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ORIGINAL PAPER
Characteristics and outcomes of anterior hyaloidalfibrovascular proliferation in lasered retinopathyof prematurity. The Indian Twin Cities Retinopathyof Prematurity Study (ITCROPS) report number 4
Vivek Pravin Dave • Subhadra Jalali •
Padmaja Kumari Rani • Tapas Ranjan Padhi
Received: 12 March 2013 / Accepted: 5 August 2013 / Published online: 14 September 2013
� Springer Science+Business Media Dordrecht 2013
Abstract To describe the characteristics and treat-
ment outcomes of an unreported, late vitreous hem-
orrhage due to anterior hyaloidal fibrovascular
proliferation in laser-regressed retinopathy of prema-
turity (ROP). Interventional case series. In the ongoing
Indian Twin Cities ROP study database, consecutive
cases with isolated late vitreous hemorrhage at least
one year after laser-regressed disease were analyzed
retrospectively. Anterior hyaloidal fibrovascular pro-
liferation was diagnosed primarily using scleral
depression. Anterior retinal cryopexy with adjunctive
treatments was performed. The main outcome mea-
sure was clinical resolution of new vessels with no
recurrent hemorrhage over a 1-year period. Vitreous
hemorrhage, at two to eight years of age, developed in
three eyes of three children out of 1,168 ROP lasered
eyes. All had received laser for zone I disease as
neonates, with no subsequent sequelae. Evaluation
revealed filiform new vessels at the posterior vitreous
base involving inferior 180� with absence of any other
source of hemorrhage. All underwent anterior retinal
cryopexy to the affected area. Simultaneous additional
treatment, based on intraoperative findings, included
one case each of peripheral laser photocoagulation,
lens-sparing vitrectomy and intravitreal bevacizumab.
All three showed successful regression and non-
recurrence of vitreous hemorrhage with improvement
of vision[20/40 at an intermediate follow-up of two
years. Anterior hyaloidal fibrovascular proliferation is
an unreported and rare cause of vitreous hemorrhage,
appearing years after laser-regressed ROP. It has a
good response to interventional treatment. Meticulous
scleral depression of the vitreous base under anesthe-
sia is useful to detect this rare source of vitreous
hemorrhage.
Keywords Anterior hyaloids fibrovascular
proliferation � Anterior retinal cryopexy �Bevacizumab � Retinopathy of prematurity
Introduction
Regressed retinopathy of prematurity (ROP) has been
reported as an important cause of spontaneous vitreous
hemorrhage in young children [1]. Decreased vision in
V. P. Dave � S. Jalali (&) � P. K. Rani
Srimati Kanuri Santhamma Centre for Vitreoretinal
Diseases, LV Prasad Eye Institute, Kallam Anji Reddy
Campus, LV Prasad Marg, Banjara Hills,
Hyderabad 500034, India
e-mail: subhadra@lvpei.org
S. Jalali
Jasti V.Ramanamma Childrens’ Eye Care Centre,
LV Prasad Eye Institute, Kallam Anji Reddy Campus,
L V Prasad Marg, Banjara Hills, Hyderabad 500034,
India
T. R. Padhi
Department of Retina Vitreous, LV Prasad Eye
Institute, Bhubaneswar, Orissa, India
123
Int Ophthalmol (2014) 34:511–517
DOI 10.1007/s10792-013-9843-2
ROP can occur due to causes such as neovascular
sequelae in active ROP or various retinal vascular and
vitreoretinal interface changes (e.g., tractional detach-
ment, macular and disc dragging, etc.) in regressed
cicatricial stages of ROP. These changes have been
described extensively in the literature. However,
information on vitreous hemorrhage as a late compli-
cation of ROP is scant [2]. Abnormal vitreoretinal
traction and the consequent vascular manifestations in
regressed ROP are hypothesized to cause vitreous
hemorrhage [3]. Anterior hyaloidal fibrovascular pro-
liferation (AHFVP) has been implicated as an impor-
tant cause of post-vitrectomy recurrent vitreous
hemorrhage in patients with proliferative diabetic
retinopathy. Late-onset vitreous hemorrhage in
patients with regressed ROP due to AHFVP has not
been described to date. Here we describe clinical
characteristics and treatment outcomes of late-onset
vitreous hemorrhage in laser-regressed ROP due to
AHFVP seen in our ongoing Indian Twin Cities ROP
study (ITCROPS) database.
