RETINAL DETACHMENT, pathogenesis, types, treatment.

1. Dr. Neeraj Agarwal

2. ANATOMICAL
CONSIDERATION
 Pars Plana
 The ciliary body starts 1 mm from the limbus and extends
posteriorly for about 6 mm.
 The first 2 mm consist of the pars plicata and the
remaining 4 mm comprises the flattened pars plana.

3. In order not to endanger the lens or
retina, the optimal location for a pars
plana surgical incision is 4 mm from the
limbus in phakic eyes and 3.5 mm from
the limbus in pseudophakic eyes.

4. Ora Serrata
 The ora serrata forms the junction between the
retina and ciliary body.
 Ora serrata is 2.1 mm wide temporally and 0.7-
0.8 mm wide nasally.
 Its distance from limbus is 7mm temporally and
6mm nasally.

5.  At the ora, fusion of the sensory retina with the retinal
pigment epithelium (RPE) and choroid limits forward
extension of subretinal fluid.
 However, there being no equivalent adhesion between
the choroid and sclera, choroidal detachments may
progress anteriorly to involve the ciliary body
(ciliochoroidal detachment).

8. Vitreous base
 The vitreous base is a 3–4 mm wide zone straddling the
ora serrata.
 The cortical vitreous is strongly attached at the vitreous
base, so that following acute posterior vitreous
detachment (PVD), the posterior hyaloid face remains
attached to the posterior border of the vitreous base.
 Pre-existing retinal holes within the vitreous base do not
lead to RD.
 Severe blunt trauma may cause an avulsion of the
vitreous base.

9. The vitreous base

10. MICROSCOPIC LAYERS OF
RETINA
1. Retinal pigment epithelium
2. Rods and Cones layer
3. External limiting membrane
4. Outer nuclear layer
5. Outer plexiform layer
6. Inner nuclear layer- 1st order neuron(bipolar cells)
7. Inner plexiform
8. Ganglion cell layer- 2nd order neuron
9. Nerve fibre layer
10. Internal limiting memb.

11. DEFINITIONS

12. Retinal Detachment
 A Retinal Detachment (RD) describes the separation of
the neurosensory retina (NSR) from the retinal pigment
epithelium (RPE).
 This results in the accumulation of subretinal fluid
(SRF) in the potential space between the NSR and
RPE. The main types of RD are:

13. 1 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.
2 Tractional in which the NSR is pulled away from the
RPE by contracting vitreoretinal membranes in the
absence of a retinal break.
3 Exudative (serous, secondary) is caused neither by a
break nor traction; the SRF is derived from fluid in the
vessels of the NSR or choroid, or both.

14. 4 Combined tractional-rhegmatogenous, as the
name implies, is the result of a combination of a
retinal break and retinal traction. The retinal break is
caused by traction from an adjacent area of
fibrovascular proliferation and is most commonly
seen in advanced proliferative diabetic retinopathy.

15. Vitreoretinal traction
Vitreoretinal traction is a force exerted on the retina by
structures originating in the vitreous.
it may be dynamic or static.
The difference between the two is crucial in
understanding the pathogenesis of the various types of
RD.

16. 1 Dynamic traction is induced by eye movements and exerts a
centripetal force towards the vitreous cavity. It plays an
important role in the pathogenesis of retinal tears and
rhegmatogenous RD.
2 Static traction is independent of ocular movements. It plays a
key role in the pathogenesis of tractional RD and proliferative
vitreoretinopathy.

17. Posterior vitreous detachment
 A posterior vitreous detachment (PVD) is a separation of
the cortical vitreous from the internal limiting membrane
(ILM) of the NSR posterior to the vitreous base. PVD can
be classified according to the following characteristics:
1 Onset. Acute PVD is by far the most common. It
develops suddenly and usually becomes complete soon
after onset. Chronic PVD occurs gradually and may take
weeks or months to become complete.

18. 2 Extent
a Complete PVD in which the entire vitreous cortex
detaches up to the posterior margin of the vitreous base.
b Incomplete PVD in which residual vitreoretinal
attachments remain posterior to vitrous base.

