Introduction
Since the initial introduction of endovascular coiling techniques by Guglielmi in 1991, endovascular therapies for intracranial aneurysms have evolved. Initially, intrasaccular coiling and parent vessel occlusion with coils after balloon test occlusion were the mainstays of treatment. At the turn of the 21st century, intracranial stents were designed as support and scaffolding for coils to treat wide-necked and unruptured aneurysms. With more advanced catheter and microcatheter technology in addition to balloon-assisted and stent-assisted techniques, endovascular therapy for intracranial aneurysms has significantly diversified the management options for ruptured and unruptured intracranial aneurysms. Although these techniques now represent the forefront of endovascular therapies, the past decade has seen the advent of flow diversion as a significant aid in treating broad-based aneurysms as well as aneurysms in difficult locations. In 2011, a flow diverter, the Pipeline embolization device (PED, Medtronic, Minneapolis, Minnesota), received approval from the U.S. Food and Drug Administration (FDA) for the treatment of large and giant wide-necked aneurysms from the petrous to superior hypophyseal segments of the internal carotid artery (ICA).
Complications may occur during different phases of treatment for intracranial aneurysms. These events may be related to general issues associated with endovascular treatment including access site hematomas, retroperitoneal hematomas, femoral artery dissections, and nephrotoxic and contrast-related complications, the details of which are outside the scope of this chapter. The most common complications and plans associated with endovascular intracranial aneurysm treatment will be discussed here.
Coiling
Complications related to intrasaccular coiling can be divided into thromboembolic or hemorrhagic complications. Thromboembolic complications commonly arise as a result of coil extrusion from the aneurysm into the parent vessel in addition to the thromboembolic risk associated with the neuroangiographic procedure itself. Hemorrhagic complications are primarily associated with entry of the microcatheter into the aneurysm dome and initial placement of the framing coil.
Thromboembolic Complications
As with any neuroangiographic procedure, embolic material can materialize on catheters and guidewires. In addition, during coiling procedures, coil mesh in contact with blood or stagnation from near-occlusive guide catheters or prolonged arterial vasospasm can increase the chance of embolic material causing ischemia. In addition, arterial dissection and vasospasm caused by the guide catheter prior to microcatheter and microwire manipulation can be associated with thromboemboli. The rate of thromboembolic complications in unruptured aneurysm series ranges from 3.7% to 6.9%. The investigators of the Analysis of Treatment by Endovascular approach of Nonruptured Aneurysms (ATENA) study demonstrated an overall thromboembolic complication rate of 7.1% in 700 procedures. Among patients who suffered from thromboembolic complications in the study, 4.1% died and 24.5% had permanent neurological deficits. It is difficult to identify the etiology of thromboembolic complications based on aneurysm location and morphology. Although aneurysm neck morphology may alter management plans, the use of intrasaccular coiling itself does not seem to be associated with high-risk features. In addition, the ATENA investigators have shown that the safety of the remodeling technique in unruptured aneurysms is similar to that of conventional coiling procedures.
The rate of thromboembolic complications during intrasaccular coiling of ruptured aneurysms ranges between 4.7% and 6%. The investigators of the Clinical and Anatomic Results in the Treatment of Ruptured Intracranial Aneurysms (CLARITY) study demonstrated a higher thromboembolic complication rate of nearly 12.5% for ruptured aneurysm treatment. This study evaluated 782 ruptured aneurysms, and 3.8% of patients with thromboembolic complications had permanent neurological deficits or died. In another study, van Rooij et al. described a higher rate of thromboembolic complications for aneurysms >10 mm in diameter, with aneurysm necks larger than 4 mm, and in patients who were smokers.
Thromboembolic complications are associated with high morbidity and mortality, and precautionary steps are taken to prevent such events. Full heparinization with a goal for activated coagulation time (ACT) between 250 and 300 seconds during unruptured aneurysm treatment is suggested. Heparinization helps reduce rates of thromboemboli but presents a clinically significant challenge while treating ruptured aneurysms. Our experience has shown that half heparinization prior to coiling and full heparinization after the aneurysm has been secured is a good protocol and approach to limit thromboemboli formation. If there is concern for iatrogenic vasospasm from the guide catheter, verapamil can be locally administered proximally to the vessel concerning for spasm at a dose ranging from 10 to 20 mg. Surgeons should be keenly aware of the different physiological and biological factors associated with vasospasm in the setting of ruptured aneurysms in addition to other variables that may predispose patients with ruptured aneurysms to altered states of coagulation.
