Aneurysmal SAH: Current Management and Complications Associated With Treatment and Disease

Abstract: The purpose of this article is to give an overview of the management of the most common complications encountered during subarachnoid hemorrhage and endovascular treatment of intracranial aneurysms. We reviewed the literature and identified the complications encountered during endovascular treatment of intracranial aneurysms. We report current management strategies of complications associated with subarachnoid hemorrhage and the interventional procedure. Aneurysmal subarachnoid hemorrhage remains a devastating condition, with high mortality and poor outcome among survivors. The successful treatment of intracranial aneurysms requires a multidisciplinary approach and the treating physicians need to be aware of predisposing factors for complications, their frequency, and also their management.

J INVASIVE CARDIOL 2014;26(1):30-37

Key words: endovascular treatment, subarachnoid hemorrhage, intracranial aneurysms

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Approximately 4% of all strokes are due to rupture of an intracranial saccular aneurysm,^1,2 which subsequently results in subarachnoid hemorrhage (SAH). Approximately 3%-6% of the general population harbor an intracranial aneurysm and are asymptomatic until the aneurysm ruptures.³ The risk of aneurysm rupture is about 1% (0.05%-2%) per year and may vary with location, size, type, and history of previously ruptured aneurysms.^4-10

SAH still presents a clinically severe and devastating event that often leads to death or severe disability. Population-based mortality rates remain as high as 38%,¹¹ with a high rate of morbidity among survivors.^5,7,8,10 Nearly 50% of patients die within the first month after the initial bleeding event.^12,13

According to a multinational World Health Organization study, the incidence of SAH ranges from 2-23 cases/100,000 population/year depending on the country.^11,14 Important factors for prognosis and quality of life include occurrence of rebleeding, vasospasm-associated neurological deficits, and development of hydrocephalus.¹⁵

Ruptured Aneurysms

A very intense and severe headache, mostly described by patients as the “worst headache of their lives,” is characteristic of SAH. In addition, patients may report of short loss of consciousness, neck stiffness, nausea, and vomiting. In severe cases, acute swelling of the brain may cause hemiparesis, aphasia, memory loss, and stupor.¹⁵

In case of aneurysmal SAH, surgical clipping or endovascular coiling should be performed to reduce the rate of rebleeding.

Treatment

(1) Surgical Clipping

In this neurosurgical approach, the operator gains access to the subarachnoid space via craniotomy. Size and shape of the clip is determined by the size and shape of the neck of the aneurysm. The goal of this technique is to exclude the aneurysm from the blood circulation. Until introduction of endovascular coiling in the 1990s, this approach was the standard treatment option for cerebral aneurysms.

(2) Endovascular Coiling

Today, endovascular coiling represents the gold standard in aneurysm treatment. The most commonly used embolization devices for the treatment of intracranial aneurysms are bare platinum coils that come in different shapes, sizes, and coil diameters. Packing density has been discussed as a factor that might influence recanalization rate after coiling¹⁶ and commonly a combination of framing and filling coils is used to achieve higher packing density.

Also, bioactive coil systems have been introduced. They differ in the way in which polyglycolic/polylactic acid (PGLA) is incorporated into the platinum coil. A convincing beneficial effect of PGLA regarding better stability at follow-up has so far not been established.^17-19

The Matrix coil (Stryker) is coated with an absorbable copolymer, which represents almost 70% of the coil volume.¹⁸

Nexus Detachable Coils (Covidien) are standard complex platinum coils with interwoven PGLA microfilament threads. The HydroCoil (Microvention, Inc) is constructed as a platinum coil with an inner core of hydrogel and a stretch-resistant filament. When exposed to blood, the hydrogel swells with the aim to improve packing density.

The Cerecyte coil (Codman) consists of a regular bare-platinum coil with PGA running through the lumen of the primary platinum wind. The Cerecyte study of 500 patients showed no significant difference at 6 months in the angiographic outcomes between Cerecyte coils and bare-platinum coils.¹⁷

Endovascular access is gained via placement of a femoral sheath. This approach is a minimally invasive technique in which a microcatheter is placed into the aneurysm lumen and platinum coils are delivered to support thrombus formation. Detachment of the coils occurs either mechanically or electrolytically. 

