Endovascular Arterial Occlusion Accomplished Using Microcoils Deployed with and without Proximal Flow Arrest: Results in 19 Patients

After Serbinenko published his description of arterial occlusion with the use of detachable latex balloons in 1974 (1), permanent endovascular occlusion of the carotid and vertebral arteries was rapidly adopted for treatment of a variety of vascular disorders. The efficacy of endovascular carotid and vertebral artery occlusion for treatment of aneurysms, pseudoaneurysms, arteriovenous fistulas, neoplasms, and traumatic injuries is now widely acknowledged. For over two decades, detachable balloons made from silicone or latex have been considered the appropriate device for endovascular occlusion of the carotid and vertebral arteries. Until May 1998 (subsequent to treatment of the patients described in this report), no detachable balloons had been approved by the Food and Drug Administration, and these devices were available only on a limited basis. Alternative methods for arterial occlusion were used in some cases, and only a few reports had been published concerning the use of coils for cerebrovascular arterial occlusion (2–6). More recently, Graves et al (7) described safe endovascular arterial occlusion using complex platinum microcoils placed during temporary proximal flow arrest in a series of 19 patients. In this report, we describe the use of microcoils for occlusion of 11 vertebral and eight carotid arteries in 19 patients. Unlike the technique reported by Graves et al, we used temporary proximal flow arrest for only six (32%) of these cases.

Methods

Nineteen patients, 12 women and seven men, 23 to 82 years old (mean age, 58 years), underwent permanent endovascular occlusion of 19 arteries (Table1). The occluded vessels included six internal carotid, two common/internal carotid, and 11 vertebral arteries. The treated lesions included nine aneurysms, one carotid-cavernous fistula with a pseudoaneurysm, seven neoplasms, and two arterial dissections. Nondetachable balloons were used to arrest proximal blood flow during occlusion of six (32%) arteries. Anticoagulation was used in 18 (95%) of the cases. All of these patients received intravenous bolus injections of heparin (5000 U) 5 to 10 minutes before microcoil placement. Laboratory analyses of the effects on coagulation profiles were not performed. In all 19 cases, the coaxial catheter systems were perfused continuously with normal saline flush solutions containing heparin (5000 U/L). The additional amount of heparin introduced through the catheter systems was estimated to be approximately 1500 U. To reduce the risk of air emboli, all coil introducers were flushed with an identical heparinized saline solution before coil introduction. The number of coils used in each case ranged from three to 88 (mean, 18). Complex fibered platinum microcoils (Boston Scientific Corp, Watertown, MA, and Cook, Inc, Bloomington, IN) were used for all cases, and Guglielmi detachable coils (GDCs) (Boston Scientific Corp) were also used in two patients. Complete pre- and postocclusion neurologic evaluations were performed in all patients.

These 19 patients do not represent a consecutive series. During the same time period (December 1993 to December 1997), five additional patients underwent carotid artery occlusion for treatment of aneurysms and carotid-cavernous fistulas with detachable silicone balloons under our physician-sponsored investigational device exemptions (IDEs) for this device. Our IDEs did not cover vertebral artery occlusion with these balloons, which accounts for the relatively higher number of vertebral arteries occluded with microcoils. Patients treated with detachable latex balloons were also excluded. Additional patients in whom temporary arterial balloon test occlusion had failed and who had bypass grafts placed before arterial occlusion were also excluded from this report.

Results

Microcoils provided rapid and durable arterial occlusion in 17 (89%) of the 19 patients. Routine follow-up angiograms were not obtained. Arterial recanalization was not evident clinically in any case. The follow-up period ranged from 4 to 36 months (mean, 19 months). No new neurologic deficits developed in 16 (84%) patients after arterial occlusion. No patient had an acute event that suggested an embolic complication.

Patient 7 (treated for a ruptured PICA aneurysm by occlusion of the vertebral artery across the PICA origin) continued to incur slowly progressive neurologic deficits attributed to severe vasospasm and inadvertent surgical ligation of the AICA. No abrupt or significant change in neurologic status was noted on the day of the procedure to suggest an embolic complication.

Patient 18 (with a cavernous aneurysm) had transient upper extremity weakness and mild dysphasia 24 hours after internal carotid artery occlusion. Whether this represented collateral vascular insufficiency or a delayed embolic event could not be determined reliably. This patient's deficits resolved significantly within 1 week.

Four patients died during the follow-up period. One patient (case 9) had a fatal hemispheric infarction after arterial occlusion to treat acute carotid rupture. A near exsanguinating hemorrhage had precluded either temporary occlusion testing or subsequent bypass graft placement. Infarction was most likely related to carotid artery occlusion and severe hypotension, but we cannot exclude the possibility of a procedure-related thromboembolic complication. Three additional patients (cases 1, 4, and 8) died of progressive malignant tumors 2 to 11 months after arterial occlusion. Their deaths were not related to our treatment.