19. COMPLICATION OF PVD
 NO COMPLICATION occur in most eyes because vitreo-
retinal attachment are weak.
 RETINAL TEAR may occur at same time at the site
of abnormally strong adhesion. Sometimes may be
delayed upto weeks so pt. should be reexamined after
1-6 weeks.
 AVULSION OF PERIPHERAL BLOOD VESSEL
resulting in vitreous haemorrhage.

20. Retinal break
A retinal break is a full-thickness defect in the sensory
retina. Breaks can be classified according to
(a) pathogenesis, (b) morphology and (c) location.
1 Pathogenesis
a Tears are caused by dynamic vitreoretinal traction and
have a predilection for the superior fundus.
b Holes are caused by chronic atrophy of the sensory
retina and may be round or oval. They have a predilection
for the temporal fundus.

21. 2 Morphology
a U-tears (horseshoe, flap or arrowhead) consist of a flap,
the apex of which is pulled anteriorly by the vitreous, the
base remaining attached to the retina.
b Incomplete U-tears, which may be linear, L-shaped or
J-shaped, are often paravascular.
c Operculated tears in which the flap is completely torn
away from the retina by detached vitreous gel.

22. d Dialyses are circumferential tears along the ora
serrata with vitreous gel attached to their posterior
margins.
e Giant tears involve 90° or more of the
circumference of the globe. They are most frequently
located in the immediate post-oral retina or, less
commonly, at the equator..

23. Retinal tears.
(A) Complete U-shaped; (B) linear; (C) Lshaped; (D) operculated; (E) dialysis

24. (A) Giant retinal tear involving the
immediate post-oral retina;
(B) vitreous cortex is attached to the
anterior margin of the tear

25. 3 Location
a Oral breaks are located within the vitreous base.
b Post-oral breaks are located between the posterior
border of the vitreous base and the equator.
c Equatorial breaks are at or near the equator.
d Post-equatorial breaks are behind the equator.
e Macular breaks (invariably holes) are at the fovea.

26. Finding the primary break
 The primary break is the one responsible for the RD.
 A secondary break is not responsible for the RD because it was
either present before the development of the RD or formed
after the retina is detached. Finding the primary break is of
paramount importance and aided by the following
considerations.
 1 Distribution of breaks in eyes with RD is approximately
as follows: 60% in the upper temporal quadrant; 15% in the
upper nasal quadrant; 15% in the lower temporal quadrant;
10% in the lower nasal quadrant.
• It should also be remembered that about 50% of eyes with RD
have more than one break, and in most eyes these are located
within 90° of each other.

27. 2 Configuration of SRF is of relevance because SRF spreads
in a gravitational fashion, and its shape is governed by
anatomical limits (ora serrata and optic nerve) and by the
location of the primary retinal break.
• If the primary break is located superiorly, the SRF first spreads
inferiorly on the same side as the break and then spreads
superiorly on the opposite side of the fundus.
• The likely location of the primary retinal break can therefore be
predicted by studying the shape of the RD.

28. a A shallow inferior RD in which the SRF is slightly
higher on the temporal side points to a primary break
located inferiorly on that side.

29. b A primary break located at 6 o’clock will cause an
inferior RD with equal fluid levels.

30. c In a bullous inferior RD the primary break usually lies above
the horizontal meridian.
d If the primary break is located in the upper nasal quadrant the
SRF will revolve around the optic disc and then rise on the
temporal side until it is level with the primary break.

31. e A subtotal RD with a superior wedge of attached retina points
to a primary break located in the periphery nearest its highest
border.
f When the SRF crosses the vertical midline above, the primary
break is near to 12 o’clock, the lower edge of the RD
corresponding to the side of the break .

32. • The above points are important because they aid in
prevention of the treatment of a secondary break whilst
overlooking the primary break.
• It is therefore essential to ensure that the shape of the RD
corresponds to the location of a presumed primary retinal
break.
3 History. Although the location of light flashes is of no
value in predicting the site of the primary break, the quadrant
in which a visual field defect first appears may be of
considerable value.
• For example, if a field defect started in the upper nasal
quadrant the primary break is probably located in the lower
temporal quadrant.

33. Ultrasonography
 B-scan ultrasonography (US) is very useful in the
diagnosis of RD in eyes with opaque media, particularly
severe vitreous haemorrhage that precludes visualization
of the fundus.

