OCR Text |
Show Optic Nerve Sheath Decompression: A Surgical Technique With Minimal Operative Complications Annie Moreau, MD, Kenneth C. Lao, MD, Bradley K. Farris, MD Background: The purpose of this study was to determine the safety and efficacy of optic nerve sheath decompression (ONSD) with a medial transconjunctival approach for a vari-ety of indications in a larger population of patients than has previously been reported. Methods: A retrospective chart review was performed on consecutive patients who underwent ONSD between January 1992 and December 2010. Before ONSD, all patients had documented evidence of progressive loss of visual acuity or visual field, or both. Postoperative follow-up visits were scheduled at 1 week, 1 month, and then every 3-6 months. Main outcome measures were visual acuity, visual fields, and surgical complications. Results: Five hundred seventy-eight eyes of 331 patients underwent ONSD for progressive vision loss due to various indications, which included but were not limited to idiopathic intracranial hypertension (IIH), progressive nonarteritic ische-mic optic neuropathy, and optic nerve drusen (OND). During a mean follow-up of 18.7 months (range, 1 week to 10 years), postoperative visual acuity remained stable or improved in 536 of 568 eyes (94.4%) and progressively worsened in 32 of 568 eyes (5.6%). Visual fields remained stable or improved in 257 of 268 eyes (95.9%) and progressive visual field loss occurred in 11 of 268 eyes (4.1%). There were no reported intraoperative complications. The most common postopera-tive complication was diplopia (6.0%). Conclusions: To our knowledge, this review represents the largest series of patients who have undergone ONSD for any indication. Our data are consistent with current literature supporting ONSD as a safe and effective procedure for IIH. Other indications for ONSD, such as progressive visual field loss associated with OND, warrant further study. Regard-less of the indication, complications following ONSD with the technique described in this report are infrequent. Journal of Neuro-Ophthalmology 2014;34:34-38 doi: 10.1097/WNO.0000000000000065 © 2013 by North American Neuro-Ophthalmology Society Optic nerve sheath decompression (ONSD), also known as optic nerve sheath fenestration, was first described by the French ophthalmologist De Wecker (1) in 1872 for the treatment of neuroretinitis, where it was thought to alleviate "strangulation of the nerve to remove pain and inconve-nience." ONSD has since become a well-established surgical procedure for papilledema associated with idiopathic intra-cranial hypertension (IIH). The most devastating consequence of untreated IIH is visual loss. Visual field defects are detected in more than 90% of patients, and severe impairment of visual acuity has been reported in up to 10% of patients (2,3). ONSD has been demonstrated in multiple studies to be an effective and safe method of stabilizing progressive visual loss in IIH patients (4-9). After medical treatment strategies are exhausted or unable to be tolerated and there is progression of disease, ONSD is a mainstay of management to avoid further deterioration of acuity or visual field. The majority of surgical complications following ONSD are typically transient and benign and include diplopia, anisocoria, and corneal dellen. Severe complications are infrequent but have been reported to include central retinal artery occlusion, intraoperative angle-closure glaucoma, and iatrogenic traumatic optic neuropathy. In 2 of the largest published series of ONSD, there were reported rates of permanent vision loss as a direct result of the surgery in less than 1% and 2% of patients, respectively (9,10). There were also concerns of adverse events associ-ated with ONSD during the Ischemic Optic Neuropathy Decompression Trial (IONDT), which ceased recruit-ment early at the recommendation of the Data and Safety Monitoring Committee (11). Department of Ophthalmology (AM, BKF), Dean A. McGee Eye Institute, University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma; and Department of Ophthalmology (KCL), Scott & White Eye Institute, Texas A&M Health Science Center,Temple, Texas. Supported in part by an unrestricted grant to the Department of Ophthalmology, University