Very Large and Giant Aneurysms

Introduction

In the initial Cooperative Aneurysm study published in 1960, giant aneurysms were defined as lesions with a diameter equal to or greater than 1 inch (25 mm). The reasons behind selection of that diameter are unclear, other than earlier authors in describing small series of very large aneurysms had apparently arbitrarily used these dimensions. In fact, as Roberto Heros points out, as a rule the morphology of aneurysms changes dramatically at diameters of 15 to 17 mm, so that lesions of this size and larger have much more in common with the 25 mm aneurysm than with the much more routine 7 to 13 mm variety. This chapter discusses the unique problems and some potential solutions in the surgical management of aneurysms 15 mm in diameter and larger.

There are three specific factors that set very large and giant (VLG) aneurysms apart from their smaller counterparts, only one of which relates specifically to their diameter. Certainly the sheer mass effect of these lesions produces uncommon effects on the surrounding brain tissue, cranial nerves, adjacent dura, and underlying bone. Almost invariably, a large percentage of the circumference of large aneurysms lies not free in the subarachnoid space but rather invaginated into the brain itself, often with significant pial adhesions and parenchymal edema. Symptoms related to cranial nerve compression are a common presentation of these aneurysms, just as permanent cranial nerve injury is one of the most frequent sources of morbidity in their treatment. Extensive and pernicious adhesions to the surrounding dura mater are often themselves hidden by overlying skull base components, both of which require meticulous surgical technique to remove. All of these factors related to size make adequate exposure of the proximal and distal vasculature, and the aneurysm itself, more difficult and fraught with more risk of brain and cranial nerve injury than is encountered in dealing with smaller lesions. More simply said, the aneurysmal mass makes visualization of the pathology harder for the surgeon and more risky for the patient.

Morphology refers to the external shape or configuration of the aneurysm; specifically, the aneurysm’s relationship to its afferent and efferent vasculature. There is obviously a continuum ranging from small aneurysms with a dainty, well-circumscribed neck completely discrete from the emerging branch arteries to lesions in which the parent vessel disappears into an aneurysm sac from which emerge, at some distance, two and infrequently three arterial branches; however, some version of the latter scenario occurs with monotonous regularity in larger aneurysms, regardless of the impressions drawn from preop angiography. As a rule, the more expansive the lesion, the more extreme the incorporation of the parent artery terminal end and the origins of the branch vessels. For a surgeon to operate on a VLG aneurysm assuming otherwise is an unfortunate triumph of hope over experience.

The final unique factor that differentiates these aneurysms is the almost uniform presence of intraluminal thrombosis and intramural calcification. The unique hemodynamic stresses that give rise to these two features are as yet unclear, and the degree and extent of each is variable in almost identical aneurysms; nonetheless, these two anomalies can and do significantly complicate surgical reconstruction. Their presence, if not their actual extent, can routinely be appreciated by review of preop magnetic resonance imaging (MRI) and computed tomographic (CT) studies (only the CT scan accurately demonstrates the degree of calcification), and early recognition can be important in prioritization of the potential alternatives in surgical treatment.

These alternatives include direct reconstruction, proximal (Hunterian) ligation, trapping of the aneurysm-bearing segment, and combinations of the above, plus the addition of one or more revascularization techniques. The possible need for and consequence of each of these approaches should be considered prior to actual operation of each VLG aneurysm; it’s almost impossible to “over think” the management of these lesions, unless of course the cognitive process should lead to paralysis by analysis.

Rules to Live By

1. You never have enough information about VLG aneurysms. Furthermore, just having the information won’t cut it. Intense study of all of the routine imaging tests, including CT, MRI, and angiograms, is a prerequisite for surgery on the lesions. Often a trial balloon occlusion (TBO) study is also indicated, if the possibility of parent vessel sacrifice exists.

2. With as clear an understanding of the anatomical and hemodynamic realities as the imaging studies can provide, you must evaluate the operative landscape and prepare for the inevitable surprises. This is best done by engaging in a series of “if-this-happens-then-what-do-I-do?” questions and hopefully answers. For example, in dealing with a very large internal carotid artery (ICA)-ophthalmic origin aneurysm, the sequence might go like this:

a. “If I drill the clinoid, remove the optic strut, open the falciform ligament, dissect the dural ring, and still can’t see the proximal neck, meaning I don’t have proximal control, then what?” (Suggestion: expose the cervical internal carotid artery.)

b. “If I have the thing exposed and the neck is too broad/atherosclerotic/turgid to close with a clip, what then?” (Suggestion: try temporary proximal occlusion, then crush the neck gently with a fine hemostat, blades sheathed in a fine French catheter.)

c. “If the neck shears when my clip closes, will the patient tolerate a trapping procedure? With/without a bypass? What caliber of bypass? From where to where?” (Suggestion: your TBO should answer most of these questions and make you prepare the appropriate alternatives.)

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