Ruptured Anterior Communicating Artery Aneurysms

Ruptured aneurysms need to be treated urgently to prevent rerupture ( 1 in algorithm ). Exceptions to treatment include poor clinical status on presentation ( 3 in algorithm ; e.g., if a patient remains a Hunt and Hess grade 5 despite having a working ventriculostomy placed in the absence of a large IC hemorrhage), the patient′s previous wishes due to multiple medical morbidities prior to aneurysm rupture (e.g., terminal cancer or debilitating chronic illness), and “do not resuscitate, do not intervene” orders.

Unruptured Anterior Communicating Artery Aneurysms

ACoA aneurysms are unique because of their relative high risk of rupture, even at a small size. The International Study of Unruptured Intracranial Aneurysms (ISUIA) showed that the smaller the aneurysm, the less likely the rupture ( 2 in algorithm ). Aneurysms in the anterior circulation less than 7 mm were associated with a less than 1% annual rupture rate. However, more recent studies have shown that ACoA aneurysms tend to rupture at less than 7 mm. The prospective Japanese Unruptured Cerebral Aneurysm Study (UCAS) showed that aneurysms located in the ACoA had a higher rate of rupture compared to aneurysms at other locations. Similar to the ISUIA study, the larger the aneurysm, the more likely the rupture. However, of the small ruptured aneurysms (< 7 mm) that ruptured, the ACoA was the most common location.

Bijlenga et al showed in more than 900 patients that ACoA aneurysms of 4 to 7 mm have a similar risk of rupture to posterior circulation aneurysms. Lee et al showed that in a series of 200 ruptured aneurysms, 47% were small (< 5 mm), with the most frequent site of rupture coming from the ACoA. Further, very small aneurysm (< 3 mm) ruptures were more likely to occur in hypertensive patients with ACoA aneurysms. Matsukawa et al showed that ACoA aneurysm ruptures were more likely to occur in younger patients (younger than 60 years), with hypercholesterolemia, and an aneurysm dome pointing anteriorly with daughter sac(s).

At our institution, the decision on whether to treat unruptured ACoA aneurysms is based on multiple factors, including patient preference, size, and associated risk factors. We offer treatment for patients with aneurysms greater than 3 mm. We encourage treatment in patients with risk factors for subarachnoid hemorrhage (SAH), including an ACoA aneurysm characterized by a daughter sac(s), an irregular shape, or radiographic evidence of interval growth, and the following modifying risk factors: hypertension, smoker, and personal or family history of SAH ( 5 in algorithm ). If the patient had prior aneurysm treatment, we wait for 4 to 6 weeks before proceeding with additional treatment. If after weighing the relative risks and benefits, the patient and family prefer conservative treatment, we follow the patient with magnetic resonance angiography (MRA) ( 6 in algorithm ) and re-discuss whether to treat in 6-month to 1-year intervals ( 7 in algorithm ).

Anterior Communicating Artery

The ACoA complex, comprising the bilateral A1, A2, and ACoA segments, is variable, with the classic “H” configuration seen in only 20% of patients. With a relative common flow asymmetry from unequally sized A1s that make sharp turns into the ACoA and A2s, the walls of the ACoA are vulnerable to aneurysm formation.

Anterior Communicating Artery Perforators

Perforators project from the superior and posterior aspects of the ACoA, perpendicular to the A2 origin, often invisible to the surgeon′s standard view. They may be eccentric on the dominant A1 or medial in symmetric A1s. These supply the anterior perforate substance, optic chiasm, pituitary stalk, hypothalamus (suprachiasmatic and anterior areas), fornix, limbic system, and inferior frontal lobe. Although there may be collateral circulation to these structures, damage to the ACoA perforators can lead to memory deficits, loss of conciousness (LOC), personality change, and electrolyte imbalances.

Adjacent Anatomy

The ACoA is bordered inferiorly by the optic apparatus (e.g., optic cistern, optic chiasm, optic nerve, or optic tract). ACoA aneurysms can compress these structures, leading to one-third of patients with ruptured ACoA aneurysm reporting visual symptoms. Inferior to the optic apparatus is the pituitary stalk, with damage associated with diabetes insipidus and hormone abnormalities. The close proximity of the ACoA aneurysm with the hypothalamus has been hypothesized as the reason for its associated higher rate of hyponatremia.

The position of the dome relative to the adjacent anatomy helps determine which ACoAs are easier to clip.

Superior and posterior to the ACoA is the lamina terminalis. ACoA aneurysm rupture through the lamina terminalis can present with intraventricular hemorrhage (IVH). Surgical fenestration of the lamina terminalis with let off of cerebrospinal fluid (CSF) can help relax the brain. Superior and medial to the ACoA is the gyrus rectus, which can be safely resected for wider exposure. Lateral to the gyrus rectus is the inferior frontal lobe, with injury associated with the classic ACoA syndrome of memory loss, confabulation, and altered personality. Because of improved open surgical and endovascular techniques, the ACoA syndrome is less common, with deficits more recently specified as altered risk-taking behavior associated with damage to the ventromedial prefrontal cortex.

Clinical Evaluation and Imaging

Clinical evaluation and imaging for ACoA aneurysms is dependent upon the clinical and rupture status of the patient, similar to other ruptured aneurysm. An early decision is the placement of an external ventricular drain (EVD) generally in patients that have a Hunt and Hess grade higher than 2. The EVD will assist in the management of the IC pressures (ICPs) as well as CSF diversion that will facilitate surgical exposure. Before placement of an EVD, coagulation factors need to be corrected and platelets administered if antiplatelet agents were used. EVDs should be set at 15 to 20 mm Hg not only to alleviate high ICPs, but also to not overdrain in the setting of an untreated aneurysm.

A computed tomography angiography (CTA) three-dimensional (3D) TeraRecon (Foster City, CA) image can help further characterize the aneurysm and facilitate treatment planning (▶ Fig. 29.2 and ▶ Fig. 29.4 ). Careful attention is directed at the ACoA aneurysm′s relationship to adjacent vascular anatomy (including the dominant A1), its relationship to the interhemispheric fissure, anterior clinoid, sella, the height of the ACoA complex from the cranial base, its orientation in the coronal and sagittal planes, and associated calcifications near the aneurysm neck. The CTA is invaluable in identifying thrombosed aneurysms that may not be seen on the digital subtraction angiogram (DSA).

In the cases where the CTA does not provide enough information to characterize the aneurysm or it is felt that the aneurysm is amenable for coil embolization, a DSA is performed with the intent to treat (▶ Figs. 29.2 – 29.5 ). Compared to other IC aneurysms, ACoA aneurysms are associated with the highest false-negative rates because of the relative competition of incoming blood from the contralateral A1. Ethmoidal dural arteriovenous fistulas have a similar pattern of hemorrhage on CT, and in some cases the diagnosis is not seen without a catheter angiogram. Some neurointerventionalists will manually occlude the contralateral ICA to magnify the flow from an ipsilateral ICA injection if an ACoA aneurysm is not visualized on DSA and highly suspected on CT/CTA. In extreme cases, simultaneous bilateral carotid injections are performed to characterize the ACoA complex (▶ Fig. 29.4 ). Once an ACoA aneurysm is identified on DSA, a 3D spin is performed to better characterize the aneurysm and its adjacent vascular anatomy in preparation for treatment.