Onyx (MTI), a liquid embolic system, has also been used for the treatment of intracranial aneurysms.^20-23 The use of Onyx involves placement of a balloon over the neck of the aneurysm while the material is injected endosaccularly.

The technique is challenging and has some intrinsic limitations. The main limitations are that leakage has to be controlled by balloon inflation across the aneurysm neck, that there is no possibility to reposition or retrieve the cast, and that fixation of the microcatheter is somewhat common.²⁴ Liquid embolic is thus only used in selected patients. Onyx liquid embolic agent has also been used in the aneurysm sac to achieve a more durable result after (and in addition to) coil embolization.²⁵

It is often necessary to perform balloon- or stent-assisted coiling. The implantation of a stent over the aneurysm neck provides a scaffold for the coils and prevents protrusion into the parent vessel. A microcatheter can then be guided through the stent struts into the aneurysm lumen to deliver the coils.

(3) Flow Diverter

The concept of parent vessel reconstruction with so-called flow diverters is a new approach of aneurysm treatment. Previous covered stents have had limited usage in the intracranial vasculature due to their stiffness.²⁶

The flow diverter is a tight, meshed, stent-like device that covers the aneurysm neck and redirects blood flow, thus supporting intra-aneurysmal blood stasis. At the same time, the flow diverter is sufficiently permeable to allow arterial branches to be adequately perfused. It requires antiplatelet medication and thus makes its use in patients with ruptured aneurysms difficult.²⁷ In contrast to the traditional intrasaccular aneurysm treatment, often there remains a residual postinterventional filling of the aneurysm sac, which will subside over a period of months.²⁸ To reflect this different occlusion pattern, different grading scales for aneurysms treated with flow diverters were introduced.^29,30

Currently, the role of flow diverters in the treatment of intracranial aneurysms is not yet defined. Additionally, the role of intrasaccular flow diverters is yet unknown.

(4) Clipping Versus Coiling

The International Subarachnoid Aneurysm Trial (ISAT) was a randomized, controlled, prospective study that compared both endovascular (n = 1073) and surgical (n = 1070) aneurysm treatment options. The study was stopped prematurely due to a significant benefit of the patients enrolled into the endovascular treatment arm (23.7% vs 30.6% dead or dependent at 1 year).³¹ Even 10 years after ISAT, the benefit of endovascular coiling over clipping was still evident in this patient group. The risk of death at 5 years was significantly lower in the coiling group than in the clipping group (relative risk, 0.77; 95% confidence interval [CI], 0.61-0.98; P=.03).³²

A recently published trial³³ evaluating the superiority in safety and efficacy of clipping versus endovascular coiling for the treatment of ruptured cerebral aneurysms observed a better 1-year outcome in patients treated with coil embolization (n = 233) in comparison to microsurgical clipping (n = 238).A poor outcome was defined as an mRS score >2, which was observed in 33.7% in the surgical arm and in 23.2% of the patients undergoing aneurysm coiling (odds ratio [OR], 1.68; 95% CI, 1.08-2.61; P=.02). No recurrent hemorrhage was seen after aneurysmal coil embolization.

Thus, for patients with ruptured aneurysms judged by an experienced team of cerebrovascular surgeons and endovascular practitioners to be technically amenable to both endovascular coiling and neurosurgical clipping, endovascular coiling can be beneficial (class I, level of evidence B).³⁴ Nevertheless, it is reasonable to consider individual characteristics of the patient and the aneurysm in deciding the best means of repair and management in centers offering both techniques (class IIa, level of evidence B).³⁴

Complications Associated With Aneurysmal SAH 

(1) Rebleeding Before Treatment

Untreated ruptured intracranial aneurysms carry a high rebleeding rate, which is quoted in the literature to be 4% on the first day post SAH, 15%-20% in the first 2 weeks and reaching a risk of 50% at 6 months.³⁵ Therefore, early treatment is crucial and reduces the risk of rebleeding after SAH.

