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Clinical Policy Bulletin:
Optic Nerve Decompression Surgery
Number: 0415


Policy

  1. Aetna considers optic nerve decompression surgery medically necessary for the treatment of papilledema accompanying pseudotumor cerebri (idiopathic intracranial hypertension).

  2. Aetna considers optic nerve decompression surgery medically necessary for traumatic optic neuropathy.

  3. Aetna considers optic nerve decompression surgery experimental and investigational for non-arteritic anterior ischemic optic neuropathy (NAION) and all other indications because of insufficient evidence in the peer-reviewed literature.



Background

Optic nerve decompression surgery involves cutting slits or a window in the optic nerve sheath to allow cerebrospinal fluid to escape, thereby reducing the pressure around the optic nerve.

Pseudotumor cerebri (also known as idiopathic intracranial hypertension) is a syndrome of increased intracranial pressure without a discernable cause.  There is a distinct female preponderance from the teens through the fifth decade.  If medical treatment has failed (i.e., Diamox, Lasix, corticosteroids), and disc swelling with visual field loss progresses, direct fenestration of the optic nerve sheaths via medial or lateral orbitotomy has been shown to be an effective and relatively simple procedure for relief of papilledema.

Non-arteritic anterior ischemic optic neuropathy (NAION) is a common cause of sudden loss of vision, especially in the elderly.  It is caused by infarction of the short posterior ciliary arteries supplying the anterior optic nerve.  There is no direct treatment for NAION, although corticosteroids are sometimes used to reduce optic nerve edema.  Treatment goals are aimed at controlling the systemic vascular disease (i.e., hypertension, diabetes, and atherosclerosis) or collagen vascular disease that precipitated NAION in hopes of preventing or delaying bilateral involvement.

Initial results of uncontrolled studies suggested that optic nerve sheath decompression was a promising treatment of progressive visual loss in patients with NAION.  Other investigators who evaluated this surgical procedure reported varying degrees of success.  To resolve the controversy over the effectiveness of optic nerve decompression for NAION, the National Eye Institute sponsored the Ischemic Optic Neuropathy Decompression Trial, a multicenter, randomized controlled clinical trial of optic nerve decompression surgery for patients with NAION.  The study found no benefit from surgery in NAION patients with progressive visual loss; in fact, significantly more patients in the surgery group had progressive loss of vision than patients who received only careful follow-up.  The investigators concluded that optic nerve decompression surgery is not an effective treatment for NAION, and in fact, may increase the risk of progressive visual loss in NAION patients.

A structured evidence review (Dickersin and Manheimer, 2002) concluded that “[r]esults from the Ischemic Optic Neuropathy Decompression Trial indicate that optic nerve decompression surgery for nonarteritic ischemic optic neuropathy is not effective."

A Cochrane review (Dickersin et al, 2012) concluded that results from the single trial indicate no evidence of a beneficial effect of optic nerve decompression surgery for NAION.  Pletcher and associates (2006) stated that the indications and outcomes for endoscopic decompression of the optic nerve remain controversial.

Atkins et al (2010) stated that NAION is the most common clinical presentation of acute ischemic damage to the optic nerve.  Most treatments proposed for NAION are empirical and include a wide range of agents presumed to act on thrombosis, on the blood vessels, or on the disk edema itself.  Others are presumed to have a neuroprotective effect.  Although there have been multiple therapies attempted, most have not been adequately studied, and animal models of NAION have only recently emerged.  The Ischemic Optic Neuropathy Decompression Trial, the only class I large multi-center prospective treatment trial for NAION, found no benefit from surgical intervention.  One recent large, non-randomized controlled study suggested that oral steroids might be helpful for acute NAION.  Others recently proposed interventions are intra-vitreal injections of steroids or anti-vascular endothelial growth factor (anti-VEGF) agents.  There are no class I studies showing benefit from either medical or surgical treatments.  Most of the literature on the treatment of NAION consists of retrospective or prospective case series and anecdotal case reports.  Similarly, therapies aimed at secondary prevention of fellow eye involvement in NAION remain of unproven benefit.

Traumatic optic neuropathy (TON) is a complication of head trauma; and there is no uniformly accepted treatment protocol for this condition.  Endoscopic, minimally invasive decompression of the optic nerve in its bony canal ihas been used as an alternative to conservative approach.  Sieskiewicz et al (2008) performed endoscopic optic nerve decompression in 6 patients with blindness or severe impairment of vision caused by head trauma.  In 5 of them, direct optic nerve injury might have been suspected due to presence of bony fractures in the region of the optic canal and the orbital apex.  The time from the trauma to the surgical intervention varied from 8 hours to 30 days.  All patients were treated with steroids before the attempted surgery, however the doses and time of this treatment varied significantly.  There were no complications of the surgery; patients were mobilized on the day of operation and reported no problems with nasal breathing.  Improvement in vision was observed in only 2 of 6 patients (33.3 %).