34. B-scan image showing vitreous haemorrhage and
flat retina;
B-scan image showing vitreous haemorrhage and
funnel-shaped retinal detachment

35. RHEGMATOGENOUS
RETINAL DETACHMENT

36. Symptoms

37. 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 the photopsia is often described as an arc of golden or white
light induced by eye movements and is more noticeable in dim
illumination. It tends to be projected into the patient's
temporal peripheral visual field.
- Occasionally photopsia precedes PVD by 24–48 hours.

38. 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.
c A sudden shower of minute red-coloured or dark spots usually
indicates vitreous haemorrhage secondary to tearing of a peripheral
retinal blood vessel. Vitreous haemorrhage associated with acute
PVD is usually sparse due to the small calibre of peripheral retinal
vessels.

39. (A) Weiss ring;
(B) B-scan
shows a
Weiss ring
associated
with
posterior
vitreous
detachment

40. 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.

41. Signs
General
1 Marcus Gunn pupil (relative afferent pupillary defect) is
present in an eye with an extensive RD irrespective of the type.
2 Intraocular pressure is usually lower by about 5 mmHg
compared with the normal eye. If the intraocular pressure is
extremely low, an associated choroidal detachment may be present.
3 Iritis is very common but usually mild. Occasionally it may be
severe enough to cause posterior synechiae. In these cases the
underlying RD may be overlooked and the poor visual acuity
incorrectly ascribed to some other cause.
4 ‘Tobacco dust’ consisting of pigment cells is seen in the
anterior vitreous.

42. 5 Retinal breaks appear as discontinuities in the
retinal surface. They are usually red because of the
colour contrast between the sensory retina and
underlying choroid. However, in eyes with
hypopigmented choroid (as in high myopia), the
colour contrast is decreased and small breaks may be
overlooked unless careful slit-lamp and indirect
ophthalmoscopic examination is performed.
6 Retinal signs depend on the duration of RD and
the presence or absence of proliferative
vitreoretinopathy (PVR) as described below.

43. Fresh retinal detachment
1 The RD has a convex configuration and a slightly opaque and
corrugated appearance as a result of retinal oedema. There is loss of the
underlying choroidal pattern and retinal blood vessels appear darker
than in flat retina, so that colour contrast between venules and
arterioles is less apparent.
2 SRF extends up to the ora serrata, except in the rare cases caused
by a macular hole in which the SRF is initially confined to the posterior
pole. Because of the thinness of the retina at the fovea, a pseudohole is
frequently seen if the posterior pole is detached. This should not be
mistaken for a true macular hole, which may give rise to RD in highly
myopic eyes or following blunt ocular trauma.
3 B-scan ultrasonography shows good mobility of the retina and
vitreous.

44. Fresh retinal
detachment.
(A) U-tear in detached
retina;
(B) superior bullous
retinal detachment;
(C) shallow temporal
retinal detachment;
(D) B-scan shows a
totally detached retina
with linear echogenic
structures inserting
onto the optic nerve
head to form an open
funnel

45. Long-standing retinal detachment
 The following are the main features of a long-standing
rhegmatogenous RD:
1 Retinal thinning secondary to atrophy is a characteristic finding
which must not be mistaken for retinoschisis.
2 Secondary intraretinal cysts may develop if the RD has been
present for about 1 year; these tend to disappear after retinal
reattachment.

46. 3 Subretinal demarcation lines (‘high water
marks’) caused by proliferation of RPE cells at the
junction of flat and detached retina are common and
take about 3 months to develop. They are initially
pigmented but tend to lose this with
time. Demarcation lines are convex with respect to the
ora serrata and, although they represent sites of
increased adhesion, they do not invariably limit spread
of SRF.

47. Long-standing
retinal
detachment.
(A) Secondary
retinal cyst;
(B) B-scan shows
a retinal cyst;
(C) ‘high water
mark’ in an eye
with an inferior
retinal
detachment

48. Proliferative vitreoretinopathy
 Proliferative vitreoretinopathy (PVR) is caused by epiretinal and
subretinal membrane formation.
 Cell-mediated contraction of these membranes causes tangential
retinal traction and fixed retinal folds.
 Usually, PVR occurs following surgery for rhegmatogenous RD
or penetrating injury.
 However, it may also occur in eyes with rhegmatogenous RD that
have not had previous vitreoretinal surgery.
 The main features are retinal folds and rigidity so that retinal
mobility induced by eye movements or scleral indentation is
decreased.