Recently, a single-center study by Philips et al showed that early treatment of ruptured intracranial aneurysm had a relative risk reduction for dependency or death at 6 months of 82% and 10.2%, respectively.³⁶

Blood pressure management is also an important factor that decreases the risk for preoperative rebleeding.³⁷ Short-acting continuous antihypertensives are best to reach the target blood pressure of 160-150 mm Hg (systolic), and blood pressure spikes need to be avoided.³⁴

(2) Vasospasm

Complications after aneurysm rupture are common. A possible complication is cerebral vasospasm. This represents a narrowing of the affected vessel resulting in a cerebral perfusion deficit.

Treatment of vasospasm is not yet defined. Treatment options for symptomatic cerebral vasospasm differ regarding the timepoint of appearance. Vasospasm that occurs during the interventional procedure and is caused by catheter manipulation will usually disappear within a few minutes. In severe cases, it can be treated with intraarterial nimodipine, a dihydropyridine calcium-channel blocker, or intraarterial papaverine, a synthetic opium alkaloid with prominent spasmolytic and anticholinergic action.

SAH-induced vasospasm will be treated either with triple-H therapy (hypervolemia, arterial hypertension, hemodilution), intravenous nimodipine, or in severe and/or in cases refractory to medical therapy, with transluminal balloon angioplasty and/or intraarterial nimodipine.^34,38,39 Triple-H therapy and intravenous nimodipine is the standard of care in most institutions.

The intraarterial vasodilator papaverine is hardly used due to its numerous adverse effects and its transient action.⁴⁰ However, several intraarterial vasodilators are efficient, including nimodipine, nicardipine, milrinone, verapamil, and fasudil, but no direct comparison of their efficacy is available. Balloon angioplasty in the proximal vasculature has been described as a successful treatment method,⁴⁰ although it has not been demonstrated in a prospective randomized series.

(3) Hydrocephalus 

Acute hydrocephalus is seen in about 20%-30% of patients after SAH. It is more frequent in patients with a poor clinical presentation.^40-44 Acute hydrocephalus develops as a result of blood clots obstructing the cerebral spinal fluid (CSF) circulation or inhibiting its reabsorbance. Disturbances in CSF circulation result in an increase of intracranial pressure (ICP). Signs of elevated ICP include headache, vomiting, altered mental status, and loss of consciousness. The therapy of choice is placement of a permanent ventricular shunt to drain the CSF and normalize the ICP.

(4) Seizures

An analysis regarding the event of seizures among the ISAT study population revealed a significantly lower rate within the endovascular group compared to the surgical group (8.3% vs 13.6% in the endovascular and neurosurgical allocations; P=.01). Also, the aneurysm location seemed to be an important factor regarding the occurrence of seizures. Regardless of the treatment option, Hart et al state that more seizure events occurred in patients with middle cerebral artery (MCA) aneurysms.⁴⁵

Although there exists no evidence that seizure prophylaxis is indicated after aneurysmal SAH,⁴⁶ antiepileptic drugs are commonly prescribed for prophylaxis and treatment, with phenytoin the most common, followed by phenobarbital and carbamazepine in a small percentage.⁴⁷ Multidrug regimes are rare. 

The main arguments for offering antiepileptic drug (AED) prophylaxis after SAH are the risk of seizure precipitating rerupture secondary to increased blood pressure, and seizure causing undue cerebral metabolic stress leading to pathologic increases in intracranial pressure or cerebral metabolic demand during a period of reduced cerebral blood flow either from brain swelling or vasospasm. Rosegart et al⁴⁷ and Naidech et al⁴⁸ showed that AEDs were associated with poorer neurological outcome compared to patients who did not receive prophylactic antiepileptic medications, with non-severe adverse effects occurring in around 4% of patients.⁴⁶

Considering these points, prophylactic administration of antiepileptic drugs in the setting of ruptured intracranial aneurysms remains controversial. Factors that are thought to increase the risk for seizures post SAH are younger age (<40 years old), loss of consciousness of >1 hour at ictus, and Fisher grade of 3.⁴⁹

Procedural Complications

Overall complication rates during endovascular treatment of aneurysms have been reported in 11.3%-19.4%.^50-53

(1) Aneurysm Perforation

Aneurysm perforation typically occurs during aneurysm cannulation and can happen with the microwire, microcatheter, or coil. Aneurysm perforation has been reported in 2.5%-5.4%.^31,50,52-56

A predisposing factor for aneurysm rupture is size, with higher rupture rates reported in smaller aneurysms.^57,58 Increased intraprocedural rupture rate in very small aneurysm is due to the difficulty of safe navigation of a microcatheter and the subsequent coil placement.

