This document provides information on rhegmatogenous retinal detachment including: - The pathogenesis which involves vitreoretinal traction from liquefaction of the vitreous gel creating a hole that allows fluid into the subretinal space. - Symptoms include photopsia, floaters, and visual field defects. - Signs include Marcus Gunn pupil, low intraocular pressure, retinal breaks, and mild iritis. - Treatment options depend on factors like location and size of retinal break, state of vitreous gel, and include laser photocoagulation, cryotherapy, scleral buckling, pneumatic retinopexy, and drainage of subretinal fluid in

1. Rhegmatogenous Retinal
detachment
DR SAMUEL PONRAJ

2. Anatomy of Peripheral Retina
 Pars plana
 Ora serrata
Normal variants - Dendate process
- Oral bay
-meridonial fold
-enclosed oral bay
-granular tissue

4.  Peripheral –innocuous lesios:
-microcystic degeneration
- Pavingston degeneration
-Honey comb degeneration
- Drusen

5.  Vitreous base
 Vitreous adhesions
-normal
-abnormal

6.  It is characterized by the presence of a retinal break
held open by vitreoretinal traction.
 Rhegmatogenous (rhegma – break), occurs
secondarily to a full-thickness defect in the sensory
retina, which permits fluid derived from synchytic
(liquefied) vitreous to gain access to the subretinal
space.

7. Pathogenesis - Dynamic Vitreoretinal traction
liquefaction of the
vitreous gel
hole in the posterior
hyaloid membrane
Fluid tru defect into
retrohyaloid space
vitreous gel collapses
synchytic fluid in space
Detachment of posterior
vitreous from ILM
Acute PVD

8. Symptoms
 1
Photopsia is the subjective sensation of a flash of light. In eyes
with acute PVD it is probably caused by traction at sites of vitreoretinal
adhesion.
 The cessation of photopsia is the result of either separation of the
adhesion or complete tearing away of a piece of retina (operculum).
 In PVD an arc of golden or white light induced by eye movements - in
dim illumination. --patient's temporal peripheral visual field.
2 Floaters are moving vitreous opacities which are perceived when
they cast shadows on the retina. Vitreous opacities in eyes with acute
PVD are of the following three types:
a Weiss ring is a solitary floater consisting of the detached
annular attachment of vitreous to the margin of the optic disc
b Cobwebs are caused by condensation of collagen fibres within
the collapsed vitreous cortex.

9. 
c A sudden shower of minute red-coloured or dark spots
usually indicates vitreous haemorrhage secondary to tearing of a
peripheral retinal blood vessel.
3 A visual field defect is perceived as a ‘black curtain’. In
some patients it may not be present on waking in the morning, due
to spontaneous absorption of SRF while lying inactive
overnight, only to reappear later in the day. A lower field defect is
usually appreciated more quickly by the patient than an upper field
defect. The quadrant of the visual field in which the field defect first
appears is useful in predicting the location of the primary retinal
break, which will be in the opposite quadrant. Loss of central vision
may be due either to involvement of the fovea by SRF or, less
frequently, obstruction of the visual axis by a large upper bullous
RD.

11. Signs:
 Marcus gunn pupil
 Low IOP relative
 ‘Tobacco dust’[shafer’s sign]
 Retinal breaks
 Mild iritis

13. Lattice degeneration
 More commonly in moderate myopes and is the most
important degeneration directly related to RD.
 Laterality- bilateral
 Location: Commonly -temporal superiorly fundus.
 40% of eyes with RD.
Pathology
Discontinuity of internal limiting membrane
Atrophy of the underlying NSR.
Vitreous - Overlying an area of lattice is synchytic
-attachments around the margins are
exaggerated

14. 3 Signs
Spindle-shaped areas of retinal thinning
between the equator and the posterior border of
the vitreous base.
• Arborizing network of white lines within the
islands
• Associated with ‘snowflakes’ (remnants of
degenerate Müller cells.
• Associated hyperplasia of the RPE is common .
• Small holes within lattice lesions are common and
usually innocuous

16. Snailtrack degeneration
 Sharply demarcated bands of tightly packed




‘snowflakes’ - white frost-like appearance.
longer islands than in lattice degeneration
Associated with overlying vitreous liquefaction
Vitreous traction at the posterior border of the
lesions is seldom present so that tractional U-tears
rarely occur,
Round holes within the snailtracks may be present

18. White with pressure’
 Translucent grey appearance of the retina -
indenting the sclera.
 In normal eyes
 Associated with abnormally strong attachment of
the vitreous gel
 Along the posterior border of islands of
degenerations.

