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

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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.

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