A 2002 meta-analysis by Cloft et al⁵⁹ studied 17 retrospective reports that presented a total of 2008 cases involving 1248 ruptured and 760 unruptured aneurysms, and found the risk of perforation was significantly higher in ruptured aneurysms than in unruptured aneurysms (4.1% vs 0.7%).

In a more recent meta-analysis conducted by Brinjikji et al⁶⁰ on 71 consecutive patients with aneurysms of ≤3 mm, the intraprocedural rupture rate in unruptured aneurysms was found to be 5.0% compared to 10.7% in small ruptured aneurysms.

Management of aneurysm perforation. Obviously, when treating small aneurysms, extra care should be given to avoid contact of the microcatheter and microwire with the aneurysm dome. The rotating hemostatic valve around the microcatheter should be tightened to avoid accidental movement within the aneurysm. 

Often, the first sign of aneurysm perforation is a decrease in blood pressure. If not obscured by coils, the tip of the microcatheter might become visible outside the aneurysm lumen on the road map image, which is essential during the coiling procedure. Other factors are bradycardia or a rise in ICP. If the patient already has an extra ventricular drainage, this might show an increase in draining blood.

If perforation is suspected, a guide catheter angiogram should be performed immediately for confirmation, while keeping the road map image. On no account should the perforating device be pulled out, as this could still be sealing at least part of the perforation. Since endovascular treatment should be performed under general anesthesia, the anesthetist should be asked to reverse any heparin with protamine. Protamine sulfate should be given by very slow intravenous injection (rate not exceeding 5 mg/minute), with a maximal dose of 50 mg.^61-63

At the same time, the main aim remains to rapidly occlude the aneurysm to stop bleeding.

It is advisable to choose a coil of long length; even if the coil is partially deployed into the subarachnoid space, the microcatheter can gradually be withdrawn in order to deploy the remainder of the coil within the aneurysm.

If balloon-assisted coiling is performed, the balloon can be inflated to diminish blood loss. Another option might be the introduction of a second microcatheter into the aneurysm to avoid withdrawal of the perforating device.

As a last option, it might be necessary to consider occlusion of the parent vessel with coils.

Further guide catheter angiograms will show if bleeding has stopped. Once the aneurysm is sealed off, imaging can then show the extent of the bleed and contrast extravasation. Modern angiography machines using DYNA-CT do not necessitate transfer of the patient and have been shown reliable in detecting hemorrhage and also hydrocephalus.⁶⁴ Continuous ICP monitoring should be conducted.

(2) Device Failure

(a) Stretching. The reported rate of coil stretching during embolization varies between 0.2%-6.5%.^65-67 Rordorf et al⁶⁸ reported 3 cases of stretching with subsequent coil fracture among 46 patients treated with GDC coils. In 1 patient, coil stretching with herniation into the ICA led to a large MCA stroke. In a series by Gallas et al,⁶⁷ coil stretching occurred in 5 patients (1.7%) without any clinical complications in any cases. Im et al reported 1 case of stretching in 435 patients (0.23%).⁶⁵ In order to address the issue of stretching, SR coils are now on the market. Here, tiny filaments extend between the two ends of the coil to prevent it from unravelling unintentionally when pulled on.

(b) Failure to detach. Failure of the coil to detach is a known complication, but this topic has not been explored in more detail.⁶⁹ Ideally, the coil can still be retrieved without dislodging the coil package. Depending on the detachment system, mechanical manipulation and twisting of the pusher wire can lead to detachment.

(3) Thromboembolic Events

Thromboembolic events are considered one of the most serious complications in endovascular procedures. We differentiate between intraprocedural thrombus formation, which may or may not become symptomatic, and thromboembolic lesions as seen on diffusion-weighted imaging (DWI). Often, the term thromboembolic event is used as a synonym for symptomatic stroke, thus extra care must be given when reviewing the literature. 