In a retrospective study, Wang and associates (2008) examined the effectiveness of endoscopic optic nerve decompression in patients with TON.  Patients (n = 46) were first treated with methylprednisolone for 6 days.  Forty-four patients (46 eyes) who did not improve with methylprednisolone treatment were offered endoscopic optic nerve decompression.  In 38 eyes with no light perception vision pre-operatively, 21 eyes (45.6 %) had improvement in visual acuity.  These patients had post-operative light perception in 17 eyes, hand movement in 3 eyes and 60/200 in 1 eye.  Four of 5 eyes with light perception pre-operatively had post-operative vision for hand movement in 2 eyes, finger counting in 1 eye and 20/200 in 1 eye.  For 3 eyes with pre-operative visual acuity of hand movement, the post-operative visual acuities were 60/200, 60/200 and 120/200.  Neither worsening of vision nor major complications was encountered in this series.  The authors concluded that endoscopic optic nerve decompression in experienced surgeons' hands can improve visual acuity in TON with minimal morbidity.

On the other hand, Li et al (2008) reported that there were no difference (statistically) between steroids and steroids plus optic nerve decompression in treating TON.  A total of 237 patients were treated with steroids; 176 also consented to endoscopic optic nerve decompression.  The total vision improvement rate was 55 % in the 176 patients treated with both steroids and endoscopic optic nerve decompression, compared with 51 % in the 61 patients treated with steroids alone; this difference was not statistically significant (p > 0.05).

Wu and co-workers (2008) stated that serious injury to the optic nerve, including direct and indirect events, induces significant visual loss and even blindness.  For the past decade corticosteroids and/or optic canal decompression surgery have been widely embraced as therapeutic paradigms for the treatment of TON.  However, the authors noted that there is little clinical evidence to support the effectiveness of these strategies, raising questions about the efficiency of current therapy for improving visual outcomes.

A Cochrane systematic evidence review (Yu Wai Man and Griffith, 2005; Yu Wai Man and Griffith, 2007) found no randomized controlled trials for either the use of corticosteroids or surgical treatment for traumatic optic neuropathy.  Citing reports of visual recovery rates of 40 to 60 % with conservative management, the authors concluded that the decision to proceed with surgery or high-dose corticosteroids depends on the clinical judgment and surgical skills of the surgeon as well as informed consent of the patient to appreciate the benefits and risks of both treatments.  More recently, a randomized a placebo-controlled trial of the use of intravenous high-dose corticosteroids versus saline in 31 patients with traumatic optic neuropathy (Entezari et al, 2007) found no statistically significant improvement in visual acuity between the 2 groups.

The International Optic Nerve Trauma Study was organized to compare corticosteroids or surgery and corticosteroids, but after failure to enroll sufficient numbers of patients, the study was transformed into an observational study.  Comparing no treatment (observation) versus corticosteroids or surgical decompression, the authors found no difference in the final visual acuity and commented that the decision to treat or not treat should be made on an individual patient basis (Levin et al, 1999). 

Some authorities have recommended optic canal decompression if visual acuity does not improve to 20/400 or better despite 24 to 48 hours of steroid therapy or if visual acuity is 20/200 or better but deteriorates during or after completion of steroid therapy (Kountakis et al, 2000).

