Retinopathy of prematurity is a disease of the developing retina which develops as a result of disruption of the internal milieu of the developing retina leading ultimately to retinal detachment and blindness.

1. RETINOPATHY OF
PREMATURITY
BY
DR UGO OSUJI

2. OUTLINE
• INTRODUCTION/DEFINITION
• EPIDEMIOLOGY
• RISK FACTORS
• EMBRYOLOGY OF RETINAL VASCULATURE
• PATHOPHYSIOLOGY OF RETINOPATHY OF PREMATURITY
• CLINICAL FEATURES
• CLASSIFICATION
• SCREENING PROTOCOLS
• MANAGEMENT
• COMPLICATIONS/SEQUELAE
• DIFFERENTIAL DIAGNOSES
• CONCLUSION
• BIBLIOGRAPHY

3. INTRODUCTION/DEFINITIO
N

4. Retinopathy of prematurity (ROP) is a vaso-proliferative disorder of
the developing retinal blood vessels in preterm infants who are low
birth weight and is caused by the arrest of complete retinal
vascularization
It is a leading cause of childhood blindness, especially in developed
countries

5. In almost all term infants, the retina and retinal vasculature are fully
developed, and, therefore, ROP cannot occur
In preterm infants, the development of the retinal vessels, which
proceeds peripherally from the optic nerve head during the course
of gestation, is incomplete
The extent of the immaturity of the retinal vessels depends mainly
on the degree of prematurity at birth

6. The disease has a typical progression pattern which is demonstrated in
stages
While earlier stages can regress spontaneously, later stages of the
disease can be characterized by vitreous haemorrhage and/or
tractional retinal detachment

7. The end stage of untreated ROP is the development of a dense
fibrovascular white plaque behind the lens and total tractional
retinal detachment
It was discovered by Theodore L. Terry in 1942 who gave it the
name retrolental fibroplasia from his description of the end stage
of the disease

8. EPIDEMIOLOGY

9. The incidence of ROP is known to be higher in developed countries
because of available resources to take care of premature infants:
• A study by Fielder et al in 1992 in London, England showed that out of 572
infants with birthweight of </= 1700g studied, acute ROP developed in
about 51%

10. In developing countries, the incidence and prevalence of ROP is on
the rise with the increasing establishment of neonatal intervention
initiatives to ensure survival of premature infants
• A study by Adekeye in 1996 on the causes of blindness children in NE
Nigeria showed prevalence of ROP to be 0.5%
• An isolated pilot study by Baiyeroju-Agbeja et al in Ibadan in 1998 showed a
prevalence of 5.5%
• A study by Adio et al in 2012 at UPTH showed an ROP prevalence of 47.2%
in the 53 premature infants studied (although the sample size was small)
• Another study in Ilorin by Ademola-Popoola in 2013 showed ROP
prevalence of 89.6%

11. Race:
Palmer et al showed that ROP is commoner in Caucasian babies than
babies of African or Caribbean descent
Sex:
Incidence is slightly greater in males than females as demonstrated by
Yang et al in 2006
Age:
The more premature the infant, the higher the incidence of ROP:
• A study on ROP in South Korea published in January 2021 found that
incidence of ROP was 4.3% higher in babies born at GA less than 28
weeks than in babies born at GA 28 weeks and above

12. RISK FACTORS

13. 1. Premature birth (</= GA 32 weeks, especially < 30 weeks GA)
2. Low Birth Weight (</= 1500 grams, especially < 1250 grams)
These are the major risk factors.
The Cryotherapy for Retinopathy of Prematurity (CRYO-ROP)
Cooperative Group found that the incidence of ROP in preterm
infants </= 1250g is about 66% and the incidence in preterm
infants </= 1000g is about 82%

14. 3. Excessive use of supplemental oxygen in the early postnatal
period
• A study conducted in 1956 found that exposure to >50% oxygen
resulted in increased incidence of ROP as compared to an oxygen-
curtailed group.
• Flynn et al in 1992 found that for every 12 hour period with tcPO2 of
>/= 80mmHg, the risk of severe ROP nearly doubled

