PEER REVIEWED
Primary Retinal Detachment: A Review
of Mechanisms, Management, and Controversies
BY
REZA IRANMANESH, MD WILLIAM M. SCHIFF, MD
Retinal detachment occurs when the neurosensory
retina separates from the underlying retinal pigment epithelium (RPE). In a rhegmatogenous
retinal detachment (RRD), liquefied vitreous gains access to the subretinal space
through a full-thickness retinal break. Retinal detachment occurs with an estimated
frequency of 1/10000 people per year.1
Roughly 95% of all RRD are ultimately repaired;2
however, it remains a serious disorder that can lead to significant loss of vision
or blindness.
Repair of retinal detachment prior to the 20th century was
generally unsuccessful because the pathophysiology of the disease was not well understood.
In 1918, Gonin was the first to demonstrate the importance of localizing and sealing
retinal breaks through transscleral cautery, a procedure termed ignipuncture.3
Scleral buckling techniques, introduced by Custodis4
and later refined by Schepens among others, have revolutionized repair of RRDs,
with success rates reported as high as 80%–90%.5-7
More recently, alternative techniques such as pars plana vitrectomy (PPV)and pneumatic
retinopexy have been utilized to treat RRD.8,9
Advances in surgical instrumentation, intraoperative visualization, and the use
of short-term intraoperative tamponades have facilitated the surgical management
of RRD by vitrectomy.
MECHANISM OF RHEGMATOGENOUS RETINAL
DETACHMENT
There are 4 major categories of retinal detachment: rhegmatogenous,
tractional, combined tractional and rhegmatogenous, and exudative. A RRD develops
from a full- thickness retinal break. This type of retinal detachment is the most
common, and is the category that will be discussed in this review.
Acute posterior vitreous separation often precedes the development
of RRD. Aging causes syneresis of the vitreous gel. Large liquefied pockets of gel,
known as lacunae, form.10
With time, the liquefied gel passes into the subhyaloid space creating a true posterior
vitreous separation.11
As the posterior vitreous separates from the inner retina, tears
can develop, especially in regions in which the cortical gel was or remains firmly
adherent. Typical flap-shaped horseshoe tears are the result of excessive and abnormal
traction often occurring at posterior insertions of the vitreous base and regions
of lattice degeneration. A RRD often develops when persistent vitreous, adherent
to the anterior flap of a tear, causes traction allowing liquid vitreous access
to the subretinal space. Eye movement, causing internal eddy currents, may facilitate
this process.
PREDISPOSING FACTORS TO RETINAL DETACHMENT
AND PROPHYLAXIS
Asymptomatic retinal breaks may predispose patients to retinal
detachment. The indications for prophylactic retinopexy of these lesions are controversial.
Given that the prevalence of retinal breaks was found to be 83 times that of retinal
detachment, it is clear that not every break leads to retinal detachment.12
Thus, prophylactic treatment of retinal breaks should be selective and is generally
recommended for symptomatic tears13
and horseshoe tears with persistent vitreous traction.14
Thirty percent to 50% of acute, symptomatic horseshoe tears have been found to result
in retinal detachment, and prophylactic treatment reduces the frequency to 5%.13,15
Several peripheral retinal lesions are characterized by anomalous
vitreoretinal adhesions, and therefore, are predisposed to full-thickness retinal
breaks in the setting of PVD. Ora bays, meridional folds and complexes, cystic retinal
tufts, and lattice degeneration represent sites of abnormal vitreoretinal adhesions.
Lattice lesions can vary in shape, appearance, and location. Retinal
thinning and degeneration with atrophic hole formation, liquefaction of the overlying
vitreous, and firm adhesions of the vitreous at the margin of these lesions have
been identified in histopathologic studies.14,17-21
The condition is bilateral in 45% of cases,16
and it occurs more frequently in myopic eyes. Approximately 30% of patients with
retinal detachment also have lattice degeneration. However, the prevalence of lattice
is high in the general population, 7%–8% in clinical series, and 11%–16%
in autopsy series. For lattice lesions without retinal breaks, the risk of retinal
detachment is <1%, and prophylactic therapy is generally not recommended. In
addition, prophylactic therapy for atrophic holes in lattice is usually not indicated,
but considerations, such as history of detachment in the fellow eye, may influence
the decision. Clinicians generally agree that lattice lesions with tractional breaks
should be treated prophylactically, even if the patient is asymptomatic.