In both patients with acute carotid rupture, even large numbers of densely packed microcoils placed during proximal flow arrest failed to produce complete arterial occlusion. After deflation of the proximal occlusion balloons, evaluation 15 and 20 minutes after placement of the last coils revealed minimal but persistent anterograde flow. The proximal balloons were reinflated and detachable latex balloons (Nycomed, Paris, France) were then placed proximally to the coils to effect complete arterial occlusion.

Discussion

Detachable balloons have long been considered the appropriate device for endovascular occlusion of the carotid and vertebral arteries (1, 8–10). Balloons had been in use for over a decade before microcoils became available (11). The use of embolization coils to occlude the carotid and vertebral arteries has been considered an inferior technique, primarily because of the theoretical risk of distal embolic complications. In some cases, arterial tortuosity or stenosis may prevent placement of a large-diameter guiding catheter to allow the use of detachable balloons for arterial occlusion. Before their recent approval, detachable balloons were generally unavailable or informed consent for use of investigational or unapproved balloons was often impossible to obtain in emergency circumstances. The use of investigational or unapproved detachable balloons was also undesirable in situations that carried a high risk of litigation.

In 1996, Hughes et al (12) reported that sonographically detectable distal emboli associated with microcoil embolization in a canine model were virtually eliminated when proximal temporary balloon occlusion was used during coil placement. It is important to note that this study was conducted without the use of anticoagulation, which would be expected to reduce or eliminate thromboemboli. The initial clinical experience with the GDC system revealed that thromboembolic complications were relatively frequent unless anticoagulation was used. Anticoagulation is now almost universally employed when using the GDC system, and it markedly reduces thromboembolic complications.

Graves et al (7) subsequently reported satisfactory clinical results of carotid and vertebral artery occlusion in 19 patients when microcoils were placed during temporary proximal flow arrest. They reported development of neurologic deficits in five patients. Deficits were transient in four patients and permanent in only one. In three of the five patients, hypoperfusion not detected during balloon test occlusion was thought to be the underlying cause of the new deficits. Most important, none of their patients sustained a neurologic deficit suggestive of an acute embolic event related to the use of coils for vessel occlusion. They concluded that microcoils placed during temporary proximal flow arrest were safe and effective for endovascular occlusion of the carotid and vertebral arteries.

None of the three patients in our series who incurred a neurologic deficit had an acute deficit at the time of arterial occlusion. The minor stroke sustained by patient 18 was compatible with either a delayed embolic event or hypoperfusion. The fatal hemispheric infarction suffered by patient 9 was most likely related to carotid artery sacrifice combined with prolonged hypotension. Vasospasm and occlusion of both the AICA and PICA accounted for the progressive deficits in patient 7. As with the experience reported by Graves and colleagues, none of our patients had an acute event consistent with an embolic complication related to the use of microcoils placed for arterial occlusion.

In both our patients with acute carotid artery rupture (cases 4 and 9), arterial occlusion with microcoils alone failed. Complete arterial occlusion required placement of a detachable balloon proximal to the microcoils in both patients. Our results suggest that microcoils will not provide effective vessel occlusion when coagulation has been diminished by aggressive resuscitation of near exsanguinating hemorrhage. Both patients had received extensive blood product transfusions and intravenous fluid administration leading to a hypocoaguable state. Heparin administration did not seem to be a factor. Only one of these two patients had received heparin (5000 U IV) and this had been reversed with protamine (50 mg IV) before microcoil placement. Systemic anticoagulation with heparin did not prevent vessel occlusion in any other patient.

In addition to worry over thromboembolic complications associated with the use of microcoils for large-vessel occlusion, concern for inadvertent distal embolization of the microcoils has also been raised. We did not observe distal migration of a microcoil in any of the 11 patients who underwent arterial occlusion without the use of proximal flow arrest or initial placement of GDC. We prevented inadvertent distal coil embolization by selecting coils that were 33% to 50% larger than the diameter of the artery to be occluded as the first coils placed. Subsequent coils of approximately the same size as the artery were then placed within and proximally to the initial coils. The coils were packed into a dense mass.

The small number of patients in our series is a recognized limitation. In addition, routine follow-up imaging studies were not obtained to evaluate for possible clinically silent embolic complications. Moreover, laboratory evaluations to quantify the effects of our anticoagulation regimen were not performed.

Conclusion

Our results, and those reported by Graves and colleagues (7), indicate that microcoils are safe and effective for neurovascular occlusion. When anticoagulation is used as we described, proximal temporary flow arrest during coil placement does not appear to be necessary to prevent clinically apparent embolic complications. The variety of microcoil shapes and sizes, as well as the availability of electrolytically and mechanically detachable coils, allows placement without fear of distal migration. Even with the recent approval of detachable balloons, the ability to place microcoils into tortuous and stenotic arteries makes them an attractive alternative to detachable balloons in selected cases. Nonetheless, when coagulation has been markedly diminished by massive hemorrhage and transfusion, microcoils may not produce complete arterial occlusion even when temporary proximal flow arrest is used. Detachable balloons remain invaluable for such cases.