Prior Authorization Review PanelMCO Policy Submission
A separate copy of this form must accompany each policy submitted for review.Policies submitted without this form will not be considered for review.
Plan: Aetna Better Health Submission Date: 09/04/2018
Policy Number: 0415 Effective Date: Revision Date: 06/23/2017
Policy Name: Optic Nerve Decompression Surgery
Type of Submission – Check all that apply: New Policy Revised Policy* Annual Review – No Revisions
*All revisions to the policy must be highlighted using track changes throughout the document. Please provide any clarifying information for the policy below:
Clinical content was last revised on 06/23/2017. Additional non-clinical updates have been made by corporate since that time, as documented below.
08/22/2018 – This CPB was updated with additional background information and references. 04/25/2019 – Tentative next scheduled review date by corporate.
Name of Authorized Individual (Please type or print):
Dr. Bernard Lewin, M.D.
Signature of Authorized Individual:
Optic Nerve Decompression Surgery - Medical Clinical Policy Bulletins | Aetna Page 1 of 21
(https://www.aetna.com/)
Optic Nerve DecompressionSurgery
Policy History
Last Review
08/22/2018
Effective: 05/04/2000
Next Review: 04/25/2019
Review History
Definitions
Additional Information
Clinical Policy Bulletin
Notes
Number: 0415
Policy *Please see amendment forPennsylvaniaMedicaid at theend of this CPB.
Aetna considers optic nerve decompression surgery medically
necessary for the treatment of the following indications:
• Papilledema accompanying pseudotumor cerebri
(idiopathic intracranial hypertension)
• Progressive visual loss associated with craniofacial
fibrous dysplasia
• Traumatic optic neuropathy
Aetna considers optic nerve decompression surgery
experimental and investigational for the following indications
(not an all-inclusive list) because of insufficient evidence in the
peer-reviewed literature:
• Intermittent paroxysmal unilateral phosphenes (i.e.,
light flashes) associated with worsening visual field
defects
• Non-arteritic anterior ischemic optic neuropathy
(NAION)
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• Visual loss secondary to optic nerve drusen
Background
Optic nerve decompression surgery (also known as optic
nerve sheath 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
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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
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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
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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
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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
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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
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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.
Moreau et al (2014) examined the safety and effectiveness of
optic nerve sheath decompression (ONSD) with a medial
trans-conjunctival approach for a variety of indications in a
larger population of patients than has previously been
reported. 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. Post-operative follow-up visits were
scheduled at 1 week, 1 month, and then every 3 to 6 months.
Main outcome measures were visual acuity, visual fields, and
surgical complications. A total of 578 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 NAION, and optic
nerve drusen (OND). During a mean follow-up of 18.7 months
(range of 1 week to 10 years), post-operative 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 intra-operative complications.
The most common post-operative complication was diplopia
(6.0 %). The authors concluded that this review represented
the largest series of patients who have undergone ONSD for
any indication. These data were 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.
Regardless of the indication, complications following ONSD
with the technique described in this report were infrequent.
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Intermittent Paroxysmal Unilateral Phosphenes
De Ridder et al (2016) stated that microvascular
decompression surgery is standard neurosurgical practice for
treating trigeminal neuralgia and hemi-facial spasm. Most other
cranial nerves have been decompressed for paroxysmal
intermittent hyperactivity of the affected cranial nerve or in very
long-standing compressions to treat cranial nerve hypo-
functioning. These investigators described a case of
intermittent paroxysmal unilateral phosphenes (i.e., light
flashes) associated with worsening visual field defects.
Magnetic resonance imaging showed a sandwiched optic
nerve/chiasm between an inferior compression of the internal
carotid artery and a superior compression of the anterior
communicating artery. The patient was successfully treated by
microvascular decompression and anterior clinoidectomy plus
optic canal un-roofing. The authors concluded that this case
report added to the few previous case reports combining 2
previously described techniques (i.e., microvascular
decompression and anterior clinoidectomy plus optic canal un-
roofing). The major drawbacks of this study were that it was a
single-case study and its findings were confounded by the
combinational use of microvascular decompression and
anterior clinoidectomy plus optic canal un-roofing.
Progressive Visual Loss Associated with Craniofacial Fibrous Dysplasia
Bhattacharya and Mishra (2015) stated that fibrous dysplasia
(FD) is a non-malignant fibro-osseous bony lesion in which the
involved bone/bones gradually get converted into expanding
cystic and fibrous tissue. The underlying defect in FD is post-
natal mutation of GNAS1 gene, which leads to the proliferation
and activation of undifferentiated mesenchymal cells arresting
the bone development in woven phase and ultimately
converting them into fibro-osseous cystic tissue. Cherubism is
a hereditary form of fibrous dysplasia in which the causative
factor is transmission of autosomal dominant SH3BP2 gene
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mutation. The disease may present in 2 distinct forms: (i) a
less severe and limited monostotic form, and (ii) a more
aggressive and more widespread polyostotic form.