Nonphakic eyes are at an increased risk for retinal detachment
in their lifetime when compared with phakic eyes. Approximately 40% of retinal detachments
occur in the nonphakic eye.22
The incidence of retinal detachment is 0.01% in the general population, 2%–5%
following intracapsular cataract extraction, and 0%–1.4% following extracapsular
cataract extraction.22-25
Crystalline lens extraction is associated with an increase in the rate of vitreous
liquefaction and it is possible that anterior movement of the vitreous contributes
to subsequent PVD and retinal break formation.26,27
TYPES OF SURGICAL INTERVENTION
Scleral buckling is often considered the gold standard for retinal
reattachment surgery, and currently reported success rates range between 82%–91%
for a single operation.28-30
Results following scleral buckling appear to be somewhat less successful in the
pseudophakic/aphakic eye and in those detachments in which a causative break is
not identified.31 This may
be due to the small slit-like breaks often found in the nonphakic eye. Additionally,
capsular opacification and fibrosis in the pseudophakic eye can obscure the view
of the peripheral fundus, rendering identification of causative breaks challenging.
Machemer initially introduced PPV in 1970.8
At the time of surgery, the underlying source of vitreoretinal traction can be relieved
internally. Once the retina is flattened, either by internal drainage through a
posterior retinotomy or through an existing peripheral retinal break, the breaks
can then be treated directly with endolaser, avoiding excessive and extensive cryopexy.
Initially, primary vitrectomy (with or without scleral buckling) was used in the
management of retinal detachments and was thought to be high-risk for failure with
traditional scleral buckling techniques. These cases included giant retinal tears,
posterior retinal breaks, retinal detachments with significant vitreous hemorrhage,
and proliferative vitreoretinopathy (PVR). Recently, there is an increasing trend
towards utilizing primary vitrectomy for the repair of routine retinal detachments.32
Advantages of PPV over scleral buckling techniques alone include
the enhanced capability of identifying small, previously unrecognized retinal breaks.
Using a panoramic viewing system and perfluorocarbon liquids, slit-like breaks are
more readily identified, with the Schlieren phenomenon often localizing the site.33
Furthermore, minimal refractive changes following PPV without scleral buckling can
be expected.
Pneumatic retinopexy was introduced in the mid 1980s as an outpatient
procedure to treat selected retinal detachments.9
Initially, the technique was recommended when the detachment was caused by a single
retinal break, no larger than 1 clock hour and located within the superior 8 hours
of the fundus, or by a group of small retinal breaks located within 1 clock hour,
in the absence of grade C or D PVR and uncontrolled glaucoma.34
Perfuoropropane (C3F8) and sulfur hexafluoride (SF6) are the most commonly used
gases and the technique combines intravitreal injection in combination with transconjunctival
cryotherapy or laser photocoagulation of retinal tears.
These 3 surgical techniques each have their advantages. When one
reviews the literature it is not surprising that there is significant controversy
regarding the ideal procedure for primary retinal detachment. In some studies, it
appears that scleral buckling and primary vitrectomy are comparable in regards to
anatomic and visual success.35
One retrospective study found retinal reattachment rates of 91% for both groups
without significant differences in postoperative visual acuity (VA).35
Others have reported higher rates of anatomic success with primary vitrectomy compared
to scleral buckling in pseudophakic retinal detachment.
Some surgeons may prefer 1 technique to another due to their own
experiences and training preferences. Many choose buckling over vitrectomy in the
younger phakic patient to avoid cataract formation. Scleral bucking, in many instances,
is an external procedure, avoiding the well-recognized complications of intraocular
surgery. However, scleral buckling can induce myopia, diplopia, and can be associated
with significant complications, especially when external drainage of subretinal
fluid is performed. Performing segmental buckling and nondrainage procedures can
minimize many of the complications associated with buckling procedures.