Methods
The current report is an interventional retrospectively
analyzed case series. We treated three eyes of three
consecutive patients of previously lasered and well-
regressed ROP in our prospective ITCROPS database
who presented to us with late-onset vitreous hemor-
rhage between September 2002 and April 2011. The
LV Prasad Eye Institute review board approved the
analysis of our ongoing prospective ITCROP database
with respect to screening and outcomes of treatment
for ROP. In all cases informed written consent
explaining the risks, benefits and available options
for any intervention in the child, was taken from at
least one of the parents.
Our protocols for screening, laser and follow-up
care of premature babies and babies with ROP have
been published earlier [4–7]. Briefly, the screening
involves neonatal retinal evaluation for ROP starting
between 20 and 30 days of birth and confluent laser
treatment for vision-threatening ROP. For zone
I/APROP disease, we conduct confluent and repeated
laser sessions, every 3–4 days to the entire avascular
retina, including posterior pockets of avascularity and
any new skip areas that may get uncovered in follow-
up until complete regression of new vessels [6, 7].
After complete regression of ROP, babies are followed
at regular intervals. At each follow-up visit visual
acuity, refraction, ocular alignment, comprehensive
anterior and dilated posterior segment examinations
are performed. Evaluations are conducted at least
three times a year for first two years and then 1–2 times
a year until six years of age. More frequent and longer
time evaluations and whenever indicated, examina-
tions under anaesthesia including for peripheral retinal
scleral depression are performed, based on the ocular
condition in a given patient.
Results
During the study period a total of 1,168 eyes
underwent laser treatment in our ITCROPS database.
Three cases alone presented with late-onset vitreous
hemorrhage at least one year after completely
regressed and stable retinopathy and were analyzed
retrospectively for this report. Any child with ocular or
head trauma or systemic hematological diseases or
anticoagulant drug therapy was excluded from the
current report. The clinical characteristics, interven-
tions and outcomes are provided in Table 1. All three
cases had eventful neonatal period with prolonged
oxygenation and sepsis, and all three had previously
undergone bilateral laser treatment in more than one
sitting for active new vessels in zone I/APROP that
had presented late to us, in the neonatal period. Each
eye had received approximately 5,000, near confluent
laser spots to the whole avascular retina, including the
posterior avascular pockets, as per published protocol
[6, 7]. All three cases were under regular follow-up, as
per protocol [6, 7] in our prospective database.
All babies had completely regressed neovascular-
ization with no vitreous traction or vitreoretinal
interface changes seen at three months and subse-
quent follow-up. In all babies no further complica-
tion or sequelae was seen on regular follow-up until
the current episode of vitreous hemorrhage. In none
of the babies could we detect any other specific
underlying systemic, ocular or retinal cause or risk
factor for the current pathology. None of the babies
had a history of trauma or any systemic or drug
history that could be related to the current vitreous
hemorrhage. Presenting symptoms were age-depen-
dent. The two 8-year-old children presented with
reduced vision and noticing floaters a week before
512 Int Ophthalmol (2014) 34:511–517
123
presentation; the youngest, a 2-year-old child was
detected to have vitreous hemorrhage on the routine
scheduled follow-up visit and was asymptomatic.
The left eye was affected in one child while the
right eye was affected in the other two. None of the
children had bilateral vitreous hemorrhage or bilat-
eral anterior hyaloid vascular proliferation on sclera
indentation under general anesthesia, although both
eyes had been treated and had similar ocular and
retinal status at the initial neonatal period and at
subsequent follow-ups. Visual acuity in the affected
eye was poor, possibly \20/400, in the youngest
child who could not perceive any object and
resented closure of the fellow eye; 20/40 in one
child and counting fingers in the other child, while
visual acuity was [20/30 in all the fellow lasered
eyes. There was dense vitreous hemorrhage in one
child with no view of the retina, moderate hemor-
rhage in one child with a hazy view of the retina
and mild vitreous hemorrhage in the other child
where most details of the retina were visualized.