of Oklahoma, from Research to Prevent Blindness, Inc., New York, NY. The authors report no conflicts of interest. Address correspondence to Bradley K. Farris, MD, Department of Ophthalmology, Dean A. McGee Eye Institute, University of Okla-homa Health Sciences Center, 608 Stanton L. Young Boulevard, Oklahoma City, OK 73104; E-mail: bradley-farris@dmei.org 34 Moreau et al: J Neuro-Ophthalmol 2014; 34: 34-38 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. The purpose of our study was to determine the safety and results of ONSD with a medial transconjunctival approach in a larger population of patients than has previously been reported with IIH and various other causes of progressive visual loss. METHODS After obtaining University of Oklahoma Institutional Review Board approval, a retrospective chart review was performed in consecutive fashion on the preoperative and postoperative course of 578 eyes in 331 patients who underwent ONSD at the Dean A. McGee Eye Institute (Oklahoma City, OK) between January 1992 and December 2010. All patients received a full neuro-ophthalmologic examination, and all ONSDs were performed by the same surgeon (B.K.F.). When necessary to confirm the presence of buried optic nerve drusen, B-scan echography was performed, along with the 30° test to assess the amount of perineural fluid (12). Before ONSD, all patients had documented evidence of pro-gressive loss of visual acuity or visual field, or both. Until 1998, all surgeries were unilateral, allowing 1-2 weeks of healing time between each eye. Starting in 1998, if bilateral ONSD was indicated, it was performed simultaneously. A standard medial transconjunctival orbitotomy, initially described by Galbraith and Sullivan (13), was performed in all cases under general anesthesia. The medial rectus muscle was disinserted and reflected nasally with 6-0 synthetic polyester suture in typical fashion for eye muscle surgery. A traction suture was then placed through the insertion stump of the medial rectus in a baseball stitch fashion to facilitate abduction of the globe. The pupil was monitored at all times. A custom-made cupped orbital retractor was inserted along the medial scleral wall and used to retract the orbital fat and allow visual-ization of the optic nerve sheath (Fig. 1). Retraction and globe abduction were relaxed if any changes in pupil size were noted. Rhoton spatula dissectors (V. Mueller, part # NL 3785-006) were used to create adequate exposure of the optic nerve sheath and prevent damage of the posterior ciliary nerves and vessels. When adequate visualization was achieved, the dural sheath was elevated using cupped ENT forceps, and retinal scissors were used to excise a dural sheath window approximately 2 · 3 mm in size. Expulsion of cerebrospinal fluid was invariably observed with the initial incision into the dural sheath. The goal was to create a decompression pocket in the medial intraconal space as shown in Figure 2. Rhoton spatula dissectors were then used to carefully dilate the dural window and lyse any arachnoid trabeculae. When feasible, an additional posterior radial incision was made in the dura. After removal of the traction suture, the medial rectus muscle was reattached to the globe at its original insertion site. In the postanesthesia care unit, visual acuity was assessed to confirm visual preservation in the operative eye. Follow-up visits with the surgeon were scheduled at 1 week, 4 weeks, and every 3-6 months depending on the severity of the visual loss. Preoperative and postoperative visual acuities were reviewed in all patients. A change of greater than 2 lines on the Snellen acuity chart was used to define visual acuity improvement or worsening. Preoperative and postoperative results of visual field testing were reviewed. Visual fields were considered improved if the field expanded by at least 20° or a significant field defect (e.g., inferonasal defect) resolved. Any progression of the visual field defect was considered worsening. Preoperative and postoperative motility and alignment evaluation also were reviewed. All follow-up examinations included examination of the optic disc and documentation of its appearance. RESULTS Optic nerve sheath decompression was performed on 578 eyes in 331 