Iatrogenic arterial dissection is another possible cause of thromboembolic complications and should be carefully monitored throughout the procedure. During removal of the microcatheter and guide catheter, final angiographic runs should be performed to confirm no signs of arterial dissection, flow limitation, or blood stagnation.
Either intraprocedurally or during final angiographic runs, acute intraprocedural thrombus formation is usually identified if a vessel branch is not seen or if there is delayed filling of the branches surrounding and distal to the site of occlusion. If coil extrusion near the aneurysm neck or into the parent vessel is observed, the surgeon can find the cause of the flow reduction. Thrombus formation is caused by platelet aggregation in these acute settings and is treated with intra-arterial or intravenous thrombolytic therapy including glycoprotein IIb/IIIa inhibitors. Cronqvist et al. performed superselective intra-arterial therapy with urokinase for thromboemboli occurring during endovascular intracranial aneurysm therapy in 19 patients with resultant complete recanalization in ten patients and partial recanalization in nine. Furthermore, abciximab, a monoclonal antibody to the glycoprotein IIb/IIIa complex, has also been used for thrombolytic therapy. Brinjikji et al. reported higher mortality in patients receiving glycoprotein IIb/IIIa inhibitors alone. In their meta-analysis, those authors found that patients who received glycoprotein IIb/IIIa inhibitors had statistically significantly lower perioperative morbidity than patients treated with fibrinolytic therapy.
Hemorrhagic Complications/Intraprocedural Aneurysm Rupture
The risk of intraprocedural rupture with intrasaccular treatment of cerebral aneurysms is greatest during initial catheterization of the aneurysm and ranges between 2% and 8.8%. Cloft et al. conducted a meta-analysis and evaluated 1248 ruptured aneurysms and revealed that rupture occurred in 4.1% of treated aneurysms during coil embolization. These results demonstrated that there is a slightly higher risk of intraprocedural rupture in cases where the aneurysm has already ruptured. This higher risk is attributable to the fragility of the vessel wall in previously ruptured aneurysms. The most common causes include perforation from the microwire and microcatheter or perforation during coil deployment. Some authors have noted that dense packing of the aneurysm with coils can predispose aneurysms to delayed hemorrhagic complications.
Often during micronavigation of the carotid siphon, a significant amount of force can build up within the microwire and microcatheter. This potential energy can convert to kinetic energy during advancement of the microcatheter or removal of the microwire. When this occurs, either the microwire or microcatheter will begin to advance by itself. Meticulous control of the microwire–microcatheter system is imperative during these procedures; however, there are methods for minimizing the risk of the progression of a wire or catheter that could potentially go through the wall of the aneurysm.
Reducing the energy built up in the system can be performed by simply backing off the microcatheter until the tip marker is seen to move slightly prior to entering the aneurysm sac. However, this technique requires the catheter then to be advanced into the aneurysm, which may reproduce the forces that were just reduced. Our favored method is to advance the microwire past the ostia of the aneurysm and then follow it with the microcatheter. The whole system can then be withdrawn until the catheter either falls into the aneurysm sac or is in a perfect position for the microwire to be advanced into the aneurysm. This completely reduces the tension in the system prior to aneurysm catheterization and permits one-to-one movement of the devices for optimal control.