15. • Despite several studies comparing several O2 ranges, a target range
for oxygen supplementation has not been found
• The Supplemental Therapeutic Oxygen for Pre-threshold ROP (STOP-
ROP) trial found no significant differences between ranges of 84 –
94% SaO2 and 96 – 99% SaO2
• The Benefits for Oxygen Saturation Targeting Study II (BOOST-II) trial
compared SaO2 of 82 – 89% and 91 – 95% and discovered that lower
O2 levels were associated with lower rates of ROP but higher mortality
rates

16. 4. Non-black Race
This particular risk factor might have less to do with the actual race
and more to do with the racial variation in socio-economic status.
• The CRYO-ROP study and other studies on ROP in North America
showed that black premature infants had lower rates of threshold
ROP compared to white infants
• However, Aralikatti et al in 2010 discovered that black infants in the
UK had higher ROP rates than white infants

17. 5. Male gender
• A study by Enninga et al in 2015 suggested that male fetal sex is
associated with elevated maternal levels of pro-inflammatory
cytokines and angiogenic factors during pregnancy which
predispose to the development of ROP in male infants
• Yang et al in 2006 and in 2015 also suggested that the male
gender is a signficant risk factor for the development of ROP

18. 6. Twin gestation
This is associated with increased risk of preterm birth and lower
birthweight and perinatal morbidities which in themselves are risk
factors for ROP
CRYO-ROP found that singleton infants had lower risk of ROP than
twins or multiplets

19. 7. Respiratory Distress Syndrome
This might cause an infant to become hypoxic requiring mechanical
ventilation and oxygen therapy and these are risk factors for
development of ROP.
These show that RDS is a significant risk factor development of ROP

20. 8. Anemia
Impaired erythropoiesis due to inadequate production of
erythropoietin causes decreased Hb levels in premature infants and
is referred to as anemia of prematurity
Several studies have shown that the anemia itself, transfusion of
whole blood or RBCs and even recombinant erythropoietin
infusions can lead to the development of ROP

21. 9. Neonatal Sepsis
This is among the commonly identified risk factors for any ROP and
for severe ROP
A New York State cohort study and the Extremely Low Gestational
Age Newborns (ELGAN) study revealed that neonatal sepsis and
late bacteremia are significant risk factors for development of ROP.

22. EMBRYOLOGY OF
RETINAL VASCULATURE

23. Retinal blood vessels start developing at about 16 weeks gestation
and reach the nasal ora serrata by 36 weeks GA and the temporal
ora serrata by 40 weeks GA
Prior to 16 weeks GA, the inner retina is supplied by the hyaloid
vasculature
As hyaloid vessels start regressing at about 16 weeks GA, retinal
vessels start developing

24. Retinal blood vessels develop via two means:
VASCULOGENESIS
ANGIOGENESIS

25. VASCULOGENESIS
• First stage of retinal vascular development
• De novo synthesis of blood vessels by the differentiation of stem
cells into endothelial cells
• In the retina, it is responsible for the development of the main
retinal vessels (branch retinal arteries and veins)
• The stem cells that are involved in this process are called
Vascular Precursor Cells (VPCs)

26. • VPCs can be identified in the primitive retina as early as 12 weeks
GA especially in the developing RNFL surrounding the primitive
optic nerve head (ONH)
• By 16 weeks GA, the VPCs start migrating outwards from the ONH
towards the periphery.
• They migrate in such a way that there is a leading cell while the
others lag behind it in the same direction of migration
• The leading VPCs are called spindle/tip cells

27. • As they migrate further towards the periphery, the VPCs behind
the leading cells coalesce to form solid vascular cords which later
canalize to form the primitive retinal vessels.
• These vascular cords are formed in a four-lobed pattern that
corresponds to the major artery and vein pairs of the adult retina
• By 21 weeks GA, spindle cells undergo apoptosis and
vasculogenesis is complete

29. ANGIOGENESIS
• Second stage of retinal vascular development
• Involves the development of new vessels from pre-existing
vessels
• In the developing retina, this stage is responsible for the
formation of the remaining parts of the branch retinal vessels
and the retinal capillaries

30. • The fully developed retina has 3 networks of capillaries:
SUPERFICIAL PLEXUS
INTERMEDIATE PLEXUS
DEEP PLEXUS

32. • The vascular products of vasculogenesis cannot supply all the
metabolic needs of the developing retinal cells and axons in the
inner two-thirds of the retina, hence the need for angiogenesis
• The increasing metabolic demands of developing retinal cells and
axons as they increase in size and quantity in the face of
inadequate blood supply from the branch retinal vessels cause the
development of physiologic hypoxia in the retina.

