These are considered to be congenital anomalies even when there is considerable atherosclerosis in their walls. They may become enormous in size, by definition greater than 2.5 cm in diameter, but sometimes twice or more as large. Most are located on a carotid, basilar, anterior, or middle cerebral artery, but also are found on the vertebral artery (Fig. 33-29). They grow slowly by accretion of blood clot within their lumens or by the organization of surface blood clots from small leaks. At a certain point they may compress adjacent structures, for example, those in the cavernous sinus, optic nerve, or lower cranial nerves. The giant fusiform aneurysm of the midbasilar artery, with signs of brainstem ischemia and lower cranial-nerve palsies, is a relatively common form. Clotting within the aneurysm may cause ischemic infarction in its territory of supply, as mentioned in the case of berry aneurysms. Giant aneurysms may also rupture and cause subarachnoid hemorrhage, but not nearly as often as saccular aneurysms. These clinical observations were confirmed by the International Study, referred to above.
Treatment of saccular aneurysms is surgical if the lesion is symptomatic and it is accessible; endovascular techniques have been employed if the lesion is in the vertebral or midbasilar artery. Obliteration of the lumen, coupled with vascular bypass procedures, has been successful in the hands of cerebrovascular neurosurgeons, but the morbidity is high. Some giant aneurysms can be ligated at their necks, others by trapping or by the use of an intravascular detachable balloon. Drake summarized his surgical experience in the treatment of 174 such cases in past years. Some fusiform aneurysms have been wrapped in muslin or similar material with mixed results. We have followed one such patient who had been operated on by
T. Sundt more than 35 years ago. Recent attempts at stabilizing the expansion of the aneurysm by deploying an intravascular stent are under study.
The term mycotic aneurysm designates an aneurysm caused by a localized bacterial or fungal inflammation of an artery. (Osler introduced the misnomer mycotic aneurysm to describe an infectious process in the wall of a vessel.) With the introduction of antibiotics, mycotic aneurysms have become less frequent, but they are still being seen in patients with bacterial endocarditis and in intravenous drug abusers. Peripheral arteries are involved more often than intracranial ones; about two-thirds of the latter are associated with bacterial endocarditis caused by streptococcal infections. In recent years, the number of mycotic aneurysms caused by staphylococcal infections and acute endocarditis has increased. The usual pathogenic sequence is an embolic occlusion of a small artery, which may announce itself clinically by an ischemic stroke with white blood cells in the CSF. Later, or sometimes as the first manifestation, the weakened vessel wall ruptures and causes a subarachnoid or brain hemorrhage. An important point is that the aneurysm may appear within days of seeding of the vessel and rupture at any time, although the rates of rupture with subarachnoid hemorrhage are low.