Polyostotic form may be associated with various endocrine
abnormalities, which require active management apart from
the management of FD. Management of FD is not free from
controversies. While total surgical excision of the involved
area and reconstruction using newer micro-vascular technique
is the only definitive treatment available from the curative point
of view, but this can be only offered to monostotic and very few
polyostotic lesions. In polyostotic varieties on many occasions
these radical surgeries are very deforming in these slow
growing lesions and so their indication is highly debated. The
treatment of craniofacial FD should be highly individualized,
depending on the fact that the clinical behavior of lesion is
variable at various ages and in individual patients. A more
conservative approach in the form of aesthetic re-contouring of
deformed bone, orthodontic occlusal correction, and watchful
expectancy may be the more accepted form of treatment in
young patients. Newer generation real-time imaging guidance
during re-contouring surgery adds to accuracy and safety of
these procedures. Regular clinical and radiological follow-up is
needed to watch for quiescence, regression or reactivation of
the disease process. Patients must be warned and watched
for any sign of nerve compression, especially visual
impairment due to optic nerve compression. Rather than
going for prophylactic optic canal decompression (which does
more harm than good), optic nerve decompression should be
done in symptomatic patients only, and preferably be done via
minimal invasive endoscopic neurosurgical approach than the
conventional more morbid open craniotomy approach. The
authors noted that there is growing research and possibilities
that newer generation bisphosphonate medication may change
the management scenario, as these medications show
encouraging response in not only reducing the osteoclastic
activity, but simultaneously also stimulating the osteoblastic
and osteocytic activities. Belsuzarri and associates (2016)
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noted that FD is a benign fibro-osseous lesion related to an
abnormal bone development and replacement by fibrous
tissue. Fibrous dysplasia has 3 clinical patterns: (i)
monostotic, (ii) polyostotic, and (iii) the McCune-Albright
syndrome (MAS). McCune-Albright syndrome is a rare genetic
disorder (about 3 % of all FDs) that comprises a triad of
polyostotic FD, cafe-au-lait skin macules, and precocious
puberty; MAS can involve the orbit region and cause stenosis
in the optic canal, leading the patient to a progressive visual
loss. These investigators reported a case of craniofacial FD in
MAS in a 9-year old male with progressive visual loss,
submitted to optic nerve decompression by fronto-orbito-
zygomatic approach, with total recovery. A research was
made at Bireme, PubMed, Cochrane, LILACS, and Medline
with the keywords: FD/craniofacial/McCune-Albright/Optic
compression for the clinical review. A clinical review of the
disease was made, the multiple, clinical, and surgical
management options were presented, and the case report was
reported. The authors concluded that MAS is a rare subtype
of FD with endocrinopathy. The FD of the orbital region can
lead to optic nerve compression and possibly to visual loss.
They stated that there is no evidence to support the benefits of
prophylactic surgery in children with normal visual fields and
optic canal narrowing, shown by the CT or MRI, and there is
no method to predict which child will stabilize or deteriorate the
visual loss. The cystic degenerations can lead to sudden
visual loss and is the only possible indication for prophylactic
surgery, but the risk of nerve damage should be considered
and well-explained. In all other cases of normal visual fields
and CT/MRI optic canal narrowing, prophylactic surgery is not
indicated, and follow-up should be done. On the other hand,
early decompression of symptomatic children is a great
standard for a better chance of visual loss reverse..
In a retrospective, chart-review study, DeKlotz and colleagues
(2017) evaluated visual outcomes and potential complications
for optic nerve decompression using an endoscopic endonasal
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approach (EEA) for FD. Patients with FD causing extrinsic
compression of the canalicular segment of the optic nerve that
underwent an endoscopic endonasal optic nerve
decompression at the University of Pittsburgh Medical Center
from 2010 to 2013 were included in this trial. The primary
outcome measure assessed was best-corrected visual acuity
(BCVA) with secondary outcomes, including visual field
testing, color vision, and complications associated with the
intervention. A total of 4 patients and 5 optic nerves were
decompressed via an EEA. All patients were symptomatic
pre-operatively and had objective findings compatible with
compressive optic neuropathy: decreased VA was noted pre-
operatively in 3 patients while the remaining patient
demonstrated an afferent pupillary defect; BCVA improved in
all patients post-operatively. No major complications were
identified. The authors concluded that EEA for optic nerve
decompression appeared to be a safe and effective treatment
for patients with compressive optic neuropathy secondary to
FD. Moreover, they stated that further studies are needed to
identify selection criteria for an open versus an endoscopic
approach.