Investigation
Two eyes with hazy media underwent B-scan ocular
ultrasonography to assess the posterior segment, along
with immersion scan. One child also had ultrasound
biomicroscopy (UBM) to assess the anterior hyaloids
(Fig. 1). The imaging showed attached retina, no
tractional bands and fine membranes anteriorly behind
the lens in both cases besides a varying amount of
vitreous hemorrhage echoes.
Management and intervention
Complete evaluation under anesthesia showed varying
amounts of vitreous hemorrhage based on which
further intervention was planned. In eyes with clear
media (Fig. 2) non-vitrectomy options were explored
while in eyes with dense vitreous hemorrhage, vitrec-
tomy was necessary to clear the media and assess the
site and source of the hemorrhage. Vitrectomy was
performed in one eye and but was not necessary to
Table 1 Clinical characteristics, interventions and outcomes in anterior hyaloidal fibrovascular proliferation (AHFVP) in late-onset
vitreous hemorrhage after laser-regressed retinopathy of prematurity (ROP)
Characteristics Baby 1 Baby 2 Baby 3
Gestational age at
birth (weeks)
28 30 34
Birth weight (g) 1,200 1,200 1,790
Type of ROP Aggressive posterior, zone I Aggressive posterior, zone I Aggressive posterior, zone I
Post-conceptional
age at laser
(weeks)
32 36 37
Age at vitreous
hemorrhage
2 years 8 years 8 years
Presenting
symptoms and
visual acuity
Asymptomatic (too young); visual
acuity \20/400 possibly
Floaters and blurred vision;
visual acuity 20/40
Floaters, blurred vision; visual acuity,
counting fingers 2 m
Fundus Dense vitreous hemorrhage. AHFVP
on intraoperative scleral indentation
Mild vitreous hemorrhage.
AHFVP on scleral
indentation
Moderate vitreous hemorrhage.
AHFVP on scleral indentation
Ultrasonography Posterior vitreous echoes, anterior
vitreous membranes on immersion
scan
Not indicated Posterior vitreous echoes, anterior
vitreous membranes on immersion
scan
Ultrasound
biomicroscopy
Not performed Not performed Anterior hyaloidal membranes
Treatment Lens sparing vitrectomy;
intraoperative anterior retinal
cryopexy
Anterior retinal cryopexy;
additional peripheral laser
Anterior retinal cryopexy; intravitreal
bevacizumab
Outcome at 2-year
follow-up
No recurrence; visual acuity 20/40 No recurrence; visual acuity
20/30
No recurrence; visual acuity 20/40
Int Ophthalmol (2014) 34:511–517 513
123
ascertain and treat the underlying pathology in the
other two eyes. In all three eyes, at least 180 degrees of
inferior vitreous base and the anterior hyaloid was
found to have abnormal, filiform, elevated neovascu-
lar tufts with minimal gliotic/fibrotic component and a
predominantly vascular component. No other point of
vitreoretinal traction, retinal tears, posterior vitreous
detachment, avascular retina or neovascular tufts were
detected even after detailed fundus examination using
indirect ophthalmoscopy and scleral depression. All
the eyes had been adequately lasered without any
evidence of skip areas as ascertained during the
intervention and the follow-up once the vitreous
hemorrhage resolved. Based on the evaluation, in all
cases the source of vitreous hemorrhage was ascer-
tained to be AHFVP. The peripheral 2 mm retina/ora
underlying the neovascular tufts appeared to have poor
vascularity and no capillary network, but this could
not be ascertained definitively due to inability to
conduct a fluorescein angiogram of this area.
For treatment of AHFVP, all eyes underwent
anterior retinal cryopexy (ARC) to the whole area of
abnormal neovascular tufts at the posterior vitreous
base and adjoining ora serrata including the 2–3 mm
of the partly avascular-appearing underlying periph-
eral retinal strip under visualization by indirect
ophthalmoscope. In the eye where lens-sparing vit-
rectomy was performed for dense vitreous hemor-
rhage, ARC was completed intraoperatively.