In a Cochrane review, Dickersin et al (2012) evaluated the safety and effectiveness of surgery compared with other treatment or no treatment in people with NAION.  These investigators searched CENTRAL (which contains the Cochrane Eyes and Vision Group Trials Register) (The Cochrane Library 2011, Issue 11), MEDLINE (January 1950 to November 2011), EMBASE (January 1980 to November 2011), the metaRegister of Controlled Trials, ClinicalTrials.gov, and the WHO International Clinical Trials Registry Platform.  There were no date or language restrictions in the electronic searches for trials.  The electronic databases were last searched on November 19, 2011.  All randomized trials of surgical treatment of NAION were eligible for inclusion in this review.  These researchers obtained full copies of all potentially relevant articles.  One author extracted data which was verified by another author.  No data synthesis was required.  The 1 included trial randomized 258 participants and was stopped early for futility.  At the time of the 24-month report the follow-up rate was 95.3 % for 6 months and 67.4 % for 24 months (174 participants; 89 careful follow-up and 85 surgery).  There was no evidence of a benefit of surgery on visual acuity.  Measurements of visual acuity and visual fields were performed by a technician masked to the treatment received.  At 6 months 32.0 % of the surgery group had improved visual acuity by 3 or more lines compared with 42.6 % of the careful follow-up group (unadjusted relative risk (RR) 0.75, 95 % confidence interval (CI): 0.54 to 1.04).  At 24 months 29.4 % of the surgery group had improved compared with 31.0 % of the careful follow-up group (unadjusted RR 0.95, 95 % CI: 0.60 to 1.49).  Participants who underwent surgery had a greater risk of losing 3 or more lines of vision, although the increased risk was not statistically significant.  At 6 months 18.9 % in the surgery group had worsened compared with 14.8 % in the careful follow-up group (RR 1.28; 95 % CI: 0.73 to 2.24).  At 24 months 20.0 % in the surgery group had worsened compared with 21.8 % in the careful follow-up group (RR 0.92; 95 % CI: 0.51 to 1.64).  Participants who received surgery experienced both intra-operative and post-operative adverse events, including central retinal artery occlusion during surgery and light perception vision at 6 months (1 participant); and immediate loss of light perception following surgery and loss of vision that persisted to the 12-month visit (2 participants).  In the careful follow-up group, 2 participants had no light perception at the 6-month follow-up visit; 1 of these had improved to light perception at 12 months.  Pain was the most common adverse event in the surgery group (17 % in surgery group versus 3 % in the careful follow-up group at 1 week).  Diplopia (double-vision) was the next most common complication (8 % in the surgery group versus 1 % in the careful follow-up group at 1  week); at 3 months there was no statistically significant difference in proportion of participants with diplopia between the 2 groups.  The authors concluded that results from the single trial indicate no evidence of a beneficial effect of optic nerve decompression surgery for NAION.  They stated that future research should focus on increasing the understanding of the etiology and prognosis of NAION; new treatment options should be examined in the context of randomized clinical trials.

 
CPT Codes / HCPCS Codes / ICD-9 Codes
CPT codes covered if selection criteria are met:
67570
ICD-9 codes covered if selection criteria are met:
348.2 Pseudotumor cerebri
377.01 Papilledema associated with increased intracranial pressure
950.0 Optic nerve injury
ICD-9 codes not covered for indications listed in the CPB:
377.41 Ischemic optic neuropathy [non-arteritic anterior ischemic optic neuropathy (NAION)]


