retinal detachment classification and etiology

1. Refrence:- kanski, yanoff, RYAN
atlus of rd wenbin wei

4.  The neurosensory retina is a highly specialized
outgrowth of the brain that has evolved to capture
photons of light, transduce that light into electrical signals,
and initiate the processing of the resulting image. The
neurosensory retina has 9 layers Beginning on the
vitreous side and progressing to the choroidal side,
 9Layers after rpe is known as neuro sensory retina
Cross-sectional histologic preparations of
the retina

5. Ora serrata
 The ora serrata is the junction
between the retina and ciliary
body.
 Variants and anatomy of ora:-
• Dentate processes are
tapering extensions of
retina onto the pars plana;
they are more marked nasally
than temporally and display
marked variation in contour.
• Oral bays are scalloped
edges of pars plana
epithelium between dentate
processes.

6. • Meridional folds (Fig. 16.2A) are
small radial folds of thickened
retinal tissue in line with dentate
processes, most commonly in the
superonasal quadrant. A fold may
occasionally exhibit a small retinal
hole at its apex
• Enclosed oral bays (Fig. 16.2B)
are small islands of pars plana
surrounded by retina as a result of
meeting of two adjacent dentate
processes. They should not be
mistaken for retinal holes.
Normal variants of the ora
serrata. (A) Meridional
fold with a small retinal hole
at its base; (B) enclosed oral
bay
A
B

7. Blood Supply of the Retina
 The central retinal artery supplies the five inner
layers of theretina, while the uveal ciliary
arteries supply the four outer layers of the
neurosensory retina and the retinal pigment
epitheliallayer.
 These two circulations are both terminal
branches, which are ended at the outer
plexiform layer and the ora serrata. Due to poor
blood flow, these two areas are prone to
degeneration and then lead to retinal
detachment

8.  DEFINITION:-
 Separation of the neurosensory retina (NSR)
from the retinal pigment epithelium (RPE)
caused by breakdown of the forces that attach
the NSR to the RPE. This results in the
accumulation of subretinal fluid (SRF) in the
potential space between the NSR and RPE.

9. RD
RHEGMATOGENOUS/
PRIMARY RD
NON-
REGMATOGENOUS
/ SECONDARY
Tractional Retinal
Detachments
Exudative Retinal
Detachments

10.  • Rhegmatogenous (Greek rhegma – break) RD
requires a full-thickness defect in the sensory retina,
which permits fluid derived from synchytic (liquefied)
vitreous to gain access to the subretinal space. It is
sometimes referred to as primary or idiopathic retinal
detachment.
.
 • Tractional RD. The NSR is pulled away from the RPE
by contracting vitreoretinal membranes in the absence
of a retinal break. The causes of tractional retinal
detachments include cellular proliferation resulting from
 retinal hemorrhage and vitreous hemorrhage of retinal
vascular disease,(DIABETIC RETINOPATHY)
 cicatricial contraction in trauma,
 intraocular foreign body extraction, and
 incision of surgery

11. • Exudative (serous, secondary) RD. SRF is derived from
the vessels of the NSR and/or choroid. Exudative retinal
detachment is associated with systemic disease or ocular
dysemia
• Combined tractional–rhegmatogenous RD results when a
retinal break is caused by traction from an adjacent area of
fibrovascular proliferation.
• Subclinical RD is generally used to refer to an
asymptomatic break surrounded by a relatively small
amount of SRF, by definition extending further than one
disc diameter away from the edge of the break but less
than two disc diameters posterior to the equator. It does
not usually give rise to a subjective visual field defect. The
term is sometimes also used to describe an asymptomatic
RD of any extent.

12.  MPS matrix in sub retinal space.
 Oncotic pressure difference b/w choroid and
SRF
 Hydrostatic or hydraulic forces related to iop
 Metabolic transfer of ions and fluids by
RPE.( Outer blood retinal barrier)

13. - HIGH Myopia
- Epiretinal membrane formation
- Chorioretinal inflammation
- Vitreous hemorrhage
- Trauma – Blunt> Penitrating
- After cataract Sx- Aphakia> pseudophakia

15.  EPIRETINAL MEMBRANE:-
- These could arise from the RPE.
- Differentiate in to active fibroblast and leads to
proliferative vitreoretinopathy.
 VITREOUS HEMORRHAGE:-
- Leads to vitreous liquefaction.
- Epiretinal mb. Formation and their retraction
- Iron ions, precipitate Insoluble hyaluronate
formation which causes loss of water from vitreous
gel. Leucocytes and platelets form the vitreous mb.
 CHOREORETINAL INFLAMMATION:-
Choreoretinitis and peripheral uveitis causes-
- Syneresis.
- Partial liquefaction of vitreous gel.
- Formation of epiretinal mb.