patients. The most common indication for the procedure was progressive vision loss due to IIH (455 eyes FIG. 1. Farris-Tang orbital retractor (Bausch & Lomb, #SP7- 53436). The rounded edges reduce trauma to the sur-rounding intraorbital tissues and the distal notch limits any apical compression of the optic nerve. (The authors have no financial interest in the retractor). FIG. 2. T2 axial magnetic resonance imaging demonstrates pockets of cerebral spinal fluid in the anteromedial orbit con-firming patent bilateral optic nerve sheath decompressions. Moreau et al: J Neuro-Ophthalmol 2014; 34: 34-38 35 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. from 236 patients), followed by progressive nonarteritic anterior ischemic optic neuropathy (pNAION; 47 eyes from 44 patients) and optic nerve drusen (OND; 13 eyes from 11 patients). The procedure was also performed on 63 eyes of 40 patients with a variety of other conditions (Table 1). Four eyes from 3 patients had ONSD for progressive optic nerve head swelling with normal intracranial pressure and unknown etiology after extensive investigation. Surgical complications were seen in 23 of 331 (6.9%) patients and are summarized in Table 2. The most common postoperative complication was an ocular motility distur-bance causing diplopia. Esotropia was noted in 11 patients, with 5 requiring eye muscle surgery for persistent diplopia. Exotropia occurred in 4 patients, with 3 of them managed surgically. Three patients developed postoperative esopho-ria, and 2 patients were found to have an exophoria. Those patients not requiring strabismus surgery were managed with prism spectacles or had spontaneous resolution of symptoms. Three patients experienced anterior segment complica-tions. Corneal dellen secondary to postoperative conjunctival swelling occurred in 2 patients, and both resolved following aggressive lubrication. One patient was found to have a conjunctival pyogenic granuloma, which was successfully treated with topical antiinflammatory eye drops. Follow-up ranged from 1 week to 10 years, with a mean of 18.7 months. Six patients were seen for the 1-week postoperative visit and subsequently co-managed by their ophthalmologist, limiting the availability of further post-operative data. Postoperative visual acuity was not available for 10 eyes. During follow-up, 536 of 568 eyes (94.4%) had stable or improved visual acuity (Table 3). Only 268 eyes had available postoperative automated visual fields for com-parison with their preoperative study. Overall, visual fields remained stable or improved in 257 of 268 (95.9%) eyes (Table 4). Although visual acuity worsened in 32 of 568 eyes and visual fields worsened in 11 of 268 eyes, none of these were directly related to the surgery itself but attributed to progression of the underlying disorder or due to a comorbidity. Fifteen eyes of 11 patients underwent repeat ONSD after an initially successful primary ONSD. The time from first to second ONSD ranged from 49 days to 3703 days (average, 823 days). All reoperations were performed in patients with IIH. The chief indication for repeat ONSD was progressive visual loss, as previously defined, in the setting of unresolved or recurrent papilledema. There were no intraoperative or postoperative complications associated with the second surgery. Fourteen of 15 eyes had stable or improved visual acuity. All 15 eyes experienced resolution of papilledema after the repeat ONSD. The procedure was performed with the same medial transconjunctival approach, although scar tissue was encountered in isolating the medial rectus muscle and exposing the retrobulbar optic nerve. TABLE 1. List of conditions in patients treated with optic nerve sheath decompression Condition No. of Patients No. of Eyes IIH 236 455 pNAION 44 47 OND 11 13 Other* 40 63 Venous sinus thrombosis 7 14 Diabetic papillopathy 6 8 Meningioma 5 5 Meningitis 2 4 Ependymoma 2 4 Inflammatory ON 2 3 Traumatic ON† 2 2 Frontal astrocytoma 1 2 Brainstem astrocytoma 1 2 Gun shot wound 1 2 Oligodendroglioma 1 2 AVM with SAH 1 2 SDH from NAT 1 2 Glioblastoma multiforme 1 2 Polycythemia vera 1 2 Hydrocephalus 1 1 Close head injury 1 1 Orbital pseudotumor 1 1 Unknown 3 4 *All patients had optic disc swelling (acute or chronic) with pro-gressive