33. • The prevailing physiologic hypoxia causes the expression vascular
endothelial growth factors (VEGFs) by astrocytes and microglia in
the retina
• The expressed VEGFs cause endothelial cell proliferation from the
already formed branch arterioles and venules to form capillary
networks
• The superficial plexus is formed first, followed by the intermediate
and then the deep plexus
• Angiogenesis continues till the whole retina is duly vascularized
and VEGF levels fall(36 – 40 weeks GA)

34. PATHOPHYSIOLOGY OF
ROP

35. ROP occurs in two phases (especially in infants born before
31weeks GA):
• Phase 1 occurs before GA 31 weeks:
• Results from the increase in the infant’s systemic oxygen tension as
breathing commences
• Leads to the reduction in the expression of angiogenic factors that drive
angiogenesis in the developing retina.
• As such, angiogenesis and vascular development ceases.
• A demarcation line thus develops between the vascularized posterior and
non-vascularized peripheral portions of the retina

36. • Phase 2 begins from GA 31 to 34 weeks:
• With cessation of angiogenesis but continued retinal growth, the retina
becomes ischemic again and further angiogenic factors are released
• This time, the angiogenic factors cause disordered and disorganized
vascular growth
• This disorganized growth leads to the formation of a fibrovascular ridge
at the demarcation line, from which vascular proliferation from the retina
into the vitreous occurs
• Finally, there is involution of the disorganized blood vessels with
cicatricial contraction of the fibrovascular membranes leading to
tractional retinal detachment

37. CLINICAL FEATURES
Early stages of ROP might not show any symptoms but severe
ROP can manifest symptoms such as:
• Nystagmus
• Leukocoria
Most of the signs seen in ROP are seen on fundoscopy and will be
discussed under “Classification”

38. CLASSIFICATION OF
ROP

39. An international classification system was needed to aid consistent
description, staging and study of ROP.
International Classification of ROP (ICROP) was developed in 1984
for this reason. It was revised in 1989 and also revised again in
2005.

40. ICROP developed classification concepts with prognostic and
pathophysiologic importance which include:
• Location of involvement (zone)
• Disease severity (stage)
• Clock-hours of involvement (extent)
• Presence or absence of plus disease

41. LOCATION (ZONE) OF INVOLVEMENT

42. DISEASE SEVERITY (STAGE)
Stage 0:
Immature Retinal
Vascularization

43. Stage 1:
Presence of a demarcation
line between vascularized
retina posteriorly and
avascular retina anteriorly

44. Stage 2:
Presence of a ridge with
height and width, with or
without small tufts of
fibrovascular proliferation
(popcorn)

45. Stage 3:
Ridge with extraretinal
fibrovascular proliferation which
might be mild, moderate, or
severe

46. Stage 4:
Subtotal/Partial
Retinal
Detachment
4A: extrafoveal
4B: with foveal
involvement

47. Stage 5:
Total Retinal Detachment

48. CLOCK-HOURS OF INVOLVEMENT (EXTENT)

49. PRESENCE OR ABSENCE OF PLUS DISEASE
Plus disease: arteriolar tortuosity and venous engorgement in at
least 2 retinal quadrants

50. FURTHER ITEMS OF
CLASSIFICATION FOR ICROP
• Pre-Plus Disease
• Venous dilatation and arteriolar tortuosity in the posterior pole that is
not as severe as the vascular abnormalities seen in frank plus disease

51. • Aggressive posterior ROP (Rush disease)
• Zone I or posterior Zone II ROP associated with plus disease
involving all 4 quadrants of the posterior pole retinal vessels,
shunt vessels, and flat neovascularization at the junction
between vascularized and non-vascularized retina
• AP-ROP is difficult to treat, has worse prognosis, does not
progress in the typical fashion and its stage 3 disease can
appear as flat neovascularization

52. SCREENING FOR ROP

53. The CRYO-ROP Cooperative Group determined that signs of ROP
were present in about 66% of infants with birthweight of </=
1250g and in 82% of patients with birthweight of </= 1000g.
Hence there is a need to always screen patients who are at risk of
developing ROP.

