise high-grade brain AVMs. Unfortunately, SM grade, although an established predictor of surgical risk, fails to predict the likelihood of complications related to endovascular embolization.


Alternative grading scales have been developed to attempt to quantify the risks undertaken during endovascular embolization of AVMs. In 2010, the AVM neurovascular grade was developed from a review of the literature on embolization-related complications using either Onyx or n-butyl cyanoacrylate glue. This schema scores an AVM on the number of feeding vessels (1 point for <3, 2 points for 3–6, and 3 points for >6), the eloquence of the surrounding brain (similar to SM system), and the presence of an arteriovenous fistula (0 points if absent, 1 point if present). Fistulae can be defined according to the criteria of Yuki et al. as the direct communication of a feeding artery to draining vein without intervening nidus, or as abnormal dilatation to twofold or greater enlargement of the feeding artery compared with a comparable vessel (e.g., in the same territory as the feeding vessel, or compared with the contralateral side). A retrospective validation study of 127 patients demonstrated good interrater reliability and significant differences in scores for patients who were cured with endovascular techniques (median score = 2), patients who required multimodal therapy (median score = 3), and patients who suffered complications attributed to embolization (median score = 4).


In 2015, the Buffalo score was described. This score is determined by the number of arterial pedicles feeding the AVM (1 point for 1 or 2, 2 points for 3 or 4, and 3 points for 5 or more), the diameter of the arterial pedicles (0 points for most >1 mm, 1 point for most <1 mm), and the nidus location (similar to the SM system). In their initial retrospective application of this scale to 50 patients, the Buffalo group demonstrated correlation between their score and complication risk, with >50% risk of complications after embolization for patients with scores of 4 or 5. More recently, however, neither the SM scale, nor the AVM neurovascular grade, nor the Buffalo score was seen to be predictive of complications when retrospectively applied to a group of patients undergoing 55 embolization procedures. The small sample size and low numbers of grade 4 (<10%) or 5 (0%) lesions contribute to this result, however.



Red Flags





  • Many small feeder vessels



  • Close proximity of nidus to circle of Willis



  • Deep venous drainage through single draining vein



  • Marked hypertrophy of feeding artery



  • Significant perilesional edema or gliosis



  • Prenidal aneurysms






AVM Hemorrhage and Hemorrhagic Complications


Hemorrhage continues to be the primary mode of symptom presentation in surgical series of patients with previously undiagnosed AVM, although increasingly, unruptured AVMs are being identified incidentally due to high sensitivity and availability of modern noninvasive imaging modalities. Hemorrhage is also the most common and most devastating complication after endovascular embolization. Hemorrhagic complications can generally be thought of in two categories: those resulting from technical issues, such as vessel perforation or rupture, or those that occur spontaneously and are unrelated to inadvertent vessel rupture. We will discuss these categories separately.


Spontaneous Postembolization Hemorrhage


Spontaneous postembolization hemorrhage is among the most vexing and devastating complications of AVM embolization. There are multiple theories of spontaneous AVM hemorrhage before treatment, and it is believed that these factors contribute to hemorrhage after embolization as well, usually due to changes in transmural vessel pressures or blood flow patterns. The most important concept to be discussed in this regard is that of normal perfusion pressure breakthrough.


The normal perfusion pressure breakthrough hypothesis was posited in 1978 by Spetzler as a mechanism to explain postoperative hemorrhage seen in the brain after complete excision of a high-flow AVM. In normal brain parenchyma, perfusion pressures are maintained within a narrow window by vessel caliber regulation through means that are both extrinsic and intrinsic to the vessels themselves. Cerebral capillary perfusion pressures can be regulated over a wide range of arterial blood pressures as a result. Although extrinsic sympathetic regulation of vascular tone does play a role in the central nervous system, it is primarily through intrinsic smooth muscle autoregulation that capillary perfusion is maintained. Importantly, arterioles appear to have a greater ability to dilate in response to hypotension than they do to constrict in response to hypertension.


In the brain of a patient harboring an AVM, there is an area of low vascular resistance due to the loss of the capillary bed and enlargement of feeding arterial and draining venous calibers. Parallel vascular beds are therefore subjected to relative hypotension with respect to perfusion pressures. The AVM essentially presents a short circuit through which blood will preferentially flow. As a result, vessels irrigating normal brain near the AVM will become chronically dilated in a constant effort to maintain flow to these relatively ischemic regions of the brain. These vessels may either lose their autoregulation abilities, or their autoregulatory set points may be dramatically shifted to remain dilated even in the face of relatively high capillary perfusion pressures. Chronically low tissue oxygen tension may also result in effusive neovascularization with frail, “leaky” capillaries.