Endolaser was not performed as the area was far too
anterior with risk of lens touch. The eye with moderate
vitreous hemorrhage in an 8-year-old child received
transconjunctival ARC to the area of abnormal new
vessels and adjoining 1.00 mm avascular strip of
retina as far as visualized, but due to hazy view, the
adequacy of treatment could not be ascertained; hence,
treatment was supplemented at the same session with
1.25 mg (0.05 ml) of intravitreal bevacizumab. In one
eye with clear media, the ARC to the relatively
avascular retinal strip was supplemented with periph-
eral additional laser using indirect ophthalmoscope
delivery, in the same session; this was performed as an
out-patient procedure under short general anesthesia.
The postoperative regimen included topical beta-
methasone eye drops four times a day, tapered over the
following 2–4 weeks depending on the extent of
inflammation and adnexal reaction. Eyes with intra-
ocular procedure also received topical tobramycin
four times a day for one week. The periodic follow-up
regimen as described earlier [7] was followed. All eyes
had attached retina, clear media with a clinically
normal macula and no vitreous pathology at last
follow-up. The treated new vessels completely
regressed and the avascular retina showed scars of
treatment only with no residual significant fibrosis/
gliosis/traction clinically. Visual acuity at two years of
post-intervention follow-up was 20/30 and 20/40 in
the two older children. The youngest child (2 years old
at treatment) improved to 20/40 and is receiving
amblyopia treatment with 2-h patching of the fellow
Fig. 1 Ultrasound
biomicroscopy of child 3
showing retrolental echoes
near vitreous base due to
fibrovascular proliferations
514 Int Ophthalmol (2014) 34:511–517
123
eye that has a visual acuity of 20/30. None of the eyes
developed any recurrent vitreous hemorrhage or any
complication of the intervention.
Discussion
Although the management of the vasoproliferation of
acute-stage vision-threatening ROP has been exhaus-
tively described in literature and in randomized
prospective trials [5–11], vitreous hemorrhage is
rarely described. Hutcheson et al. [12] found that
babies with vitreous hemorrhage in active acute ROP
had a worse visual and anatomical prognosis as
compared to those with no vitreous hemorrhage.
Information regarding late-onset vitreous hemorrhage
in treated and regressed ROP is scarce. The only
substantial report is a retrospective study by Ruth et al.
[3] which described 14 eyes of 13 patients with late
vitreous hemorrhage after regressed ROP. The retro-
spective study group was non-homogenous and
included eyes with trauma, retinal detachments and
non-lasered patients many of whom were treated and
followed up elsewhere. Detailed evaluation under
anesthesia and ultrasonography was not reported
uniformly. A definitive source of vitreous hemorrhage
could not be ascertained in a number of eyes [3].
Hence, the information available currently is very
sparse and inadequate with no clear guidelines for the
evaluation and management strategies for eyes with
late-onset isolated vitreous hemorrhage in lasered
ROP patients.
Ruth et al. [3] hypothesized various mechanisms for
this late vitreous hemorrhage in regressed ROP
including abnormal vitreoretinal traction caused by
contracture of the regressed fibrotic tissue leading to
shearing of the normal retinal vasculature or vitreo-
schisis with traction [3] on the retinal surface as seen in
diabetic eyes [13]. Whether these phenomena actually
occur in ROP eyes is speculative and not proven.