49. TRACTIONAL RETINAL
DETACHMENT

50.  The main causes of tractional RD are
(a) proliferative retinopathy such as diabetic and retinopathy
of prematurity, and
(b) penetrating posterior segment trauma

51. Pathogenesis of diabetic tractional
retinal detachment
1 Pathogenesis of PVD.
- Tractional RD is caused by progressive contraction of fibrovascular
membranes over large areas of vitreoretinal adhesion.
- In contrast to acute PVD in eyes with rhegmatogenous RD, PVD in
diabetic eyes is gradual and frequently incomplete.
- It is thought to be caused by leakage of plasma constituents into the
vitreous gel from a fibrovascular network adherent to the posterior
vitreous surface.
-

52. - Owing to the strong adhesions of the cortical vitreous
to areas of fibrovascular proliferation, PVD is usually
incomplete.
- In the very rare event of a subsequent complete PVD,
the new blood vessels are avulsed and RD does not
develop.

53.  2 Static vitreoretinal traction of the following three types is
recognized.
a Tangential traction is caused by the contraction of epiretinal
fibrovascular membranes with puckering of the retina and distortion
of retinal blood vessels.
b Anteroposterior traction is caused by the contraction of
fibrovascular membranes extending from the posterior retina,
usually in association with the major arcades, to the vitreous base
anteriorly.
c Bridging (trampoline) traction is the result of contraction of
fibrovascular membranes which stretch from one part of the
posterior retina to another or between the vascular arcades, tending
to pull the two involved points together.

54. Tractional retinal
detachment
associated with
anteroposterior
and bridging
traction

55. Diagnosis
1 Symptoms. Photopsia and floaters are usually absent because
vitreoretinal traction develops insidiously and is not associated with
acute PVD. The visual field defect usually progresses slowly and may
become stationary for months or even years.
2 Signs.
• The RD has a concave configuration and breaks are absent.
• Retinal mobility is severely reduced and shifting fluid is absent.
• The SRF is shallower than in a rhegmatogenous RD and seldom
extends to the ora serrata.
• The highest elevation of the retina occurs at sites of vitreoretinal
traction.
• If a tractional RD develops a break it assumes the characteristics of
a rhegmatogenous RD and progresses more quickly (combined
tractional-rhegmatogenous RD).

56. (A) Tractional retinal
detachment in
severe proliferative
diabetic
retinopathy;
(B) B-scan image of
another patient
shows incomplete
posterior vitreous
detachment and a
shallow tractional
retinal
detachment

57. 3 B-scan ultrasonography shows incomplete posterior
vitreous detachment and a relatively immobile retina

58. EXUDATIVE RETINAL
DETACHMENT

59. Pathogenesis
 Exudative RD is characterized by the accumulation of SRF in the
absence of retinal breaks or traction.
 It may occur in a variety of vascular, inflammatory and neoplastic
diseases involving the NSR, RPE and choroid in which fluid leaks
outside the vessels and accumulates under the retina.
 As long as the RPE is able to compensate by pumping the leaking
fluid into the choroidal circulation, no fluid accumulates in the
subretinal space and RD does not occur.
 However, when the normal RPE pump is overwhelmed, or if the
RPE activity is decreased, then fluid starts to accumulate in the
subretinal space

60. The main causes are the following:
1 Choroidal tumours such as melanomas, haemangiomas and
metastases; it is therefore very important to consider that exudative RD is
caused by an intraocular tumour until proved otherwise.
2 Inflammation such as Harada disease (Part of VKH syndrome) and
posterior scleritis.
3 Bullous central serous chorioretinopathy is a rare cause.
4 Iatrogenic causes include retinal detachment surgery and panretinal
photocoagulation.
5 Subretinal neovascularization which may leak and give rise to
extensive subretinal accumulation of fluid at the posterior pole.
6 Hypertensive choroidopathy, as may occur in toxaemia of
pregnancy, is a very rare cause.
7 Idiopathic such as the uveal effusion syndrome.