(a) Periprocedural thromboembolic events. The first source of thrombus formation is the introduction of the guidewire. This can induce vasospasm with subsequent flow reduction or stasis in the parent vessel. Any interventional procedure will cause small endothelial damage, which will induce release of vascular endothelial growth factor. This will activate the intrinsic coagulation cascade, which will remain active for 48 hours.^70-72 In addition, the devices — catheters, wires, stents, and balloons — are thrombogenic.⁷³

Fiber coils were manufactured to be especially thrombogenic in order to induce rapid thrombosis of the aneurysm. Fibered coils are standard bare-platinum coils with additional polymer microfilament threads protruding from the primary coil. For example, the Axium coil (eV3 Endovascular, Inc) is available as a bare-platinum coil and as a microfilament coil with either polymer polyglycolic-lactic acid or nylon. However, in case of coil loop protrusion or coil dislodgment, the risk of thrombus formation here is even higher.¹⁹

Other identified risk factors for thromboembolic events are wide-necked aneurysms, coil retrieval, and balloon-assisted coiling.⁷⁴

In the CLARITY study, a higher rate of thromboembolic events was observed in patients with large aneurysms (>10 mm P<.001), in smokers (P=.02), and in aneurysms with a neck larger than 4 mm (P=.01).

(b) Thromboembolic events as seen on DWI. Silent DWI lesions after diagnostic angiography have been reported in up to 44% in patients with a history of vasculopathy. The significance of these lesions is unknown. The appearance of lesions was significantly correlated with whether vessels were difficult to probe (P=.01), amount of contrast medium needed (P<.01), fluoroscopy time (P<.01), and use of additional catheters (P=.02).⁷⁵

In a study conducted by Grunwald et al,⁷⁶ 68 patients underwent endovascular treatment of asymptomatic aneurysms. Hyperintense lesions visible on DWI imaging were evaluated in 50 of these patients. New DWI lesions were found in 42%. There was no correlation between the occurrence of thromboembolic events as well as clinical findings and aneurysm localization, size, number of coils implanted, total embolization time, and patient age. A higher incidence of DWI lesions was reported in ruptured aneurysms.^77,78

Management of thromboembolic complications. DWI cannot only act as a diagnostic tool, but also as a quality control for the interventionalist.

A saline flush is mandatory on each line using heparinized saline to continuously flush sheath, guide catheter, distal access catheter, and microcatheter to avoid thrombus formation; systematic anticoagulation with heparin (usually 5000 units per 70 kg body weight) has also been proposed.^50,76,79,80 Empty or turned-off flush lines can be the cause of thrombus formation and present a frequent and serious risk to the patient. All flush lines should be monitored continuously and carefully.

The guide catheter should not be placed directly against a bend in order to limit guide-catheter induced vasospasm. Especially in unruptured aneurysms, many centers will use aspirin prior to or during the coiling procedure. In an experimental study in rabbits, Grunwald et al could not show an influence of aspirin or heparin on stable aneurysm occlusion.⁷⁰

A study conducted by Ries et al evaluated the use of aspirin on endovascular complications during endovascular aneurysm coiling. Thromboembolic events occurred more often in the non-anticoagulation group (17.6%) in comparison to the aspirin group (8.8%). The authors concluded that administration of aspirin led to a significant reduction of thromboembolic events during endovascular coil embolization.⁷⁹

Usually, in cases of acute thrombus formation, the thrombus will continuously grow. It is advisable to compare angiographic runs with a preprocedural angiographic run to detect filling defects at an early stage.

Thrombus formation can also occur around the catheter tip or aneurysm neck. Depending on the occlusion of the aneurysm, abciximab (ReoPro), a glycoprotein IIb/IIIa receptor antagonist that inhibits platelet aggregation, can be administered either intravenously or intraarterially. It has a short plasma half-life. Platelet aggregation returns to normal in about 96-120 hours after discontinuation. Abciximab is a clear and non-pyrogenic solution. The recommended dosage in cardiac interventions in adults is a 0.25 mg/kg intravenous bolus, followed by intravenous infusion of 125 ng/kg/min (maximum, 0.01 mg/min)^81-83 and it is suggested that lower doses are more effective when given intraarterially.⁸⁴

Interventional techniques like the Penumbra aspiration catheter (Penumbra, Inc) or stent-trievers can also be used to re-open an occluded vessel.

