Endoscopic Endonasal Surgery for Tumors of the Cavernous Sinus: Experience of 234 Cases

Object: For many years, tumors of the cavernous sinus (CS) were considered inoperable given the high density of neurovascular structures within the CS. During the past two decades detailed microsurgical studies have described numerous approaches to the CS. We present our experience with endoscopic endonasal surgery (EES).

Methods: We retrospectively reviewed the outcome of 234 patients (55.5% male) that underwent EES to address CS tumor involvement between April 2002 and November 2012. CS invasion was confirmed intraoperativelly in every case. The cohort included 175 (75%) pituitary adenoma cases and 59 (25%) non-adenomatous lesions.

Results: The majority of pituitary adenomas with invasion of the CS was non-functioning (75.5%). This subgroup included 115 macro- and 60 giant adenomas with unilateral invasion of the CS in 152 cases (87%) and bilateral in 23 (13%). Other than hypersecretion syndromes in functional adenomas and visual deterioration with optic apparatus compression, clinical presentation included palsies of the intracavernous cranial nerves (CN) in 22 patients (12.6%). Following EES, total radiographic tumor resection from the CS was achieved in 36.6%. Preexisting CN palsies improved/resolved in 18 cases (81.8%) and remained unchanged in 4 (18.2%). New permanent CN palsies developed in 4 patients (2.3%). The rate of CSF leak in pituitary adenomas was 6.3%. Three patients (1.7%) suffered a carotid artery injury resulting in a postoperative death in one (mortality 0.6%) and no sequelae in two.

The subgroup of non-adenomatous lesions (n = 59) with CS invasion included 28 meningiomas (47.5%), 14 chordomas (23.7%) and 17 more rare sellar/parasellar lesions. Unilateral CS invasion was noticed in 46 cases (78%) and bilateral in 13 (22%). Clinical presentation included intracavernous CN palsies in 34 patients (57.6%). The goal of EES was decompression/biopsy in 17 cases; among the remaining cases, total tumor resection from the CS was achieved in 16 (38.1%) based on imaging studies. Preexisting neuropathies improved/resolved in 15 patients (44.1%) and remained unchanged in 19 (55.9%). New permanent CN palsies were observed in 11 patients (18.6%) affecting the abducens nerve in 5 patients and branches of the trigeminal in 6 cases. The rate of CSF leak in the group of non-adenomatous lesions was 11.9%. Among two cases (3.4%) with carotid artery injury, one patient died (mortality 1.7%) and the other remained intact.

Conclusion: Tumors invading the CS are difficult to access without new neurological deficits. Given its medial corridor, EES provides acceptable results in the management of these tumors. Symptomatology due to CS invasion is more likely to improve in pituitary adenoma cases and the rate of surgical complications is higher in non-adenomatous cases. The risk of intracavernous carotid artery injury remains high but the overall perioperative mortality due to vascular injury is less than 1% and the risk of stroke, in our experience, is 0%.