The anterior vitreous cortex or anterior hyaloid is
the anterior surface layer or condensation of the
vitreous body. There is no specialized membrane that
constitutes the anterior vitreous cortex, but instead
there is a greater density of collagen fibrils. Neovas-
cularization of this area, termed as AHFVP, has been
described in literature following diabetic vitrectomy
[14, 15]. UBM in diabetic vitrectomized eyes has
shown AHFVP at scleral port sites [16]. It is also
described as a cause of late-onset vitreous hemorrhage
in lasered, non-vitrectomized diabetic retinopathy
eyes and is thought to be due to unlasered ischemic
anterior retinal tissues. There are also few reports of
AHFVP in diabetic eyes after cataract surgery [17] and
as an idiopathic entity in non-diabetic non-operated
otherwise healthy individuals [18]. AHFVP is char-
acterized by peripheral extra-retinal fibrovascular
proliferation that extends circumferentially along the
anterior hyaloid at the vitreous base to the posterior
surface of the lens edge at the equator. The fibrovas-
cular tissue contracts and causes recurrent vitreous
hemorrhage and sometimes tractional detachment of
the peripheral retina. Fibrovascular proliferation in
vitrectomized non-regressed acute-stage ROP eyes
has been described on the posterior pole [19] but not at
the vitreous base as seen in our patients. In none of our
three lasered and non-vitrectomized children could we
find any recurrent/residual new vessels at the posterior
Fig. 2 Fundus photograph
of patient 2 showing inferior
peripheral fresh vitreous
hemorrhage, old confluent
laser marks and absence of
any posterior traction or
proliferation
Int Ophthalmol (2014) 34:511–517 515
123
pole either before, during or after the surgery. To the
best of our knowledge, fibrovascular proliferation at
the anterior hyaloid and vitreous base causing vitreous
hemorrhage has not been described in ROP literature.
The previous literature that describes delayed-onset
vitreous hemorrhage in regressed ROP has no mention
of scleral depression or UBM evaluation of the
vitreous base and the anterior hyaloid [3, 19]. AHFVP
as the actual cause of vitreous hemorrhage in some of
those cases cannot be ruled out. We could detect the
pathology due to our meticulous search for the source
of the vitreous hemorrhage by careful scleral depres-
sion and evaluation of the vitreous base, which is our
routine protocol for all adult and pediatric vitreous
hemorrhages. As retinal surgeons, our familiarity with
AHFVP in diabetic and non-diabetic adult eyes helped
to diagnose this entity in the ROP eyes.
As seen in our three cases, AHFVP could be an
important though rare cause of isolated late-onset
vitreous hemorrhage in regressed ROP and may be
missed if not actively looked for by peripheral scleral
depression under general anesthesia. Clinical charac-
teristics of these cases included a stable and well-
regressed retinopathy following laser for severe
APROP, a time lag of minimum of about 24 months
and as long as 8 years, no trauma and no new vessels
or incomplete vitreous separation at the posterior pole.
The presence of filiform and frond-like fibrovascular
tufts found circumferentially at the vitreous base just
behind the lens equator confirms the diagnosis. The
proliferations can also be seen on appropriate ultraso-
nographic evaluation like UBM and sometimes on
meticulous immersion B-scan. In all our cases the
AHFVP was limited inexplicably to the inferior half of
the eye. Extensive posterior and peripheral retinal
ischemia and young age were proposed as risk factors
in diabetic eyes [14]. What caused only these three
unilateral eyes to develop AHFVP amongst hundreds
of treated ROP in our database is not clear and the
underlying cause is purely speculative. It is possible
that a small 1–2 mm rim of the peripheral avascular
retina was inadvertently left untreated and this part of
the retina continued to grow as it is known that the
stem cells of retinal growth are present in the most
anterior parts of the retina–ciliary epithelium junction.
This new retina could develop with poor vascularity
anterior to the heavily ablated laser scars, as the baby
and the eye grew in size in postnatal weeks/months;
this anterior avascular retina could have triggered the
late-onset anterior hyaloids proliferation. The long
quiescent period of 2–8 years is, however, a little
difficult to explain. It is possible that small minor
bleeds/tufts in the far periphery near the ora could have
been overlooked during the regular follow-ups and
were detected only when they caused significant
symptoms/signs to warrant sclera depression during
evaluation under anesthesia. No particular neonatal,
postnatal or ocular characteristic of these three eyes
could be identified that appeared different from fellow
eyes or other zone I/APROP eyes that we treated.