54. Some guidelines were put in place jointly by the Royal College of
Ophthalmology and British Association of Perinatal Medicine in
1995 and also jointly by the American Academy of Pediatrics –
Section on Ophthalmology, the American Association for Pediatric
Ophthalmology and Strabismus and the American Academy of
Ophthalmology for the ROP screening.
Different countries have modified the screening guidelines to
formulate protocols to suit their peculiar needs and regional
variations in presentation of ROP cases.

55. Screening for ROP should be a concerted effort between
neonatologists and ophthalmologists
There are differences in degree of awareness among
pediatricians/neonatologists on the need for ROP screening in
premature infants:
• A study by Uhumwangho et al in Benin in 2013 showed that among
48 pediatricians, even though about 96% had some knowledge of
the risk factors of ROP, only 29% had knowledge of the screening
guidelines
This translated to a poor knowledge of available treatment
modalities

56. In Nigeria, screening for ROP is still in its nascent stages so there is
no standardized National Screening Protocol in use but some
centres have developed protocols for the purpose of the screening.
The following couple of slides look at the screening protocol in use
in University of Benin Teaching Hospital, Benin.

59. MOBILE PHONES FOR
ROP SCREENING
• There is a place for the use of mobile phones in screening for
ROP
• An inexpensive and less cumbersome way for screening
especially when there is unavailability of the BIO
• This can also make it easier for neonatologists to be directly
involved in the screening for ROP
• A mobile phone with a good camera quality combined with a
20D or 28D lens can prove to be a great tool for screening

60. • Some mobile phone camera apps can be of greater help than the
inbuilt phone cameras
• At a demonstration done at Lagos University Teaching Hospital,
the iOS camera app Filmic Pro was used (in video mode) with an
iPhone 5.
• After pupillary dilatation, the 20D lens was used to visualize the
retinal image which was picked up by the camera and recorded all
through the duration of the examination.
• Indirect ophthalmoscopy was still done at the end of the
demonstration to make sure that there were no missed diagnoses.

61. WHEN TO STOP
SCREENING
• Zone III retinal vascularization attained without previous zone I
or zone II ROP
• Full retinal vascularization in close proximity to the ora serrata for
360 degrees
• Post-menstrual age of 50 weeks and no signs of pre-threshold
disease or more severe ROP
• Regression of ROP – it should be ascertained that there is no
abnormal vascular tissue present which may be capable of
reactivationand progression in zone II or III

62. MANAGEMENT OF ROP

63. Management of retinopathy of prematurity involves a
multidisciplinary approach centered basically around the
neonatologist and the ophthalmologist
Management would involve:
• History
• Examination
• Investigations
• Treatment

64. HISTORY
The clinician should try to ascertain a history of
• Prematurity
• Low birth weight
• Incubator care and prolonged oxygen therapy
• Respiratory distress
• Anemia and blood transfusions
• Neonatal sepsis

65. EXAMINATION
General examination: vital signs such as pulse, respiratory rate and
possibly oxygen saturation (SpO2)
Ocular examination would include:
• Assessment of visual acuity
• Examination of the iris for signs of rubeosis iridis
• Lens examination as cataract is one of the complications of severe ROP

66. • Dilated fundus examination + scleral depression with the aid of
• a Sauer speculum (to keep the lids parted)
• a 20D/28D lens
• a Flynn scleral depressor(to depress the sclera and aid peripheral retinal
examination)

67. INVESTIGATIONS
• Fundus photography
The image that will be gotten from this investigation will depend
on the stage of the disease or zone involved as depicted in the
images shown in previous slides.