visual loss. †These patients had presumed subdural sheath hematoma. AVM, arteriovenous malformation; IIH, idiopathic intracranial hypertension; NAT, nonaccidental trauma; ON, optic neuropathy; OND, optic nerve drusen; pNAION, progressive nonarteritic ischemic optic neuropathy; SAH, subarachnoid hemorrhage; SDH, subdural hemorrhage. TABLE 2. Complications of optic nerve sheath decompression Complication No. of Patients Esodeviation 14 (5*) Exodeviation 6 (3*) Corneal dellen 2 Conjunctival pyogenic granuloma 1 *Eight patients required strabismus surgery to treat their deviation and recovered without complication. TABLE 3. Results of visual acuity following optic nerve sheath decompression Visual Acuity IIH (No. of Eyes) pNAION OND Other Improved 75 23 2 20 Stable 354 16 10 36 Worse 19 8 0 5 IIH, idiopathic intracranial hypertension; OND, optic nerve dru-sen; pNAION, progressive nonarteritic anterior ischemic optic neu-ropathy. 36 Moreau et al: J Neuro-Ophthalmol 2014; 34: 34-38 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. DISCUSSION This retrospective series represents one of the largest cohort of patients undergoing ONSD by a single surgeon in the same institution over 2 decades. Although a similar study previously has been published reviewing ONSD for IIH alone (9), this review specifically examines the safety and efficacy of ONSD for multiple disorders. The 3 conditions accounting for 88% of patients who underwent surgical intervention for progressive visual loss were IIH, pNAION, and OND. Idiopathic Intracranial Hypertension Our study is consistent with previous reports of ONSD as a safe and effective intervention for progressive visual loss in the setting of IIH (5-9,14). The goal of ONSD is to either halt the progression or improve visual function. We found a 96% rate (429 of 448 eyes) of visual acuity stabilization or improvement among the IIH cohort. We further stratified the preoperative visual acuity of IIH patients into 3 groups (20/20-20/50, 20/60-20/200, or less than 20/200) to examine any differences in visual acuity outcome based on preoperative acuity (Table 5). Visual acuity results among the IIH patients based on preoperative vision revealed sta-bility or improvement of 96.2% for the first group, 88.4% for the second, and 100% for the third. The results suggest that the majority of IIH patients experience halting of vision loss following ONSD, regardless of initial visual acuity. It also demonstrates that approximately half of the patients with a preoperative vision of 20/60 or worse experience improvement in visual acuity after ONSD. Visual field stabilization or improvement was seen in 97% of our patients. However, postoperative visual field data were only available for 227 of 455 eyes in IIH patients. Many of these patients only presented for their 1-week or 1-month postoperative visit without undergoing a visual field testing before returning to their own ophthalmologist for continued care. Complications were seen in 17 of 236 IIH patients (7.2%), with 15 patients developing a postoperative ocular misalignment and 2 patients with self-limiting corneal dellen. Four patients with postoperative esotropia and 2 patients with postoperative exotropia eventually required strabismus surgery, and all patients achieved resolution of their diplopia. There were no cases of visual loss due to ONSD surgery. These results compare favorably with 2 of the largest previously published series of ONSD for IIH (8,9). Progressive Nonarteritic Ischemic Optic Neuropathy Our findings for ONSD performed on patients with progressive nonarteritic ischemic optic neuropathy (pNAION) revealed visual acuity stabilization or improve-ment in 39 of 47 eyes (83%). There was improvement in 48.9% of eyes and worsening in 17%. The IONDT showed visual acuity improvement of 3 or more lines in 42.7% and worsening in 12.4% of patients in their observation group at 6 months (11). It is important to note that the observation group in the IONDT included both patients with progressive and static nonarteritic ischemic optic neuropathy (NAION). The retrospective design in our study and the absence of a controlled NAION cohort does not allow comparison with the prospectively designed IONDT. There remains uncer-tainty as to the