Surgical Management of Intracavernous Carotid Artery Aneurysms: BNI Experience
A. Giancarlo Vishteh, MD
Suresh K. Sankhla, MD†
Michael T. Lawton, MD
Robert F. Spetzler, MD
Division of Neurological Surgery, Barrow Neurological Institute, Mercy Healthcare Arizona, Phoenix, Arizona
†Current Address: Department of Neurosurgery, University of Texas, M. D. Anderson Cancer Center, Houston, Texas
Between 1988 and 1994, 24 patients (21 females and 3 males) with 25 aneurysms of the cavernous portion of the internal carotid artery (ICA) underwent surgery. Patients presented with signs and symptoms of cranial nerve compression (n=15), subarachnoid hemorrhage (n=3), thromboembolic ischemic symptoms (n=3), bilateral carotid-cavernous fistulae (n=1), and seizures (n=1). One aneurysm was discovered incidentally. Eighteen aneurysms were confined to the cavernous sinus, while seven had subarachnoid extensions. There were 15 giant and 9 large aneurysms and 1 small aneurysm. Surgical intervention included trapping and bypassing (n=17), direct clipping (n=5), or wrapping (n=3). At a mean follow-up of 2.0 years, 22 (92%) patients were at their preoperative Glasgow Outcome Scale score or better. Two patients (8%) had deteriorated. There were no deaths related to surgery, and the treatment-associated neurological morbidity rate was 8%. Aneurysms of the cavernous ICA have become amenable to surgery, with good patient outcomes, mainly due to advances in microsurgical, vascular bypass, and endovascular techniques. Surgery, however, is recommended only for a few select cases with clear and appropriate indications.
Key Words : aneurysms, carotid artery, cavernous sinus, revascularization
Intracavernous internal carotid artery (ICA) aneurysms represent 3 to 5% of all intracranial aneurysms[16,35,49] and account for 14% of all ICA aneurysms. As neuroimaging techniques have become more sophisticated, the diagnosis of cavernous aneurysms has increased markedly. About a third of these lesions are asymptomatic at diagnosis. Their natural history suggests that a large number of such aneurysms will remain clinically asymptomatic and carry significantly lower rates of rupture and mortality compared to aneurysms situated in the subarachnoid compartment.[27,32] Therefore, most asymptomatic intracavernous ICA aneurysms do not require surgical treatment. Because the morbidity and mortality rates associated with surgical treatment are high, surgery should be reserved for cases with clear indications.[7-9,18,37,40,41,43-46,50] For example, asymptomatic aneurysms that extend into the subarachnoid space or those located at the junction of the cavernous and intradural portions of the ICA are associated with a considerable risk of subarachnoid hemorrhage (SAH) and should be considered for elective surgical management.[1-33]
Symptomatic lesions may produce considerable neurological morbidity as the result of compression (pain and cranial nerve deficits), rupture (carotid-cavernous fistula, epi staxis or SAH), or thromboembolic episodes associated with ischemia.[3,14,31,38,58] Patients with symptomatic aneurysms, particularly those who present with acute rupture or progressive neurological manifestations, may incur profound debilitating or potentially life-threatening consequences from their disease and hence require treatment. Therefore, direct surgical treatment (combined with endovascular intervention in some cases) is one approach to the management of patients with symptomatic intracavernous ICA aneurysms.[9,10] We present our experience with the surgical treatment of aneurysms of the intracavernous ICA in 24 patients. Clinical, anatomical, and surgical features are discussed. Based on our experience and review of the literature, we propose a treatment protocol for intracavernous ICA aneurysms.
Clinical Materials and Methods
Between May 1988 and April 1994, 24 patients with aneurysms arising from the intracavernous portion of the ICA were treated surgically at our institution (Table 1). There were 21 females and 3 males (mean age, 52 years; range, 6 to 78 years). Aneurysms originating outside the cavernous sinus but with part of their sac extending into the cavernous sinus as well as paraclinoid aneurysms that required entry into the cavernous sinus at surgery were excluded. Hospital and office records were examined for clinical data and radiological studies for anatomic features. All surgical procedures were performed by one surgeon (RFS). Pre- and postoperative neurological function was evaluated using Glasgow Outcome Scale (GOS) scores. Final outcome was assessed during clinic visits as well as by telephone questionnaires.
Fifteen (63%) patients presented with signs and symptoms of progressive compression of cranial nerves (II through VI) as a result of aneurysmal enlargement (Table 1
). Three (13%) patients presented with SAH, and all were Hunt and Hess grade II at diagnosis. Three (13%) patients had thromboembolic symptoms and one (4%) patient became symptomatic with seizures. One (4%) patient presented with bilateral carotid-cavernous fistulae after trauma, and one (4%) patient's aneurysm was detected incidentally during investigations for unrelated symptoms that included mild diaphoresis, nausea and confusion. By preoperative GOS criteria, 19 patients were in good condition and 5 had moderate disabilities. Twenty patients had preoperative neurological deficits.
Cerebral angiography, the gold standard for determination of the origin, configuration, and course of an aneurysm, was performed in all patients. Radiological studies demonstrated 38 intracranial aneurysms, 29 of which were located within the cavernous sinus. Of these 29 intracavernous ICA aneurysms, 25 were treated surgically and therefore included in this series. Eighteen (72%) aneurysms were confined to the cavernous sinus only; the remaining seven (28%) aneurysms extended into the adjacent subarachnoid space. There was a predominance of right-sided aneurysms (16:9). There were 15 (60%) giant (>2.5 cm in diameter) and 9 (36%) large (1.0 to 2.5 cm in diameter) aneurysms and one (4%) small (<1.0 cm in diameter) aneurysm (Table 2). Eighteen (72%) aneurysms were classified as saccular, two (8%) as fusiform, and five (20%) as pseudo aneurysms (Table 2).