Pneumatic
retinopexy is advantageous because it is technically less difficult and can be performed
in the office setting. In 1989, a randomized controlled trial compared pneumatic
retinopexy to scleral buckling and found a single-operation success rate of 73%
and 82%, respectively.34
Hilton and colleagues described a comprehensive literature review and reported a
single-operation anatomic success rate of 80%.36
Although the use of pneumatic retinopexy in phakic eyes is fairly well accepted,
its use in the pseudophakic or aphakic eye is more controversial. Primary retinal
reattachment was achieved in 67% of pseudophakic retinal detachments treated with
pneumatic retinopexy.31,34
However, because most eyes that initially failed pneumatic retinopexy ultimately
reattached with fairly good vision, the Retinal Detachment Study Group recommended
the use of pneumatic retinopexy independent of lens status.31,34
Others have also found that initial failure of pneumatic retinopexy does not adversely
affect the visual outcome.37,38
Despite these results, there are those who are skeptical regarding the use of pneumatic
retinopexy in nonideal cases.39
Ultimately, without a randomized clinical trial comparing the
3 modalities, and in numerous clinical scenarios, there will never be a definitive
answer as to which procedure is superior. For most surgeons, the decision as to
what procedure to use for primary retinal detachment will depend on the individual
clinical situation combined with each surgeon's biases, experience, and comfort
level. With vitrectomy and pneumatic retinopexy as accepted options for repair of
the routine retinal detachment, there is less exposure to scleral buckling for vitreoretinal
surgeons in training. Younger surgeons may ultimately prefer these techniques to
conventional scleral buckling. In fact, 1 study showed that the popularity of pneumatic
retinopexy was inversely proportional to the number of years that the specialist
had been in practice.40
Although
there is no proven algorithm for repair of primary RRD, it is our preference to
perform primary scleral buckling in the phakic patient with well-recognized pathology.
We prefer segmental, nondrainage procedures. We perform encircling buckles in eyes
with global pathology, and the nonphakic eye with larger detachments with limited
peripheral visualization.
|

|
|
Figure
1. An image of a posterior retinal break where a primary vitrectomy is generally
utilized.
IMAGES
COURTESY OF KEVIN LANGTON, CRA, COLUMBIA OPHTHALMOLOGY
PHOTOGRAPHY DEPARTMENT |
|
 |
|
|
Figure
2. An image of a giant retinal tear where a primary vitrectomy is generally utilized. |
|
Primary vitrectomy (with or without an encircling scleral buckle)
is generally utilized in those eyes with vitreous hemorrhage, posterior retinal
breaks (Figure 1), giant retinal tears (Figure 2), cataract or pseudophakic
status, and established PVR. In eyes with diffuse pathology, often requiring extensive
retinopexy in multiple quadrants, we feel vitrectomy may be a more ideal approach.
By applying localized and focused retinopexy, and avoiding external drainage in
the setting of a congested choroid, vitrectomy is extremely effective and safe.
We often use a 3.5-mm solid, silicone-encircling element to support the posterior
vitreous base in pseudophakic eyes, those with PVR, or those eyes with significant
global peripheral pathology. However, if primary vitrectomy is being performed in
a phakic eye with more limited pathology, such as a patient with a posterior retinal
break, then scleral buckling is generally not required. In addition, we shave the
vitreous base 360° under panoramic viewing in most patients. The retina is
flattened internally utilizing perfluorocarbon liquids. Postoperative positioning
is generally recommended for 1–2 weeks.
In our practice, we utilize pneumatic retinopexy, most often in
only the ideal cases. These include phakic patients with isolated pathology and
tears in the superior quadrants. Cryopexy of the retinal break with subsequent injection
of 0.3 cc of pure C2F6 gas, or injection followed by indirect laser retinopexy followed
by a flattening of the retina should be performed. In eyes that have failed pneumatic
retinopexy, repair with subsequent buckling can often be more challenging for several
reasons. Visualization may be impaired due to residual gas or fish eggs and often
new breaks, as a result of the gas injection, can convert a routine detachment into
a more complex case. Ultimately, vitrectomy with scleral buckling may be preferable
for repair.
PROLIFERATIVE VITREORETINOPATHY
In spite of improvements in surgical techniques and outcomes in
the repair of primary retinal detachment over the past decades, the development
of PVR remains a major obstacle to successful repair. Proliferative vitreoretinopathy
is characterized by the formation of fibrous membranes along the periretinal surface,
often causing redetachment of the retina. This process occurs in approximately 5%–10%
of all rhegmatogenous retinal detachments and is responsible for the majority of
surgical failures.