16.  Blunt trauma
Compression of A-P diameter of
globe->equatorial plane
expansion.
 more frequent cause than
Penetrating injuries.
 Myopic eyes are more prone.
 fragmentation retinal and
hemorrhegic necrosis of
choroid- Large irregular retinal
holes
 Vitreous liquefaction and post.
Vitreous separation .
 Dialysis- Bucket handle
appearance. (sup.nasal>inf.T)
 Equatorial tears.

17.  PENETRATING
INJURIES:-
 Vitreous incarceration at
the site of penetration.
Localized or wide spread
membranE. Formation
and their traction.
 Characteristic signs
are-
transvitreous sheets and
bands of fibrovascular
ingrowth.

18.  APHAKIC AND PSEUDOPHAKIC:
- Aphakics are more susceptible,
- Incidence of RRD in pseudophakics 1to2%
within 1yr of sx.
- Most common is Rhegmatogenous RD
- Due to vitreous loss
- Closely associated with
PVD(aphakic>pseudo)
- Round retinal holes may leads to RRD
following YAG laser capsulotomy.

19.  SEX AND RACE:-
Males are more prone.
Caucasians are more prone than Negroes.
 HEREDITY:-
Myopia , benign dialysis, retinoschisis of young.
 CONGENITAL EYE ANOMALIES:-
Choroidal coloboma, PHPV, optic pit.
 PREVIOUS INTRAOCULAR SX- PSEUDOPHAKIA,
 FAMILY H/O RD.
 ARN( acute retinal necrosis) SYNDROME AND CMV
RETINITIS.

20. Patients with any predisposing lesion, or indeed any high risk
features for RD, should be educated about the nature of
symptoms of PVD and RD and the need to seek review
urgently if these occur.
 Lattice degeneration
 Snailtrack degeneration
 Cystic retinal tuft
 Degenerative retinoschisis
 Zonular traction tuft
 Myopic choroidal atrophy
 White with pressure and white without pressure
 Pvd

21. It is found more commonly
in moderate Myopes and
is the most important
degeneration directly
related to RD. Lattice is
present in about 40% of
eyes with RD.
Pathology. There is
discontinuity of the
internal limiting
membrane with variable
atrophy of the underlying
NSR

22. Signs. Lattice is most commonly bilateral,
temporal and
superior.
 Spindle-shaped areas of retinal thinning,
commonly located between the equator and
the posterior border of the vitreous base
 Sclerosed vessels
 ‘snowflakes’,emnants of degenerate Müller
cells.
 Associated hyperplasia of the RPE
 Small holes
Complications.
 Tears
 Atrophic holes may rarely (2%) lead to RD;
the risk is higher in young myopes
retinal detachment with lattice on
the flap of the tear

25.  Snailtrack degeneration is characterized by
sharply demarcated bands of tightly packed
‘snowflakes’ that give the peripheral retina a
white frost-like appearance It is viewed by some
as a precursor to lattice degeneration.
 Marked vitreous traction is seldom present so
that U-tears rarely occur, although round holes
are relatively common
 Prophylactic treatment is usually unnecessary,
though review every 1–2 years may be prudent
as RD occurs in a minority.

27.  A cystic retinal tuft (CRT), also known
as a granular patch or retinal rosette,
is a congenital abnormality consisting
of a small, round or oval, discrete
elevated whitish lesion, typically in the
equatorial or peripheral retina, more
commonly
 there may be associated pigmentation
at its base. It is comprised principally
of glial tissue; strong vitreoretinal
adhesion is commonly present and
both small round holes and
horseshoe tears can occur. It is likely
to be an under-recognized
lesionthough the risk of RD in a given
eye with CRT is probably well under
1%.
Isolated uncomplicated lesion
tuft with small round hole

28.  RS is believed to develop from
microcystoid degeneration by a
process of gradual coalescence of
degenerative cavities resulting in
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. In
typical retinoschisis the split occurs in
the outer plexiform layer, and in the
less common reticular retinoschisis at
the level of the nerve fibre layer.
Circumferential microcystoid
degeneration with progression to
retinoschisis supero- and inferotemporally

29.  This refers to a common
(15%) phenomenon
caused by an aberrant
zonular fibre extending
posteriorly to be attached
to the retina near the ora
serrata, and exerts traction
on the retina at its base.
 It is typically located
nasally. The risk of retinal
tear formation is around
2%, and periodic long-term
review is generally
recommended.