(4) Coil Herniation/Migration

(a) Coil herniation. Coil herniation can cause occlusion of the parent artery or other branching vessels, carrying a high risk to induce ischemic complications when compromising blood flow.^85-87 In the literature, the incidence of this complication is reported to be 2.4%-4.2%.^65,87-89 The most common risk factors for coil herniation are detachment of an unstable coil, excessive packing of the aneurysm sack, microcatheter removal, or dislocation of a coil by subsequently placed devices.^87,90 Coil mismatch with the aneurysmal lumen size or a wide-necked aneurysm increases the risk of coil herniation.^55,87,91

(b) Coil migration. Coil migration can happen in wide-necked aneurysms due to unstable coil position or undersized coils. The frequency has been reported in about 0.5%-1.7%.^92-94 Predisposing factors for coil migration are wide-necked aneurysm, size mismatch between coils and aneurysm, and underpacking of the aneurysm sac.^95-97Phatouros et al⁹⁵ reported 4 cases of postprocedure coil migration into the parent artery after completion of endovascular coiling. One patient developed severe MCA infarct caused by most of the packed coils that had migrated out of the aneurysm. The other 3 cases were asymptomatic, as the affected parent artery remained patent.

Prevention and management. Stent- or balloon-assisted coiling can reduce the risk of coil herniation or migration. If unsure about the stability of a coil within the aneurysm, several minutes should pass before the detachment of the coil. If coil herniation occurs, the protruding loop can be fixed to the vessel wall by placement of an intracranial stent.

There have been several reports of successful coil extraction with endovascular devices, such as the Amplatz goose-neck microsnare (ev3, now part of Covidien) or the Alligator retrieval device (Covidien); recently, stent-trievers have also been utilized for ischemic stroke treatment.^86,98-100

(5) Dissection

A dissection develops when a small tear forms in the tunica intima, the innermost layer of the arterial wall. Due to separation of the inner and outer layers of the arterial wall, blood is able to enter this newly formed space and may cause stenosis or even complete occlusion of the true vessel lumen.

Periprocedurally, vessel dissection is caused by catheter and wire manipulation and has been reported in 0.1% of cases.⁵⁰

Dissections are usually treated with heparin in the acute phase and later with aspirin or clopidogrel.¹⁰¹ If the dissection shows an intimal flap and reduced flow, it might become necessary to place a stent to limit risk of thrombosis and to secure access.¹⁰²

Postprocedural Complications 

(1) Recanalization

Endovascular coiling of intracranial aneurysms is associated with a recanalization rate of up to 25%.^103,104

Aneurysm size, presence of intrasaccular thrombus material, local blood hemodynamics, primary packing density, coil material, as well as patient age and gender have been discussed as possible risk factors.^70,105-108

(2) Rebleeding After Treatment 

Wrapped or coated aneurysms and incompletely clipped or coiled aneurysms have an increased risk of rehemorrhage compared with those that are completely occluded and therefore require long-term follow-up angiography.

Although postprocedural rebleeding is an infrequent complication, it carries a high mortality.^56,109,110

In ISAT2, a total of 10 of 1005 coiled aneurysms (1%) rebled within 30 days after coiling. In the CARAT study, half of the reruptures occurred during the first 3 days after treatment.⁵⁶

Several studies could show that certain factors contribute to aneurysm rebleeding post treatment. The most important are aneurysm size and shape, and history of bleeding from the treated aneurysm, with giant aneurysm having a higher rerupture risk (33%) than large aneurysm (4%).³⁴

Conclusion 

Non-traumatic aneurysmal SAH is a major cause of morbidity and mortality worldwide. Although endovascular devices and treatment techniques are continuously developing, these minimally invasive procedures still carry treatment-specific risks. Awareness of complications, their predisposing factors, and their prevention and management can further reduce morbidity and mortality.

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