Several studies have identified clinical risk factors that are
associated with the development of PVR. Proliferative vitreoretinopathy is more
often seen in patients with large or giant retinal tears, vitreous hemorrhage, choroidal
detachment, failed retinal reattachment procedures, extensive cryopexy, and retinal
detachments involving 2 or more quadrants.41,42
Due to the complexity of PVR surgery and ultimately the disappointing visual outcomes,
adequate prophylaxis of PVR remains an important goal. Currently, there is great
interest in developing viable pharmacologic therapies in the hope of preventing
this intraocular response.
Some papers describing therapies composed of a combination of
steroids, antineoplastic agents, and/or other antiproliferative agents have shown
encouraging results for PVR prophylaxis. A randomized clinical trial combining low-molecular
weight heparin (LMWH) with 5-fluorouracil (5-FU) as adjuvant therapy for PVR reported
a statistically significant lower incidence of postoperative PVR in the LMWH/5-FU
group (12.6%) vs. the placebo group (26.4%). The final VA, however, was not significantly
different between the 2 groups.43
Additionally, others have evaluated treatment for established PVR. Williams and
colleagues randomized 62 eyes with severe (class C3 or D) PVR to infusion fluid
composed of either balanced salt solution or of balanced salt solution with added
heparin and dexamethasone.44
The authors found that there was a trend towards fewer cases of recurrent PVR in
the heparin/dexamethasone group although this did not approach statistical significance.
Despite the initial enthusiasm regarding these reports, an
agent that truly prevents the development of PVR and improves visual outcomes is
not yet on the horizon. Improvements in current management of PVR have been primarily
surgical in nature. Controlling postoperative inflammation, performing focused retinopexy
without extensive cryopexy, and successful reattachment of the retina is the best
prophylaxis for PVR.
TIMING OF INTERVENTION
Many authors have looked at duration of macular detachment and
its effects on visual prognosis. Yang and colleagues reviewed 93 patients retrospectively
and found that a final vision of 20/50 or better was noted in 53.6% of patients
with macular detachment <7 days duration, compared with 29.7% of patients with
a macular detachment of >7 days.45
Other investigators have had similar findings confirming that surgery after 1–2
weeks of macula-off retinal detachment yields poorer visual results.46,
47 Ross and Kozy evaluated patients with early macula-off
detachments and subdivided them into 3 groups based on duration of macular detachment
(1–2 days, 3–4 days, and 5–7 days). They found that there was
no statistical difference in the visual recovery between the 3 groups.48
This study suggests that surgery in macula-off detachments may be delayed for a
relatively short period without compromising visual outcomes.
Patients with macula-on retinal detachments risk the progression
to macular involvement if surgery is delayed. In general, these cases are more urgent.
Most vitreoretinal surgeons prefer to operate prior to progression. If delay is
anticipated due to factors such as operating room or surgeon availability and/or
medical issues, strict bedrest with double patching often prevents and delays progression
of the detachment into the macula. In 1992, Hartz and colleagues showed that delaying
surgery for a short time did not lead to worse visual outcomes regardless of the
status of the macula.49
CONCLUSION
As more technical advances occur in the field of vitreoretinal
surgery, there will also be more controversies regarding the best approaches in
the management of primary retinal detachment. Fortunately, current success rates
for retinal reattachment are high regardless of the technique utilized. Frontiers
that need exploring are numerous. Mechanisms and therapies that reduce the postoperative
risk of PVR, enhance visual outcomes, and improve postoperative positioning and
quality of life issues in the retinal detachment patient are paramount.
REFERENCES
1. Wilkes SR, Beard CM, Kurland LT, et al. The incidence of retinal
detachment in Rochester, Minnesota, 1970-1978. Am J Ophthalmol. 1982;94:670-673.
2. Af-Fat FG, Sharma MC, Majid MA, et al. Trends in vitreoretinal
surgery at a tertiary referral center: 1987 to 1996. Br J Ophthalmol.
1999;83:396–398.
3. Gonin J. Le Decollement de la retine. Pathogenie-traitment.
Lausanne, Switzerland: Libraire Payot;1934.
4. Custodis E. Bedeutet die plombenaufnahung auf die sklera einen
fortschritt in der operatven behandlung der netzhautablosung. Ber Dtsch Ophthalmol
Ges. 1953;58:102.
5. Lincoff HA, Baras I, McLean J. Modifications to the Custodis
procedure for retinal detachment. Arch Ophthamlol. 1965;73:160.
6. Schepens CL, Okamura ID, Brockhurst RJ. The scleral buckling
procedures. I: surgical techniques ad management. Arch Ophthalmol. 1957;58:797-811.