The above policy is based on the following references:
  1. Glaser JS. Topical diagnosis: Prechiasmal visual pathways. In: Duane's Clinical Ophthalmology. Rev. Ed. W Tasman, EA Jaeger eds. Philadelphia, PA: Lippincott-Raven; 1995;2(5):37-39, 50-58.
  2. American Academy of Ophthalmology. Eye Facts About Ischemic Optic Neuropathy. San Francisco, CA: American Academy of Ophthalmology; July 1992.
  3. Flaharty PM, Sergott RC, Lieb W, et al. Optic nerve sheath decompression may improve blood flow in anterior ischemic optic neuropathy. Ophthalmology. 1993;100(3):297-305.
  4. Sergott RC, Cohen MS, Bosley TM, et al. Optic nerve decompression may improve the progressive form of nonarteritic ischemic optic neuropathy. Arch Ophthalmol. 1989;107:1743-1754.
  5. Kelman SE, Elman MJ. Optic sheath decompression for non-arteritic ischemic optic neuropathy improves multiple visual function parameters. Arch Ophthalmol. 1991;109:667-671.
  6. Spoor TC, Wilkinson MJ, Ramocki JM. Optic sheath decompression for the treatment of progressive nonarteritic ischemic optic neuropathy. Am J Ophthalmol. 1991;111:724-728.
  7. Spoor TC, McHenry JG, Lau-Sickon L. Progressive and static nonarteritic ischemic optic neuropathy treated by optic nerve sheath decompression. Ophthalmology. 1993;100:306-311.
  8. The Ischemic Optic Neuropathy Decompression Trial Research Group. Optic nerve decompression surgery for nonarteritic anterior ischemic optic neuropathy (NAION) is not effective and may be harmful.  JAMA. 1995;273(8):625-632.
  9. No authors listed. Characteristics of patients with nonarteritic anterior ischemic optic neuropathy eligible for the Ischemic Optic Neuropathy Decompression Trial. Arch Ophthalmol. 1996;114(11):1366-1374.
  10. Kosmorsky G. Pseudotumor cerebri. Neurosurg Clin N Am. 2001;12(4):775-797, ix.
  11. Feldon SE, Scherer RW, Hooper FJ, et al. Surgical quality assurance in the Ischemic Optic Neuropathy Decompression Trial (IONDT). Control Clin Trials. 2003;24(3):294-305.
  12. Soheilian M, Koochek A, Yazdani S, Peyman GA. Transvitreal optic neurotomy for nonarteritic anterior ischemic optic neuropathy. Retina. 2003;23(5):692-697.
  13. Acheson JF. Optic nerve disorders: Role of canal and nerve sheath decompression surgery. Eye. 2004;18(11):1169-1174.
  14. Yu Wai Man P, Griffiths PG. Surgery for traumatic optic neuropathy. Cochrane Database Syst Rev. 2005;(4):CD005024.
  15. Yu Wai Man P, Griffiths PG. Steroids for traumatic optic neuropathy. Cochrane Database Syst Rev. 2007;(4):CD006032.
  16. Pletcher SD, Sindwani R, Metson R. Endoscopic orbital and optic nerve decompression. Otolaryngol Clin North Am. 2006;39(5):943-958, vi.
  17. Yang Y, Wang H, Shao Y, et al. Extradural anterior clinoidectomy as an alternative approach for optic nerve decompression: Anatomic study and clinical experience. Neurosurgery. 2006;59(4 Suppl 2):ONS253-ONS262.
  18. Levin LA, Beck RW, Joseph MP, et al. The treatment of traumatic optic neuropathy: The International Optic Nerve Trauma Study. Ophthalmology. 1999;106(7):1268-1277.
  19. Entezari M, Rajavi Z, Sedighi N, et al. High-dose intravenous methylprednisolone in recent traumatic optic neuropathy; a randomized double-masked placebo-controlled clinical trial. Graefes Arch Clin Exp Ophthalmol. 2007;245(9):1267-1271.
  20. Kountakis SE, Maillard AA, El-Harazi SM, et al. Endoscopic optic nerve decompression for traumatic blindness. Otolaryngol Head Neck Surg. 2000;123(1 Pt 1):34-37.
  21. Sieśkiewicz A, Łysoń T, Mariak Z, Rogowski M. Endoscopic decompression of the optic nerve in patients with post-traumatic vision impairment. Klin Oczna. 2008;110(4-6):155-158.
  22. Wang DH, Zheng CQ, Qian J, et al. Endoscopic optic nerve decompression for the treatment of traumatic optic nerve neuropathy. ORL J Otorhinolaryngol Relat Spec. 2008;70(2):130-133.
  23. Li H, Zhou B, Shi J, et al. Treatment of traumatic optic neuropathy: Our experience of endoscopic optic nerve decompression. J Laryngol Otol. 2008;122(12):1325-1329.
  24. Wu N, Yin ZQ, Wang Y. Traumatic optic neuropathy therapy: An update of clinical and experimental studies. J Int Med Res. 2008;36(5):883-889.
  25. Uretsky S. Surgical interventions for idiopathic intracranial hypertension. Curr Opin Ophthalmol. 2009;20(6):451-455.
  26. Atkins EJ, Bruce BB, Newman NJ, Biousse V. Treatment of nonarteritic anterior ischemic optic neuropathy. Surv Ophthalmol. 2010;55(1):47-63.
  27. Ott I, Schwager K, Hagen R, Baier G. Traumatic optic neuropathy: A review of the literature in the light of personal experiences. Laryngorhinootologie. 2010;89(11):647-652.
  28. Dickersin K, Manheimer E, Li T. Surgery for nonarteritic anterior ischemic optic neuropathy. Cochrane Database Syst Rev. 2012;(1):CD001538.


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Copyright Aetna Inc. All rights reserved. Clinical Policy Bulletins are developed by Aetna to assist in administering plan benefits and constitute neither offers of coverage nor medical advice. This Clinical Policy Bulletin contains only a partial, general description of plan or program benefits and does not constitute a contract. Aetna does not provide health care services and, therefore, cannot guarantee any results or outcomes. Participating providers are independent contractors in private practice and are neither employees nor agents of Aetna or its affiliates. Treating providers are solely responsible for medical advice and treatment of members. This Clinical Policy Bulletin may be updated and therefore is subject to change.
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