for ophthalmology residents

1. Retinoschisis
Othman Al-Abbadi, M.D

2. Definition
• Separation or splitting of the NSR into inner
and outer layers with severing of neurones
and complete loss of visual function in the
affected area.

9. Senile
• Prevalence
– 5% of the population >20 years
– Particularly in hypermetropics
• Typical retinoschisis
– Split occurs in the outer plexiform layer
• Reticular retinoschisis
– Split occurs at the level of RNFL

10. Symptoms
• NO Photopsia NOR floaters
• Visual field defect but rarely noticed
• If any, result from VH or a progressive RD

11. Signs
• Bilateral in 50-80%
• Early  Extreme Inferotemporal periphery
– exaggeration of microcystoid degeneration
• Elevation is convex, smooth, thin and relatively
immobile
• May progress circumferentially until it has
involved the entire periphery
– Typical usually remains anterior to the equator
– Reticular is more likely to spread posteriorly

14. • The surface of the inner layer may show
sclerosis of blood vessels & ‘snowflakes’
(whitish remnants of Müller cell footplates)
• Breaks may be present in one or both layers
– Inner layer breaks are small and round
– outer layer breaks are usually larger, with rolled
edges & located behind the equator

15. • Distinction between the typical and reticular
types is difficult clinically, though the inner
layer is thinner and tends to be more elevated
in the latter; differentiation is based
principally on behaviour, with complications
much more common in the reticular form

16. Complications
• RD is rare
– even in an eye with breaks in both layers the
incidence is only around 1%
– The detachment is almost always asymptomatic,
infrequently progressive and rarely requires
surgery
• Posterior extension to involve the fovea
– very rare
• Vitreous haemorrhage is rare

17. Distinction between RD & RS

19. Juvenile
• Bilateral maculopathy, with associated peripheral
retinoschisis in 50%
• Splitting occurs at RNFL
• Inheritance is XLR
• Poor prognosis
• Due to progressive maculopathy; visual acuity
deteriorates during the first two decades, but
may remain reasonably stable until the fifth or
sixth decades before further deterioration

22. Symptoms
• Presentation
– Between the ages of 5-10 years
• Reading difficulties
• squint or nystagmus occurs in infancy
– associated with advanced peripheral retinoschisis,
often with VH
• Carrier females are generally asymptomatic

23. • Foveal schisis
– Spoke-like striae radiating from the foveola,
associated with cystoid changes

24. • Whitish drusen-like dots and pigment
variation may be seen
• Peripheral schisis predominantly involves the
inferotemporal quadrant
– Does not extend
– Inner layer may develop oval defects
– Defects may coalesce, leaving only retinal blood
vessels floating in the vitreous (‘vitreous veils’)

26. Complications
• Vitreous and intra-schisis haemorrhage
• Neovascularization
• Subretinal exudation
• Rhegmatogenous or tractional RD
• Traumatic rupture of the foveal schisis

27. Investigations
• OCT
– Documenting maculopathy progression
• FAF
– spoke-like patterns
– central hypoautofluorescence with surrounding
hyperautofluorescence

28. • FA
– Mild window defects but NO leakage
• ERG
– Normal in eyes with isolated maculopathy
– Selective decrease in amplitude of the b-wave on
scotopic and photopic testing

30. Management
• Small lesions found incidentally need annual
follow-up
• Progression towards the fovea
– Retinopexy or surgical repair
• Recurrent VH
– PPV
• In cases of Maculopathy
– Topical or oral CAI
– Reduce foveal thickness and improve visual acuity in
some patients

31. After treatment with CAI