7. Schepens CL, Okamura ID, Brockhurst RJ, et al. The scleral
buckling procedures. V: synthetic sutures and silicone implants. Arch Ophthalmol.
1960;64:868-881.
8. Machemer R, Parel JM, Buettner H. A new concept for vitreous
surgery. I: Instrumentation. Am J Ophthalmol. 1972;73:1-7.
9. Hilton GF, Grizzard WS. Pneumatic retinopexy. A two-step outpatient
operation without conjunctival incision. Ophthalmology. 1986;93:626-641.
10. Byer NE. What happens to untreated asymptomatic retinal breaks,
and are they affected by posterior vitreous detachment? Ophthalmology. 1998;105:1045-1049.
11. Heller MD, Straatsma BR, Foos RY. Detachment of the posterior
vitreous in phakic and aphakic eyes. Mod Probl Ophthalmol. 1972;10:23-36.
12. Davis MD. Natural history of retinal breaks without detachment.
Arch Ophthalmol. 1974;92:183-94.
13. Byer NE. Clinical study of retinal breaks. Trans Am Acad
Ophthalmol Otolaryngol. 1967;71:461-473.
14. Combs JL, Welch RB. Retinal breaks without detachment: natural
history, management and long-term follow up. Trans Am Ophthalmol Soc. 1982;80:64-97.
15. Colyear BH Jr, Pischel DK. Clinical tears in the retina without
detachment. Am J Ophthalmol. 1956;41:773-792.
16. Foos RY, Simons KB. Vitreous in lattice degeneration of retina.
Ophthalmology. 1984;91:452-457.
17. Spencer LM, Foos RY, Straatsma B. Enclosed bays of the ora
serrata. Arch Ophthalmol. 1970;83:421-425.
18. Spencer L, Foos R, Straatsma B. Meridional folds, meridional
complexes and abnormalities of the peripheral retina. Am J Ophthalmol. 1970;70:697-714.
19. Parelhoff E, Wood W, Green WR. Radial perivascular lattice
degeneration of the retina. Ann Ophthalmol. 1980;12:25-32.
20. Straatsma BR, Zeegan PD, Foos RY, et al. Lattice degeneration
of the retina. Trans Am Acad Ophthalmol Otolarygol. 1974;78:87-113.
21. Byer N. Lattice degeneration of the retina. Surv Ophthalmol.
1978;23:213-248.
22. Haimann M, Burton TC, Brown CK. Epidemiology of retinal detachment.
Arch Ophthalmol. 1982;100:289-292.
23. Clayman HM, Jaffe NS, Light DS. Intraocular lenses, axial
length, and retinal detachment. Am J Ophthalmol. 1981;92:778-780.
24. Ridgeway AEA. Discussion of factors responsible for retinal
detachment and other late complications after intraocular lens implantation. Trans
Ophthalmol Soc UK. 1985;104:539-540.
25. Heslin KB, Guerriero PN. Clinical retrospective study: comparing
planned extracapsular cataract extraction and phacoemulsification with and without
lens implantation. Ann Ophthalmol. 1984;116:956-962.
26. Hilding AC. Alterations in the form, movement, and structure
of the vitreous body in aphakic eyes. Arch Ophthalmol. 1954;52:699-709.
27. Irvine AR. The pathogenesis of aphakic retinal detachment.
Ophthalmic Surg. 1985;16:101-107.
28. La Heij EC, Derhaag PF, Hendrikse F. Results of scleral-buckling
operation in primary rhegmatogenous retinal detachment. Doc Ophthalmol. 2000;100:17-25.
29. Sharma T, Challa JK, Ravishankar KV, et al. Scleral buckling
for retinal detachment. Predictors for anatomic failure. Retina. 1994;14:338-343.
30. Schwartz SG, Kuhl DP, McPherson AR, et al. Twenty-year follow-up
for scleral buckling. Arch Ophthalmol. 2002;120:325-329.
31. Tornambe PE, et al. Pneumatic retinopexy. A two-year follow-up
study of the multicenter clinical trial comparing pneumatic retinopexy with scleral
buckling. Ophthalmology. 1991;981115-1123.
32. Gartry DS, Chignell AH, Franks WA, et al. Pars plana
vitrectomy for the treatment of rhegmatogenous retinal detachments uncomplicated
by advanced proliferative vitreoretinopathy. Br J Ophthalmol. 1993;77:199–203.