frequency of vision recovery in patients with pNAION and perhaps this warrants further study. In our experience, patients with NAION are typically composed of static NAION, p-NAION (typically progress-ing over 2-4 weeks), and a smaller group of younger patients (,50 years old) with chronic progressive NAION (progress-ing over a month) and associated with diabetes mellitus. This last group typically is diagnosed with diabetic papillopathy. In our study, ONSD was performed on 6 patients (8 eyes) with diabetic papillopathy, with all demonstrating postoper-ative stability or improvement in visual acuity. Postoperative visual field results were only available for 5 of the 8 eyes, with 4 demonstrating visual field improvement or stability. In light of the findings from our study and the high percentage of patients who spontaneously recover vision as demonstrated in the IONDT, we no longer recommend ONSD for pNAION at our institution. Optic Nerve Drusen We examined the safety of ONSD for progressive visual loss due to OND. Our findings are based on 11 patients (13 eyes); however, postoperative visual acuity data were only available for 12 eyes and postoperative visual field informa-tion for 9 eyes. Preoperatively, all patients had developed progressive visual field loss and 3 patients demonstrated central visual acuity loss as an indication for surgical inter-vention. Eight patients (8 eyes) with OND had concomitant TABLE 4. Visual field results for the IIH, progressive NAION, OND, and other groups Visual Field IIH (No. of Eyes) pNAION OND Other Improved 142 6 3 3 Stable 78 10 5 10 Worse 7 2 1 1 IIH, idiopathic intracranial hypertension; OND, optic nerve dru-sen; pNAION, progressive nonarteritic ischemic optic neuropathy. TABLE 5. Visual acuity results for IIH patients following optic nerve sheath decompression Preoperative Visual Acuity No. of Eyes Improved Stable Worse 20/20-20/50 372 35 323 14 20/60-20/200 43 23 15 5 ,20/200 33 17 16 0 IIH, idiopathic intracranial hypertension. Moreau et al: J Neuro-Ophthalmol 2014; 34: 34-38 37 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. disc swelling that was not due to an inflammatory, demyelinating, or compressive etiology. We believed that the patients experienced drusen-associated anterior ischemic optic neuropathy (15). Although our sample size was small, ONSD showed stabilization or improvement of visual acuity in all 12 eyes and visual field stabilization or improvement in 8 of 9 eyes. We are unsure why patients with OND and progressive visual loss seem to benefit fromONSD. Although we suggest that ONSD may be beneficial in halting progres-sive visual loss due to OND, the published data for this indication are scarce and warrants further study. Overall Safety Although previous authors have reported sight-threatening surgical complications, such as central retinal artery occlusion and traumatic optic neuropathy, none were encountered in our series. Our overall complication rate of 6.9% compares favorably with the 4.9% complication rate reported by Spoor and McHenry (16) in reviewing 327 ONSD procedures. Although the risk of complications is greater with repeat ONSD (8,17), no complications were encountered in the 11 patients who underwent a second ONSD. The majority of our complications were related to postoperative ocular misalignment (20 of 331 patients). We attribute this finding to the medial transconjunctival technique that requires disinsertion and manipulation of the medial rectus muscle. All of our patients experiencing postoperative diplopia had spontaneous resolution of symptoms or were successfully managed with either prism spectacle correction or strabismus surgery. We recognize the limitations of our study that are inherent in any retrospective case series. Our visual field results are based on less than half of the study population due to the variable follow-up intervals and inconsistent availability of postoperative visual field data. The overall favorable results of visual field stabilization or improvement following ONSD must be viewed with caution. Although our retrospective study did not determine the therapeutic efficacy of ONSD for progressive visual loss due to pNAION or OND, we believe our results suggest that further study of the role of ONSD