30.  • ‘White with pressure’ (WWP) refers to
retinal areas in which a translucent
white–grey appearance can be induced
by scleral indentation
 Each area has a fixed configuration that
does not change when indentation is
moved to an adjacent area. It may also
be observed along the posterior border of
islands of lattice degeneration, snailtrack
 degeneration and the outer layer of
acquired retinoschisis.
 It is frequently seen in normal eyes and
may be associated with abnormally
strong attachment of the vitreous gel,
though may not indicate a higher risk of
retinal break formation.

31.  ‘White without pressure’
(WWOP) has the same
 appearance as WWP but Is
present without scleral
indentation WWOP corresponds
to an area of fairly strong
adhesion of condensed vitreous
 On examination a normal area of
retina surrounded by white
without pressure may be
mistaken for a flat retinal hole .
 However, retinal breaks,
including giant tears,
occasionally develop along the
posterior border of white without
pressure).
 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
considered.

32.  Diffuse choroidal/chorioretinal
atrophy in myopia is
characterized by diffuse or
circumscribed choroidal
depigmentation, commonly
associated with thinning of the
overlying retina, and occurs
typically in the posterior pole
and equatorial area of highly
myopic eyes. Retinal holes
developing in the atrophic retina
may occasionally lead to RD.
Because of lack of contrast,
small holes may be very difficult
to visualize

33.  Posterior vitreous detachment
(PVD) refers to separation of
thecortical vitreous, along with
the delineating posterior hyaloid
membrane (PHM), from the
neurosensory retina posterior to
the vitreous base.
 PVD occurs due to vitreous gel
liquefaction with age
(synchysis) to form fluid-filled
cavities), and
 subsequently condensatIon
(syneresis), with access to the
preretinal space allowed by a
dehiscence in the cortical gel
and/or PHM.

34.  SYMPTOMS:-
• Flashing lights (photopsia)
• Floaters (myodesopsia)
• Blurred vision
 SIGNS:-
• The detached PHM can often be seen clinically on slit lamp
examination as a crumpled translucent membrane in the mid-
vitreous cavity behind
• Haemorrhage may be indicated by the presence of red blood
cells in the anterior vitreous
• Pigment granules(the Shafer sign or ‘tobacco dust’)
• Vitrous cells
• Retinal breaks

36.  The retina detaches with a full-thickness
retinal break and vitreous degeneration, so it
is usually called as rhegmatogenous retinal
detachment (RRD).

37. Classified according to: pathogenisis,
morphology and location
1. Pathogenesis:-
-TEARS- By dynamic VR traction.
Upper temp.>Up asal.
-HOLES-By chr. Atrophy of sensory retina
Temp.sup>Temp.inf

38. 2. MORPHOLOGY:-
A U-tears:
 Horseshoe, flap or arrowhead.
 Apex: pulled ant. By the
vitreous.
 Base: Remaining attached to
retina
 Two ant. Horns (extension)
running forward from the apex.
B.Incomplete U- tears
 Linear
 J-shaped
 L shape
 Often paravascular.
C .Operculated tears:-
Flap- completely torn away
from the retina
by detached vitreous gel.
D . Dialysis:-
 Circumferential tear
along the ora serrata.
 Vitreous gel attached to
post. Border.

39. E Giant tears:-
 Involve 90 degree or more of the
circumference of globe .
 Vitreous gel attached to
ant. margin,
 Most frequently located in
immediate post-oral retina
 Less commonly at equator.

40. 3. Location:-
 Oral- Within the vitreous
base
 Post oral-B/w the post.
Border of vitr. Base and
equator.
 Equatorial:- Near the
equator.
 Post equatorial- Behind the
equator.
 Macular- Holes at fovea.

41.  • Distribution of breaks in eyes with RD is
approximately as follows:
 60% superotemporal quadrant,
 15% superonasal,
 15% inferotemporal and
 10% inferonasal. The upper

42.  Configuration of SRF.
 SRF spread is governed by gravity,
 Byanatomical 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 of the
fundus as the break and
 then superiorly on the opposite side, so that the
likely location of the primary retinal break can be
predicted .
 Furthur explained by:-(modified from Lincoff’s
rules):

43.  ○ 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 (Fig. A).
 ○ A primary break located at 6
o’clock will cause an inferior RD
with equal fluid levels (Fig. B).
 ○ In a bullous inferior RD the
primary break usually lies above
the horizontal meridian (Fig.
16.27C).