If intraprocedural rupture occurs while the catheter is within the aneurysm, the next best move is to deploy a slightly oversized, very long coil. Ideally, a coil around 20–30 cm in length (depending on the aneurysm dome size) is deployed in the hopes of achieving the greatest amount of occlusion of the aneurysm with a single coil. Prior to detachment of the coil, an injection of contrast material should be performed via the catheter, and frames should be captured into the late venous phase to evaluate for any continued extravasation. If continued extravasation is evident, standard management of elevated intracranial pressures (i.e., releasing cerebrospinal fluid if a ventriculostomy catheter is in place) should be simultaneously performed. The anesthesiologist should be informed and the coil can be detached after simultaneously using standard management of elevated intracranial pressure, such as releasing cerebrospinal fluid if a ventriculostomy is in place. A small compliant balloon could then be brought up to occlude the parent vessel temporarily to decrease the pressure head further and to allow for hemostasis. However, it may take precious minutes to introduce an exchange length microwire and bring it up a small, compliant balloon in a fully heparinized patient with a ruptured aneurysm. Rather, opening and inserting a long coil into the parent vessel without detaching it to occlude the vessel temporarily in the same fashion as a balloon is a more timely and quicker option. Protamine should be administered to reverse the heparin effect. If the patient is intubated, having the anesthesiologist induce “burst suppression” with sedation can possibly help reduce cerebral metabolism to decrease risk of ischemic injury. If the patient is under conscious sedation, a neurologic examination should be performed as soon as possible. If the patient is lethargic or has a concerning neurological change on examination, intubation and sedation are warranted. It may also be pertinent to place a ventriculostomy if one is not already in place. Alternatively, some interventionists may advocate simply coiling the aneurysm as quickly as possible until extravasation is no longer seen. However, this can lead to the catheter being pushed out of the aneurysm, poor placement of coils with prolapse into parent or branch vessels, and it may be ineffective in resulting in hemostasis. It is imperative that the interventionist remain calm when encountering an intraprocedural rupture as hastily made decisions and treatment attempts can result in devastating injury, bleeding, and permanent neurologic deficits for the patient.
Early Hemorrhagic Complications
Risk factors associated with early hemorrhagic complications other than intraprocedural rupture are not well understood. The greatest risk of hemorrhagic complications tends to be in the first 48 hours. In a study by Zheng et al., 1764 aneurysms were treated with 13 patients suffering from early hemorrhagic complications, more commonly seen with ruptured aneurysms.
It is believed that the risk of rebleeding after coiling is 1.1% for ruptured aneurysms with an associated mortality of 31%. Anticoagulation during microcatheter manipulation and aneurysm coiling as well as antiplatelet therapy have been suggested to be the cause of delayed aneurysm rupture not caused by perforation, although these have not been observed at our institution. Hemodynamic changes secondary to subarachnoid blood may elicit dynamic changes postprocedurally and may be additional causes of delayed hemorrhagic events.
Coil Migration
Migration of detached coils is a serious complication. Coil masses in contact with blood are highly thrombogenic. The thrombogenicity is proportionate to the surface area in contact with blood. Coil migration has been noted to have an incidence of 2.4% to 2.8% with significant morbidity and mortality related from parent vessel occlusion. Henkes et al. reported a 2.5% rate of coil migration in the treatment of 1811 aneurysms, with no significant difference between unruptured and ruptured aneurysms. Cases with large aneurysms >10 mm and broad-based aneurysm necks >4 mm tend to be associated with higher rates of coil migration. Surgeons must pay particular attention to sizing coils in these cases because the first framing coil will play a major role in the frame set for the remaining coils. Henkes et al. reported only a 0.1% risk of arterial thrombosis with coil migration into the parent vessel.
Endovascular management of coil migration has not been standardized. Many patients with coil protrusion or prolapse can be treated with anticoagulation and antiplatelet therapy. Coil protrusion with noted thrombus formation can be treated within 24 to 48 hours of anticoagulation therapy with a stroke protocol heparin drip with a goal-activated partial thromboplastin time (aPTT) of 50 to 70 seconds without a heparin bolus. This can be followed with antiplatelet therapy for 6 months ( Fig. 52.1 ). If flow limitation secondary to coil fracture, stretching, or migration occurs, there are methods to extract these coils including goose neck snares, stent retrieval devices, and trapping the coil mass against the arterial wall with an intracranial stent. To date, there are no defined or standardized methods to retrieve problematic coils. Snares and stent retriever devices are interchangeably used among surgeons based on comfort level and, if unsuccessful, interventionists may resort to trapping the coil mass via stenting.