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Endoscopic Optic Nerve Decompression for the Treatment of Idiopathic Intracranial Hypertension
Tarrats and colleagues (2017) stated that the conventional
treatment for IIH involves weight loss, steroids, diuretics,
and/or serial lumbar punctures; however, if the symptoms
persist or worsen, surgical intervention is recommended.
Surgical options include cerebro-spinal fluid (CSF) diversion
procedures, such as ventriculo-peritoneal and lumbo-
peritoneal shunts, and optic nerve decompression with nerve
sheath fenestration. The latter can be performed using an
endoscopic approach, but the outcomes of this technique have
not been firmly established. This systematic review examined
the outcomes of performing endoscopic optic nerve
decompression (EOND) in patients with IIH; 6 studies were
included for a total of 34 patients. The patients presented with
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visual field disturbances (32 of 32 [100 %]), VA disruptions (33
of 34 [97.1 %]), papilledema (26 of 34 [76.5 %]), and persistent
headache (30 of 33 [90.1 %]). The mean duration of
symptoms ranged from 7 to 32 months. Overall, the patients
showed post-EOND improvement in signs and symptoms
associated with IIH, specifically visual field deficits (93.8 %), VA
(85.3 %), papilledema (81.4 %), and headaches (81.8 %).
Interestingly, 11 cases showed post-operative improvement in
their symptoms with bony decompression of the optic canal
alone, without nerve sheath fenestration. There were no major
AEs or complications reported with this approach. The authors
concluded that EOND appeared to be a promising and safe
surgical alternative for patients with IIH who failed to respond to
medical treatment. Moreover, they stated that further
studies are needed to ascertain the clinical validity of this
procedure.
Endoscopic Endonasal Optic Nerve Decompression for the Treatment of Optic Neuropathy Secondary to Fibrous Dysplasia
DeKlotz and colleagues (2017) evaluated visual outcomes and
potential complications for optic nerve decompression using
an endoscopic endonasal approach (EEA) for fibrous
dysplasia. These researchers carried out a retrospective chart
review of patients with fibrous dysplasia causing extrinsic
compression of the canalicular segment of the optic nerve that
underwent an endoscopic endonasal optic nerve
decompression from 2010 to 2013. The primary outcome
measure assessed was BCVA with secondary outcomes,
including visual field testing, color vision, and complications
associated with the intervention. A total of 4 patients and 5
optic nerves were decompressed via an EEA. All patients
were symptomatic pre-operatively and had objective findings
compatible with compressive optic neuropathy: decreased VA
was noted pre-operatively in 3 patients while the remaining
patient demonstrated an afferent pupillary defect; BCVA
improved in all patients post-operatively. No major
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complications were identified. The authors concluded that
fibrous dysplasia is a rare disease that can lead to
compressive optic neuropathy and subsequent visual
impairment. Only patients with signs and/or symptoms of
compressive optic neuropathy are candidates for surgery. The
EEA for optic nerve decompression appeared to be a safe and
effective means of treating these patients. It is unknown if
endoscopic decompression can be successfully applied to
most or all patients with this disease component or rather if
only a select subgroup is likely to benefit and requires further
study with longer follow-up. They stated that while transcranial
approaches are expected to continue to have a role in the
management of these patients, the EEA shows promise and
may become a preferred option for therapeutic intervention
The authors stated that this study had several drawbacks.
First, it was a small study population (n = 4). Benign
pathology of the canalicular segment of the optic nerve that is
amenable to surgical decompression is rare. The limited
number of patients and interventions prevented making
definitive statements about the overall efficacy and safety.
The current study only evaluated patients affected by fibrous
dysplasia and whether this can be extrapolated to those with
other fibro-osseous lesions is unknown. The follow-up in the
current study was limited (the mean follow-up was 14.8
months). As demonstrated by 1 patient, there was the
possibility for recurrent compressive optic neuropathy following
endoscopic endonasal decompression. Although there was no
disease progression on imaging, his VA and color perception
worsened on ophthalmologic testing and prompted a lateral
decompression via craniotomy. The prevalence of the need for
additional interventions as well as timing following an
endoscopic approach is unknown. Additional work is needed
in the future to fully define the role of endoscopic optic nerve
decompression for fibrous dysplasia. More concrete
indications need to be determined to enable more widespread
acceptance. While randomized controlled trials (RCTs) are
unrealistic given the rarity of these disorders, additional
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reporting of outcomes is needed to critically analyze and
determine those likely to benefit from intervention. While
endoscopic optic nerve decompression appeared to have an
emerging role in the management of these lesions, this did not
mean that open cranial approach is now obsolete. The
potential benefits of improved visualization, preserved
olfaction, more rapid recovery, lack of scarring, decreased
operative stress, and lack of cerebral retraction would favor an
endoscopic approach in some settings, though it is not
universal. Location of the pathology (medial versus lateral) is
perhaps the most critical determinant of approach used as well
as surgeon experience and comfort with a particular technique.