20. ‘White without pressure’
 Without scleral indentation.
 Mistaken for flat holes.
 Giant tears occasionally develop along the posterior
border
 For this reason, if ‘white without pressure’ is found in the
fellow eye of a patient with a spontaneous giant retinal
tear, prophylactic therapy should be performed
 360° cryotherapy / indirect argon laser
photocoagulation, irrespective of the presence of ‘white
without pressure’, if they have not developed a PVD.

22. Fresh Retinal detachment
 The RD has a convex configuration and a slightly
opaque and corrugated appearance as a result of retinal
oedema
Loss of the choroidal pattern
Retinal blood vessels - darker than in flat retina
2 SRF extends up to the ora serrata
- rare cases caused by a macular hole in which the SRF is
initially confined to the posterior pole - thinness of the
retina at the fovea, a pseudohole is frequently seen if the
posterior pole is detached.
3 B-scan ultrasonography shows good mobility of
the retina and vitreous

23. Long-standing retinal detachment
 Retinal thinning secondary to atrophy
 Secondary intraretinal cysts disappear after retinal
reattachment.
 Subretinal demarcation lines (‘high water marks’)
caused by proliferation of RPE cells at the junction of
flat and detached retina

24. Proliferative vitreoretinopathy
 Contraction of Epiretinal & Sub retinal membranes -
tangential retinal traction and fixed retinal folds.
 following surgery for rhegmatogenous RD or penetrating
injury.
 No previous vitreoretinal surgery for RD.
 Signs
- Retinal folds and rigidity
retinal mobility induced by eye movements or scleral
indentation is decreased

25. 1 Grade A (minimal) PVR
-diffuse vitreous haze and tobacco dust.
- pigmented clumps on the inferior surface of the retina.
2 Grade B (moderate) PVR
- wrinkling of the inner retinal surface,
- tortuosity of blood vessels
- decreased mobility of vitreous gel and rolled edges of retinal breaks.
3 Grade C (marked) PVR
- rigid full-thickness retinal folds with heavy vitreous condensation and
strands.
4 B-scan ultrasonography in advanced disease shows gross
reduction of retinal mobility with retinal shortening and the characteristic
triangular sign .

28. How to find the retinal break – fundus drawing

29. Prophylaxis of RRD
 Important criteria for selection-
- Characteristics of Break
- Other considerations
Characteristics of Break :
- Type
- Size
- Symptomatic
- Location
- Pigmentation

30.  Other Considerations:
- Cataract surgery
- Myopic patients
- Family history
- Systemic diseases

32. Choice of treatment modalities
 (a) laser using a slit-lamp delivery system
 (b) laser using an indirect ophthalmoscopic delivery
system combined with scleral indentation
 (c) cryotherapy.
CONSIDERATIONS:-Location of Lesion
- Clarity of media
- Pupil size

33. Laser photocoagulation

34. CRYOTHERAPY

36. INDICATIONS FOR URGENT SURGERY
 Position of Primary break
 Size of the break
 State of Vitreous gel

37. Pneumatic retinopexy

38. Scleral buckling

41. Dr. Miratashi
R.D
.

42. Drainage of subretinal fluid

1 Indications. Although a large proportion of RDs can be treated
successfully with non-drainage techniques, drainage of SRF may be
required under the following circumstances:
a Deep SRF beneath the retinal break. In such case the application of
cryotherapy may be difficult or impossible.
• Drain the SRF to bring the break closer to the RPE.
• Air injection into the vitreous cavity to counteract the hypotony
induced by drainage.
• Cryotherapy to the break.
• Explant insertion.
b Long-standing RDs tend to be associated with viscous SRF and
may take a long time (many months) to absorb. Drainage may therefore be
necessary to restore macular attachment quickly, even if the break itself can
be closed without drainage.

43.  2
Technique
a ‘Prang’ • Digital pressure is applied to the
globe until the central retinal artery is occluded and
complete blanching of the choroidal vasculature is
achieved in order to prevent haemorrhage from the
drainage site.
• A full-thickness perforation is made in a
single, swift but controlled fashion with the tip of a
27-gauge hypodermic needle bent 2 mm from the tip.
• Following drainage of SRF, air is injected to
restore intraocular pressure.

44.  b
‘Cut-down’ • The sclerotomy site should be beneath the
area of deepest SRF but avoiding the vortex veins.
• A radial sclerotomy is performed, about 4 mm long and of
sufficient depth to allow herniation of a small dark knuckle of
choroid.
• A mattress suture is placed across the lips of the sclerotomy
(optional).
• The assistant holds apart the lips and the prolapsed knuckle is
inspected with a +20 D lens for the presence of large choroidal
vessels.
• If large choroidal vessels are absent, gentle low-heat cautery is
applied to the choroidal knuckle to decrease the risk of bleeding.
• If this does not result in drainage of SRF the choroidal knuckle
is perforated with a 25-guage hypodermic needle on a syringe.