in this condition is warranted. The medial transconjunctival approach (5,6,8,9,13) is one of the most popular approaches for ONSD with an impressive safety profile. However, newer techniques with-out detaching an extraocular muscle may prove to possess even less morbidity. The superomedial lid crease approach requires no muscle disinsertion and provides exposure to the medial intraconal space for ONSD (18,19). We are cur-rently studying a superomedial transconjunctival approach for ONSD, also without the need of disinserting the medial rectus, in hopes to reduce our incidence of postoperative diplopia. Although only described in a cadaveric study, the endoscopic medial transconjunctival approach (20) requires little to no manipulation of the muscles and may be a minimally invasive technique of the future for optic nerve sheath decompressions. Further investigation with long-term safety and efficacy data of newer techniques are needed. Acknowledgments The authors thank Michele Riggins, MD; Yoonsang Kim, PhD, MPH; Sara Fransen, MD; and Paul Tlucek, MD. REFERENCES 1. DeWecker L. On incision of the optic nerve in cases of neuroretinitis. In: Power H, ed. Report of the Fourth International Ophthalmological Congress, 1872. London, United Kingdom: Savill, Edwards and Co, 1873:11-14. 2. Wall M, George D. Idiopathic intracranial hypertension. A prospective study of 50 patients. Brain. 1991;114:155-180. 3. Rowe FJ, Sarkies NJ. Assessment of visual function in idiopathic intracranial hypertension: a prospective study. Eye. 1998;12:111-118. 4. Hupp SL, Glaser JS, Frazier-Burne S. Optic nerve sheath decompression. A review of 17 cases. Arch Ophthalmol. 1987;105:386-389. 5. Brourman ND, Spoor TC, Ramocki JM. Optic nerve sheath decompression for pseudotumor cerebri [case report]. Arch Ophthalmol. 1988;106:1378-1383. 6. Sergott RC, Savino PJ, Bosley TM. Modified optic nerve sheath decompression provides long-term visual improvement for pseudotumor cerebri. Arch Ophthalmol. 1988;106:1384- 1390. 7. Corbett JJ, Nerad JA, Tse DT, Anderson RL. Results of optic nerve sheath fenestration for pseudotumor cerebri. The lateral orbitotomy approach. Arch Ophthalmol. 1988;106:1391- 1397. 8. Spoor TC, Ramocki JM, Madion MP, Wilkinson MJ. Treatment of pseudotumor cerebri by primary and secondary optic nerve sheath decompression. Am J Ophthalmol. 1991;112: 177-185. 9. Banta JT, Farris BK. Pseudotumor cerebri and optic nerve sheath decompression. Ophthalmology. 2000;107:1907-1912. 10. Sergott RC, Savino PJ, Bosley TM. Optic nerve sheath decompression: a clinical review and proposed pathophysio - logic mechanism [review]. Aust N Z J Ophthalmol. 1990;18: 365-373. 11. Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful. The Ischemic Optic Neuropathy Decompression Trial Research Group. JAMA. 1995;273:625-632. 12. Ossoinig KC, Cennamo G, Byrne SF. Echographic differential diagnosis of optic nerve lesions. Doc Ophthalmol Proc Ser. 1981;29:327-331. 13. Galbraith JEK, Sullivan JH. Decompression of the perioptic meninges for relief of papilledema. Am J Ophthalmol. 1973;76:687-692. 14. Goh KY, Schatz NJ, Glaser JS. Optic nerve sheath fenestration for pseudotumor cerebri. J Neuroophthalmol. 1997;17:86-91. 15. Purvin V, King R, Kawasaki A, Yee R. Anterior ischemic optic neuropathy in eyes with optic disc drusen. Arch Ophthalmol. 2004;122:48-53. 16. Spoor TC, McHenry JG. Comment: complications of optic nerve sheath decompression. Ophthalmology. 1993;100:1432-1433. 17. Plotnik JL, Kosmorsky GS. Operative complications of optic nerve sheath decompression. Ophthalmology. 1993;100:683-690. 18. Pelton RW, Patel BC. Superomedial lid crease approach to the medial intraconal space: a new technique for access to the optic nerve and central space. Ophthal Plast Reconstr Surg. 2001;17:241-253. 19. Pelton RW. The anterior eyelid crease approach to the orbit. Curr Opin Ophthalmol. 2009;20:401-405. 20. Pillai P, Lubow M, Ortega A, Ammirati M. Endoscopic transconjunctival surgical approach to the optic nerve and medial intraconal space: a cadaver study. Neurosurgery. 2008;63:204-208. 38 Moreau et al: J Neuro-Ophthalmol 2014; 34: 34-38 Original Contribution Copyright © North American Neuro-Ophthalmology Society. Unauthorized reproduction of this article is prohibited. |