68. • Ocular Ultrasound B scan

69. • Flourescein Angiography

71. TREATMENT
The modalities of treatment of ROP include:
• Cryoablation
• Retinal Laser Photocoagulation
• Intravitreal Anti-VEGF injection
• Vitrectomy and Scleral Buckling Surgery

72. CRYOABLATION
This involves the use of a cryoprobe (applied externally to the
globe) to freeze and destroy the avascular retina in order to
eliminate the hypoxic stimulus for VEGF expression and reduce
overall retinal oxygen demand.
This procedure was limited to patients who had progressed to
stage 3 of the disease

74. The efficacy of cryotherapy in inducing ROP regression was first
demonstrated by Yamashita in 1972
The effects of cryoablation on the progression of ROP was studied
in the CRYO-ROP trial
The Cryotherapy for ROP (CRYO-ROP) trial was a study
conducted in 1988 to determine the effects of retinal cryoablation
on the progression and visual outcomes of ROP

75. About 1398 children with ROP (aged 5.5 years and below) were
included in the study
For an ROP eye to be included in the study, it had to have
progressed to the threshold disease stage – a term coined by the
study group.
Threshold Disease describes ROP of 5 contiguous clock hours or 8
total clock hours of stage 3 ROP in zone I or zone II in the presence
of plus disease

76. The study discovered that treatment of ROP eyes with threshold
disease by cryo-ablation of the avascular retina halved the
incidence of unfavourable complications (47% to 25% at 1 year
follow up)
Also, at 10 years follow up, treated eyes were less likely to go blind
than untreated eyes.

77. But, with all the successes of cryoablation, CRYO-ROP showed that
it had some drawbacks:
• Couldn’t eliminate all cases of retinal detachment due to ROP
• 26% of eyes with zone II threshold disease and 78% of eyes with zone I
threshold disease still had unfavourable structural outcomes despite
treatment
• Even among those that had threshold disease and had favourable
structural outcome, most of them had visual acuity worse than
6/12

78. LASER THERAPY
The drawbacks of cryoablation encouraged the need for further
advances in the treatment of ROP
.
Laser therapy involves the use of lasers to burn the peripheral
avascular retina via Pan-Retinal Laser Photocoagulation
Diode lasers are frequently used for this purpose
The treatment area should extend from the ora serrata to the
junction between the vascularized and non-vascularized retina.

80. The Early Treatment of ROP (ETROP) published in 2003
• to test the hypothesis that treatment of ROP in stages of
development of ROP earlier than the CRYO-ROP-prescribed
threshold disease cut-off will result in less unfavourable and better
visual outcomes
ETROP therefore came up with the term “pre-threshold disease”

81. Pre-threshold disease refers to all zone I and zone II ROP changes
that do not meet threshold treatment criteria (except for zone II
stage 1 and zone II stage 2 without plus disease)
This Pre-threshold disease is further grouped into:
TYPE 1 TYPE 2
Zone I, any stage with plus disease Zone I, stage 1 or 2 without plus disease
Zone I, stage 3 without plus disease Zone II, stage 3 without plus disease
Zone II, stage 2 or 3 with plus disease

82. ETROP discovered that early treatment resulted in better visual and
structural outcomes than conventionally treated eyes and this was
more noticeable in eyes with Type 1 pre-threshold disease than in
eyes with Type 2 pre-threshold disease
52% of Type 2 eyes underwent regression even without treatment
So it recommended that eyes with Type 2 disease should be closely
monitored and observed for progression to Type 1 disease before
instituting treatment

83. INTRA-VITREAL
ANTI-VEGF INJECTION
This involves the intravitreal injection of anti-VEGF agents
especially Bevacizumab in eyes with ROP
The recommended dose of Bevacizumab for the treatment of
ROP is 0.625mg
The efficacy of Bevacizumab in ROP treatment was studied and
also compared with laser therapy in the BEAT-ROP trial

84. • The Bevacizumab Eliminates the Angiogenic Threat of ROP
(BEAT-ROP)
• to determine the efficacy of Bevacizumab in promoting regression
of neovascularization in ROP
• to compare rate of ROP recurrence after 54 weeks with use of
Bevacizumab and use of laser therapy
• The study recruited about 150 infants with bilateral ROP with
Zone I or Zone II stage 3 plus disease for a total sample of 300
eyes (though it was 286 eyes that were included in the final
analysis)

85. They were randomized into two groups
• one group was to receive bilateral intravitreal bevacizumab injections
(0.625 mg for each eye) – 140 eyes
• The other group to receive bilateral laser photocoagulation treatment –
146 eyes
6 of the 140 eyes (4.29%) in the bevacizumab group had a
recurrence while 32 out of the 146 eyes (21.92%) in the laser group
had a recurrence of ROP 54 weeks post-treatment