As regards management, conservative treatment by
waiting for spontaneous resolution of the vitreous
hemorrhage was not an option considering the young
and amblyogenic age of the children and the unknown
source of the hemorrhage before our intervention and
evaluation under anesthesia. Very good visual and
anatomical outcomes were achieved by cryoablation
of the anterior abnormal neovascular and avascular
tissues as is advised for treatment of the condition in
adults [20]. No sequelae such as hypotony or tractional
detachments were noted and the new vessels regressed
with pigmented scars of retinal ablation. This required
additional vitrectomy when the vitreous hemorrhage
was dense. We used additional intravitreal bev-
acizumab where the view was hazy and we could not
confirm complete transconjunctival cryoablation of
the pathological area. This avoided unnecessary and
overtreatment of the unaffected area by blind cryo-
therapy in hazy areas of pathology.
The natural history regarding chances of worsening
or spontaneous resolution of AHFVP in ROP is
unknown though the prognosis is reported to be poor
with disease progression in many adult diabetic eyes.
Ruth et al. [3] reported that in their non-homogenous
study group, the majority of patients maintained
baseline vision over a mean follow-up period of one
year both in the treated as well as in the observed
group. However, our series cannot be compared to that
by Ruth et al. [3] due to differences in age at
presentation, severity and source of vitreous hemor-
rhage, co-morbidities and varying clinical findings.
There are a few limitations to our study including
small sample and relatively short post-treatment
follow-up of two years and inability to adequately
photograph the pathology. The fundus photographs
could capture the vitreous hemorrhage, absence of any
other fibrovascular proliferations and well-lasered
retina (Fig. 2) but could not capture the anterior
516 Int Ophthalmol (2014) 34:511–517
123
pathology in spite of our attempts at photographing the
involved area with scleral depression. However,
considering our large on-going prospective ROP
database over more than 10 years, the condition seems
to be extremely rare and hence not reported earlier. We
believe ours is the first report characterizing AHFVP
in laser regressed-APROP patients. Based on our
experience and experience of Ruth et al. [3] detailed
evaluation of the vitreous base by appropriate scleral
depression preferably under anesthesia is recom-
mended in children presenting with new signs/symp-
toms after ROP has regressed. These include change in
visual acuity, changes in visual behavior, floaters,
ocular discomfort, recent-onset squint, any vitreous
opacity, trauma, etc. UBM can be used additionally
wherever feasible. Early diagnosis and prompt man-
agement may prevent amblyopia and provide long-
term stability. Longer duration of follow-up and
pooled experience from other researchers who have
observed or may diagnose similar cases would provide
more insights into this rare clinical situation.
Acknowledgments Supported by unrestricted support from
Hyderabad Eye Research Foundation. This work received no
specific grant from any funding agency in the public,
commercial or not-for-profit sectors. Data analyzed was
collected prospectively as a part of the routine ROP screening
program and treatment protocols and was approved by the LV
Prasad Eye institutional review board, Hyderabad, India. The
tenets of Helsinki were strictly adhered to during the course of
the programme. Each treatment was carried out only after
obtaining written informed consent from the guardians
explaining the risk, benefits and available options.
Conflict of interest No conflict of interest is reported by any
of the contributors. SJ is on the Oxurdex advisory board of
Allergan and received an honorarium from Sun Pharmaceuticals
as an advisor, not connected to this study.
References
1. Spirn MJ, Lynn MJ, Hubbard GB 3rd (2006) Vitreous
hemorrhage in children. Ophthalmology 113(5):848–852
2. Tufail A, Singh AJ, Haynes RJ, Dodd CR, McLeod D,
Charteris DG (2004) Late onset vitreoretinal complications
of regressed retinopathy of prematurity. Br J Ophthalmol
88(2):243–246
3. Ruth A, Hutchinson AK, Baker Hubbard G (2008) Late
vitreous hemorrhage in patients with regressed retinopathy
of prematurity. J AAPOS 12(2):181–185
4. Jalali S, Anand R, Kumar H, Dogra MR, Azad R, Gopal L
(2003) Program planning, screening strategy in retinopathy
of prematurity. Int J Ophthalmol 51(1):89–99
5. Jalali S, Hussain A, Matalia J, R. Anand (2006) Modifica-
tion of ROP screening criteria for India, other middle-
income group countries. Am J Ophthalmol 141(5):966–968
6. Jalali S, Kesarwani S, Hussain A (2011) Outcomes of a
protocol-based management for zone I retinopathy of pre-
maturity. The Indian twin cities retinopathy of prematurity
screening program report number 2. Am J Ophthalmol
151(4):719–724
7. Jalali S, Azad RV, Trehan HS, Dogra MR, Gopal L, Na-
rendra V (2010) Technical aspects of laser treatment for
acute retinopathy of prematurity under topical anesthesia.