The result of these phenomena is a vascular system in which feeding arteries are chronically dilated with reduced capacity to respond appropriately to changes in perfusion pressure heads, and with downstream capillary beds that are prone to rupture. Embolization of an AVM results in decreased flow across the fistula and a compensatory increase in flow through these fragile systems. It would be expected, therefore, that postembolization hemorrhage would be common—and it is.


Several recent studies have evaluated hemorrhage risk after endovascular embolization. Asadi et al. reported post- or intraprocedural hemorrhages in 57 of 199 patients (29%) treated with endovascular embolization, 47% of which occurred spontaneously at a site remote from the embolization after uncomplicated completion of the embolization procedure. This hemorrhage rate is relatively high compared with other series, probably because the majority of patients in this series presented with hemorrhage from the AVM; in addition, almost all patients underwent multiple embolizations (i.e., the risk of complications from an individual embolization procedure is a fraction of these numbers), and an aggressive strategy of endovascular therapy was pursued, with 45% of patients achieving cure of the AVM without supplemental radiosurgery or open microsurgical resection.


Baharvahdat et al. reported post- or intraprocedural hemorrhages after endovascular embolization—again with the goal of complete obliteration of the lesion—in 92 of 408 patients (23% of patients, 11% of embolization procedures). Fifty-two percent of these complications were felt to be related to spontaneous hemorrhage unrelated to inadvertent vessel rupture or perforation during the procedure. Eighty-one percent of these occurred just hours or days after the procedure was complete, with a mean of 34 hours postprocedure. Once again, this study is remarkable for the fact that endovascular embolization was utilized as the sole therapeutic modality in 91% of cases. Spontaneous hemorrhages resulted in 37 patients suffering an acquired neurologic deficit, 58% of which resulted in permanent disability and 10% in death. Types of hemorrhages encountered included intracerebral, intraventricular, and subarachnoid hemorrhage; 71% of spontaneous hemorrhages were intraparenchymal. Importantly, the authors of this study identified premature embolization of the draining vein as a contributing factor in delayed hemorrhage, with 17% of hemorrhages occurring in this context, although other authors have reported successful transvenous embolization strategies in small patient samples.


In neurosurgical series using embolization as an adjunctive therapeutic modality followed by either microsurgical resection or stereotactic radiosurgery, hemorrhagic complications appear to be less common. Crowley et al. reported permanent neurologic morbidity from all causes in 9.6% of patients with only 1 death out of 327 patients treated. Six of 153 patients (4%) suffered unexpected postprocedural neurologic deficits secondary to hemorrhagic complications in an earlier, smaller series published by the same group. Only 13% and 2.3% of procedures in the smaller and larger series, respectively, were curative, whereas 70% and 79%, respectively, were performed before microsurgical resection of the lesion, thus highlighting differences in treatment strategies employed around the world and by different subspecialists. One should bear this in mind when comparing studies, because the surgical complications after craniotomy may not be included in the reported data. In an older surgical series, Taylor et al. reported permanent neurologic deficits after embolization in 18 of 201 patients (9%) and death in 4 patients (2%). Again, in this series embolization was used primarily as an adjunct to surgical resection.


In summary, periprocedural intracerebral hemorrhage after endovascular embolization of is most common in patients in whom: (1) complete embolization of the lesion is attempted in one session, (2) when embolic material enters the draining veins during subtotal embolization, and (3) when high-risk features (e.g., intranidal aneurysms) are left untreated. Hemorrhage in these situations is caused either by worsening of venous or intraaneurysmal hypertension or by normal perfusion pressure breakthrough. Avoidance of hemorrhage may therefore be accomplished by staging attempts at embolization, targeting high-risk features of the lesion early in treatment, and maintaining strict blood pressure control after embolization. The risks of hemorrhage from attempted endovascular cure of the AVM should be weighed against the risks of microsurgical resection, which are patient- specific but may be accurately predicted by the SM grading scheme.


At our institution, all cerebral AVMs are treated by neurosurgeons with training in both open surgical and endovascular treatment modalities, and with access to state-of-the-art radiosurgical therapy. Embolizations are generally staged with no more than 30% to 50% of the lesion embolized in a single session, except in very small lesions fed by a single artery, when cure may be achieved in a single sitting and partial embolization is not possible. Postoperatively, systolic blood pressures are controlled to <120 mm Hg, frequently requiring intravenous infusions of nicardipine. Labetalol is a second-line agent that is also used as a continuous infusion or, more commonly, on an as-needed basis for breakthrough hypertension. Postembolization, all patients are monitored in the neurosurgical intensive care unit at least overnight. Neurologic deterioration from delayed postembolization hemorrhage generally prompts immediate evacuation of the hematoma and resection of the AVM.

Only gold members can continue reading. Log In or Register to continue

Stay updated, free articles. Join our Telegram channel

Jun 29, 2019 | Posted by in NEUROSURGERY | Comments Off on Procedure-Related Complications: AVMs

Full access? Get Clinical Tree

Get Clinical Tree app for offline access