61. Diagnosis
1 Symptoms. Photopsia is absent because there is no vitreoretinal
traction, although floaters may be present if there is associated
vitritis. The visual field defect may develop suddenly and progress
rapidly. Depending on the cause both eyes may be involved
simultaneously (e.g. Harada disease).
2 Signs
• The RD has a convex configuration, just like a
rhegmatogenous RD, but its surface is smooth and not corrugated.

62. The detached retina is very mobile and exhibits the
phenomenon of ‘shifting fluid’ in which SRF responds
to the force of gravity and detaches the area of retina
under which it accumulates.
• For example, in the upright position the SRF
collects under the inferior retina, but on assuming the
supine position for several minutes, the inferior retina
flattens and the SRF shifts posteriorly detaching the
superior retina.

63. The cause of the RD, such as a choroidal tumour, may
be apparent when the fundus is examined, or the
patient may have an associated systemic disease
responsible for the RD (e.g. Harada disease, toxaemia
of pregnancy).
• ‘Leopard spots’ consisting of scattered areas of
subretinal pigment clumping may be seen after the
detachment has flattened.

64. Exudative retinal
detachment
with shifting
fluid.
(A) Inferior
collection of
subretinal fluid
with the patient
sitting;
(B) the subretinal
fluid shifts
upwards when
the patient
assumes the
supine position

65. Exudative retinal
detachment
caused by a
choroidal
melanoma

66. ‘Leopard spot’
pigmentation
following
resolution of
exudative retinal
detachment

67. PROPHYLAXIS
 Prophylaxis of retinal detachment is best done by
identifying predisposing retinal break and treating
them with cryotherapy and laser.
 i/c- vitroretinal traction, h/o trauma, myopia, positive
family history, prior cataract surgery or detachment in
the fellow eye.

68. CRYOTHERAPY
It is used to produce chorioretinal inflammation around
the edges of retinal break.
It may break down blood ocular barrier.
In this chorio retinal adhesion take 2-6 weeks to form.

69. LASER PHOTOCOAGULATION
 It cause less morbidity and is the treatment of choice
for prophylaxis except in very peripheral retinal break.
 It require close chorioretinal apposition for at least one
week and cannot be used in the presence of
detachment.

70. TREATMENT

71. PNEUMATIC RETINOPAXY
 It is a Minimally invasive and quick and office based
procedure.
 In this intravitreal expanding gas bubble is used to
seal a retinal break and reattach the retina without
scleral buckling.
 Most frequently use gases are Sulphur hexafluride
(SF6) and long acting Perfluoro propane (C3F8).

72.  it is used for fresh single retinal break or a group of
braks that are clustered within 1 clock hour in the
superior two third of fundus.
 Success rate is slightly less than conventional scleral
buckling surgery.

73. SCLERAL BUCKLING
 It is a procedure in which material sutured on sclera
create an inward indentation.
 Its purpose are to close retinal break by apposing RPE
to neurosensory retina and to reduce vitroretinal
traction.

74. EXPLANTS
 Explants are made from soft or hard silicone.
 in this a silicone encircling band or sectoral buckle is
sutured to sclera and indents the outside of the eye
towards the detached retina.
 The entire break should ideally surround by 2mm of
buckle.

78. BUCKLE CONFIGURATION
 RADIAL- placed at right angle to the limbus
 CIRCUMFERNTIAL- placed in parallel with limbus
to create a segmental block
 ENCIRCLING- explants are placed around the entire
circumfernce of the globe to create a 360 degree
buckle and may be augmented by local explants.

79. DRAINAGE OF SRF
 2 routes-
 External scerotomy or Internally by a flute
needle(soft, blunt, silicone tipped needle).
 It is indicated in eyes with bullous retinal detachment
or when a more marked elevation of the buckle is
required.
 Complications are choroidal hemorrhage, retinal
perforation, retinal incarceration, choroidal
neovascularisation and endopthalmitis.

80. VITRECTOMY
INDICATIONS-
 Rhegmatogenous RD- in which retinal break can’t be
visualized and in which break can’t be closed by scleral
buckling.
 Tractional RD- which threatning or involving macula and
combined tractional rhegmatogenous RD.

81. THANK
YOU