Int J Ophthalmol 58(4):505–519
8. Zilis JD, deJuan E, Machemer R (1990) Advanced reti-
nopathy of prematurity. The anatomic, visual results of
vitreous surgery. Ophthalmology 97(6):821–826
9. Early Treatment for Retinopathy of Prematurity Coopera-
tive Group (2003) Revised indications for the treatment of
retinopathy of prematurity: results of the early treatment for
retinopathy of prematurity randomized trial. Arch Oph-
thalmol 121(12):1684–1694
10. Good WV, Early Treatment for Retinopathy of Prematurity
Cooperative Group (2004) Final results of the early treat-
ment of retinopathy of prematurity (ETROP) randomized
trial. Trans Am Ophthalmol Soc 102:233–248
11. Early Treatment for Retinopathy of Prematurity Coopera-
tive Group, Good WV, Hardy RJ, Dobson V, Palmer EA,
Phelps DL, Tung B, Redford M (2010) Final visual acuity
results in the early treatment for retinopathy of prematurity
study. Arch Ophthalmol 128(6):663–671
12. Hutcheson KA, Nguyen AT, Preslan MW, Ellish NJ, Steidl
SM (2003) Vitreous, hemorrhage in patients with high-risk
retinopathy of prematurity. Am J Ophthalmol 136(2):258–263
13. Chu TG, Lopez PF, Cano MR, Freeman WR, Lean GS,
Liggett PE, Thomas EL, Green RL (1996) Posterior vit-
reoschisis. An echographic finding in proliferative diabetic
retinopathy. Ophthalmology 103(2):315–322
14. Lewis H, Abrams GW, Foos RY (1987) Clinicopathologic
findings in anterior hyaloidal fibrovascular proliferation
after diabetic vitrectomy. Am J Ophthalmol 104(6):614–618
15. Lewis H, Abrams GW, Williams GA (1987) Anterior hya-
loidal fibrovascular proliferation after diabetic vitrectomy.
Am J Ophthalmol 104(6):607–613
16. Bhende M, Agraharam SG, Gopal L, Sumasri K, Sukumar
B, George G, Sharma T, Shanmugam MP, Bhende PS,
Shetty NS, Agarwal RN, Deshpande DA (2000) Ultrasound
biomicroscopy of sclerotomy sites after pars plana vitrec-
tomy. Ophthalmology 107(9):1729–1736
17. Ulbig MR, Hykin PG, Foss AJ, Schwartz SD, Hamilton PA
(1993) Anterior hyaloidal fibrovascular proliferation after
extracapsular cataract extraction in diabetic eyes. Am J
Ophthalmol 115(3):321–326
18. Dowler JGF, Mehta JS, Landers AM, Hamilton AM (2003)
Idiopathic anterior hyaloidal vessels. Br J Ophthalmol
87(3):365–366
19. Yokoi T, Yokoi T, Kobayashi Y, Nishina S, Azuma N
(2010) Risk factors for recurrent fibrovascular proliferation
in aggressive posterior retinopathy of prematurity after early
vitreous surgery. Am J Ophthalmol 150(1):10–15
20. Neely KA, Scroggs MW, McCuen BW (1998) Peripheral
retinal cryotherapy for postvitrectomy diabetic vitreous
hemorrhage in phakic eyes. Am J Ophthalmol 126(1):82–90
Int Ophthalmol (2014) 34:511–517 517
123
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