86. The treatment effect was more noticeable in eyes with Zone I
disease:
• In the eyes with zone I disease only 2 eyes treated with
bevacizumab experienced a recurrence while 23 eyes treated with
laser had a recurrence.
• Eyes with zone II disease had similar outcomes with either treatment
The four cases of complications (1 corneal opacity and 3 lens
opacities) seen in the study were all noticed in the laser group

87. • Some drawbacks or concerns about this study include:
• Publications that have documented recurrence of ROP several months
after treatment with anti-VEGF agents therefore requiring prolonged
surveillance and retreatment if necessary --- for this reason, anti-VEGF is
not advisable for infants who are unlikely to return for frequent follow
ups

88. • Concerns that anti-VEGF injection may have deleterious effects on
developing vessels in other parts of the body and may lead to adverse
developmental outcomes
• Some abnormalities in retinal vasculature have been demonstrated by
fluorescein angiography years after anti-VEGF treatment
• Further studies are needed in order to determine the long-term ocular
and systemic side effects of anti-VEGF agents used to treat ROP

89. VITRECTOMY AND
SCLERAL BUCKLING
This is indicated in eyes with stage 4 ROP or worse
The purposes for these procedures include:
• Relieving fibrovascular traction on the retina
• Preventing further detachment of the retina
• Encouraging re-attachment of already detached retina

90. Vitrectomy involves the surgical removal of some or all of the eye’s
vitreous gel and along with it some of the fibrovascular tissue that
is pulling on the retina
At the end of the procedure, air or silicone oil is injected into the
vitreous cavity to push the detaching neurosensory retina back
towards the RPE and encourage re-attachment

92. Scleral buckling involves the attachment of a silicone plastic
material or sponge to the sclera in such a manner that the sclera,
choroid and RPE are pushed forwards towards the detaching
neurosensory retina in order to promote re-attachment.
Various materials have been used for scleral buckling such as fascia
lata, palmaris tendon, plantaris tendon and even encircling
nonabsorbable and absorbable sutures
But of all these, silicone is the most popular

94. For these two procedures, stage 4A eyes have better outcomes
(especially visual outcomes) than Stage 4B or Stage 5
Lens sparing vitrectomy in Stage 4A eyes may slow down
progression to Stage 4B or Stage 5.

95. COMPLICATIONS/SEQUELAE
The following conditions can be
seen in eyes with regressed ROP:
• Myopia with astigmatism
• Anisometropia
• Strabismus
• Amblyopia
• Cataract
• Glaucoma
• Macular pigment epitheliopathy
• Vitreo-retinal scarring
• Abnormal vitreo-retinal
adhesions
• Tractional retinal detachment
• Anomalous foveal anatomy

96. DIFFERENTIAL DIAGNOSES
• Retinoblastoma
• Coat disease
• Persistent Fetal Vasculature
• Ocular Toxocariasis
• Retinal detachment (from any other cause)
• Familial Exudative Vitreoretinopathy
• Norrie disease

97. CONCLUSION
• ROP is one of the leading causes of blindness in the world today
• As more resources are made available for medical care of premature
infants, the incidence of ROP will continue to rise
• It behooves on clinicians, especially ophthalmologists and
neonatologists, to ensure regular screening for ROP so that cases of
ROP can be caught early and treatment instituted early enough to
prevent further pathologic changes that will lead to blindness.

98. BIBLIOGRAPHY
• American Academy of Ophthalmology, Pediatric Ophthalmology and Strabismus,
2019 – 2020 Basic and Clinical Science Course, pp 325 – 335
• American Academy of Ophthalmology, Retina and Vitreous, 2019 – 2020
Basic and Clinical Science Course, pp 175 – 188
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Ophthalmol. 2005; 123: 991 – 999
• Yang, M. B., Donovan, E. F., Wagge, J. R., Race, Gender and Clinical Risk
Index for Babies (CRIB) score as predictors of severe retinopathy of
prematurity, Journal of American Academy of Pediatric Ophthalmology
and Strabismus 2006; 10(3): 253 – 261
• Ludwig, C. A., Chen, T. A., Hernandez-Boussard, T., Moshfeggi, A. A., Moshfeggi,
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101. THANK YOU