While the use of endoscopic endonasal
decompression is expected to grow with further clarification of
its indications, it is not expected to completely supplant
traditional transcranial approaches.
CPT Codes / HCPCS Codes / ICD-10 Codes
Information in the [brackets] below has been added for clarification purposes. Codes requiring a 7th character are represented by "+":
Code Code Description
CPT codes covered if selection criteria are met:
67570 Optic nerve decompression (e.g., incision or
fenestration of optic nerve sheath)
ICD-10 codes covered if selection criteria are met:
G93.2 Benign intracranial hypertension
H47.11 Papilledema associated with increased
intracranial pressure
S04.011+
-
S04.019+
Injury of optic nerve
ICD-10 codes not covered for indications listed in the CPB:
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Code Code Description
H47.011 -
H47.019
Ischemic optic neuropathy [non-arteritic anterior
ischemic optic neuropathy (NAION)]
H47.321 -
H47.329
Drusen of optic disc
H53.8 Other visual disturbances [Intermittent
paroxysmal unilateral phosphenes (i.e., light
flashes)]
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
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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.
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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.
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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.
29. Ropposch T, Steger B, Meço C, et al. The effect of
steroids in combination with optic nerve
decompression surgery in traumatic optic neuropathy.
Laryngoscope. 2013;123(5):1082-1086.
30. Moreau A, Lao KC, Farris BK. Optic nerve sheath
decompression: A surgical technique with minimal
operative complications. J Neuroophthalmol. 2014;34
(1):34-38.
31. Nishida S, Otani N, Inaka Y, et al. Usefulness of
extradural optic canal unroofing and decompression
of the optic nerve for improvement of visual acuity in
traumatic optic neuropathy. No Shinkei Geka. 2014;42
(11):1035-1038.
32. Dickersin K, Li T. Surgery for nonarteritic anterior
ischemic optic neuropathy. Cochrane Database Syst
Rev. 2015;3:CD001538.
33. De Ridder D, Sime MJ, Taylor P, et al. Microvascular
decompression of the optic nerve for paroxysmal
phosphenes and visual field deficit. World Neurosurg.
2016;85:367.e5-e9.
34. Sosin M, De La Cruz C, Mundinger GS, et al. Treatment
outcomes following traumatic optic neuropathy. Plast
Reconstr Surg. 2016;137(1):231-238.
35. Dhaliwal SS, Sowerby LJ, Rotenberg BW. Timing of
endoscopic surgical decompression in traumatic optic
neuropathy: A systematic review of the literature. Int
Forum Allergy Rhinol. 2016;6(6):661-667.
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36. Bhattacharya S, Mishra RK. Fibrous dysplasia and
cherubism. Indian J Plast Surg. 2015;48(3):236-248.
37. Belsuzarri TA, Araujo JF, Melro CA, et al. McCune-
Albright syndrome with craniofacial dysplasia: Clinical
review and surgical management. Surg Neurol Int.
2016;7(Suppl 6):S165-S169.
38. DeKlotz TR, Stefko ST, Fernandez-Miranda JC, et al.
Endoscopic endonasal optic nerve decompression for
fibrous dysplasia. J Neurol Surg B Skull Base. 2017;78
(1):24-29.
39. Tarrats L, Hernandez G, Busquets JM, et al. Outcomes
of endoscopic optic nerve decompression in patients
with idiopathic intracranial hypertension. Int Forum
Allergy Rhinol. 2017;7(6):615-623.
40. DeKlotz TR, Stefko ST, Fernandez-Miranda JC, et al.
Endoscopic endonasal optic nerve decompression for
fibrous dysplasia. J Neurol Surg B Skull Base. 2017;78
(1):24-29.
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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.
Copyright © 2001-2018 Aetna Inc.
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AETNA BETTER HEALTH® OF PENNSYLVANIA
Amendment to Aetna Clinical Policy Bulletin Number: 0415 Optic Nerve
Decompression Surgery
There are no amendments for Medicaid.
www.aetnabetterhealth.com/pennsylvania updated 08/22/2018