33. Brazitikos PD, DAmico DJ, Tsinopoulos IT, Stangos NT. Primary
vitrectomy with perfluoro-n-octane use in the treatment of pseudophakic retinal
detachment with undetected retinal breaks. Retina. 1999;19:103-109.
34. Tornambe PE, Hilton GF. Pneumatic retinopexy. A multicenter
randomized controlled clinical trial comparing pneumatic retinopexy with scleral
buckling. The Retinal Detachment Study Group. Ophthalmology. 1989;96:772-783.
35. Oshima Y, Yamanishi S, Sawa M, et al. Two-year follow-up study
comparing primary vitrectomy with scleral buckling for macula-off rhegmatogenous
retinal detachments. Jpn J Ophthalmol. 2000;44:538-549.
36. Hilton GF, Das T, Majji AB, et al. Pneumatic retinopexy: principles
and practice. Indian J Ophthalmol. 1996;44:131-143.
37. Amber JS, Meyers SM, Zegarra H, Paranandi L. Reoperation and
visual results after failed pneumatic retinopexy. Ophthalmology. 1990;97:786-790.
38. Grizzard WS, Hilton GF, Hammer ME, et al. Pneumatic retinopexy
failures. Cause, prevention, timing, and management. Ophthalmology. 1996;102:929-936.
39. Han DP, Mohsin NC, Guse CE, et al. Comparison of pneumatic
retinopexy and scleral buckling in the management of primary rhegmatogenous retinal
detachment. Southern Wisconsin Pneumatic Retinopexy Study Group. Am J Ophthalmol.
1998;126:658-668.
40. Benson WE, Chan P, Sharma S, et al. Current popularity of
pneumatic retinopexy. Retina. 1999;19:238-241.
41. Cowley M, Conway BP, Campochiaro PA, et al. Clinical risk
factors for proliferative vitreoretinopathy. Arch Ophthalmol. 1989;107:1147-1151.
42. Girard P, Mimoun G, Karpouzas I, et al. Clinical risk factors
for proliferative vitreoretinopathy after retinal detachment surgery. Retina.
1995;14:417-424.
43. Asaria RHY, Kon CH, Bunce C, et al. Adjuvent 5-fluorouracil
and heparin prevents proliferative vitreoretinopathy: results from a randomized,
double-blind, controlled clinical trial. Ophthalmology. 2001;108:1179-1183.
44. Williams RG, Chang S, Comaratta MR, et al. Does the presence
of heparin and dexamethasone in the vitrectomy infusate reduce reproliferation in
proliferative vitreoretinopathy? Graefes Arch Clin Exp Ophthalmol. 1996;234:496-503.
45. Yang CH, Lin HY, Huang JS, et al. Visual outcome in primary
macula-off rhegmatogenous retinal detachment treated with scleral buckling. J
Formos Med Assoc. 2004;103:212-217.
46. Hassan TS, Sarrafizadeh R, Ruby AJ, et al. The effect of duration
of macular detachment on results after scleral buckle repair of primary, macula-off
retinal detachment. Ophthalmology. 2002;109:146-152.
47. McPherson AR, O'Malley RE, Butner RW, et al. Visual acuity
after surgery for retinal detachment with macular involvement. Ann Ophthalmol.
1982;14:639-645.
48. Ross WH, Kozy DW. Visual recover in macula-off rhegmatogenous
retinal detachments. Ophthalmology. 1998;105:2149-2153.
49. Hartz AJ, Burton TC, Gottlieb MS, et al. Outcome and cost
analysis of scheduled versus emergency scleral buckling surgery. Ophthalmology.
1992;99:1358-1363.
Reza Iranmanesh,
MD is a retina fellow at the Department of Ophthalmology, Columbia University College
of Physicians and Surgeons, Edward S. Harkness Eye Institute in New York, NY. William
M. Schiff, MD, is assistant clinical professor of ophthalmology at the Department
of Ophthalmology, Columbia University College of Physicians and Surgeons, Edward
S. Harkness Eye Institute in New York, NY. Neither author has any financial interest
in the information reported in this article. Dr. Iranmanesh can be reached at
riranmanesh@yahoo.com
and Dr. Schiff can be reached at wms13@columbia.edu.
Retinal Physician, Issue: September 2005