44.  ○ 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 (Fig. D).
 ○ A subtotal RD with a superior
wedge of attached retina points to
a primary break located in the
periphery nearest its highest border
(Fig.E).
 ○ 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 (Fig.F).

45. PATHOGENESIS OF TRAUMATIC RRD

46.  Circulatory disturbances
 Closure of retinal
capillaries and
obliteration of arterioles
and venules
 Atrophy of inner retinal
layers and deficit in
vitreous metabolites
 Syneresis of vitreous gel
 Retinal break and RD
 Deficiency in the RPE
cells or
choriocapillaries
 Breakdown of
adhesions b/w the
Photoreceptor and RPE
RD

47.  SYMPTOM
 The classic premonitory symptoms reported in about 60% of
patients with spontaneous rhegmatogenous RD are flashing
lights and floaters
 a curtain-like relative peripheral visual field defect
 and can progress to involve central vision; in some patients
this may not be present on waking in the morning, due to
spontaneous absorption of SRF while inactive overnight, only
to reappear later in the day.
 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 to involvement of the fovea
by SRF or, infrequently, obstruction of the visual axis by a
large bullous RD.

49.  Relative afferent pupillary defect
 Intraocular pressure (IOP) is often lower by about 5
mmHg
 It may be raised, characteristically in Schwartz– Matsuo
syndrome in which RRD is associated with an apparent
mild anterior uveitis,
 the aqueous cells (displaced photoreceptor)
 Iritis
 Weiss ring and sudden shower of minute red coloured
floaters or dark spots
 Cobweb and multiple translucent lines floating in the
visual field.

50.  Posterior synechiae; the
underlying RD
 ‘Tobacco dust’ consisting of
pigment cells is commonly seen
in the anterior vitreous called
shafers sign. Pathognomic of
rrd
 substantial vitreous blood or
inflammatory cells are also
highly specific.
 • 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.

51.  FRESH RD:-
 Convex configuration
 Opaque and corrugated
appearance
 Loss of underlying choroidal
pattern
 Retinal vessels appear
darker than flat retina
 Colour contrast between
venules and arterioles less
apparent
 SRF extends up to the ora
serrata
 Pseudohole is frequently seen

52.  Long standing RD :-
- Retinal thinning due to atrophy
- Secondary intraretinal cyst (in
1 yr duration)
- Subretinal demarcation line-
High water marks
caused by proliferation of RPE
cells at the junction of flat and
detached retina.(in 3 yr
duration). Initially pigmented
later lose pigment.
- Demarcation line are convex
with respect to ora serrata,
they do not invariably limit the
spread of SRF.

55. Tractional retinal detachment can be caused by
 vitreoushemorrhage,
 proliferative diabetic retinopathy (PDR),
 retinal vein occlusion (RVO),
 retinal vasculitis,
 familial exudative vitreoretinopathy (FEVR)
 retinopathy ofprematurity (ROP).
 Eales ds
 Penetrating posterior segment trauma

56.  Diabetic tractional RD:-
The PVD jn tractional RD is gradual and incomplete
Due to strong adhesion of cortical vitreous to areas of
fibrovascular proliferation
Progressive contraction of fibrovascular mb. Over Vitreo Retinal
adhesions
Posterior Tractional RD
 ;
 Static vitreo retinal traction- main types:-
1. Tangential
2. Anteroposterior
3. Bridging
4. Table top
5. Tent
6. Peripheral traction

57.  Traumatic tractional RD
Trauma
Vitreous incarceration and
bleeding within vitreous gel
Fibroblastic proliferation
Contraction of epiretinal mb.
Ant. Tractional RD

58. Symptoms.
 Photopsia and floaters are usually absent
because vitreoretinal traction develops
insidiously and is not associated with acute
PVD.
 A visual field defect usually progresses
slowly and may be stable for months or even
years.

59.  • 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 rapidly (combined tractional–
rhegmatogenous RD).
 • B-scan ultrasonography shows incomplete
posteriorvitreous detachment and a relatively
immobile retina

61. 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
retina, 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,
RD does not occur. However, when the mechanism is
overwhelmed or functions subnormally, fluid accumulates in the
subretinal space.

62. Causes include:
• 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.
• Inflammation such as Harada disease and posterior scleritis.
• Bullous central serous chorioretinopathy is a rare cause.
• Iatrogenic causes include retinal detachment surgery and
panretinal photocoagulation.
• Choroidal neovascularization which may leak and give rise
to extensive subretinal accumulation of fluid at the posterior
pole.
• Hypertensive choroidopathy, as may occur in toxaemia of
pregnancy, is a very rare cause.
• Idiopathic, such as uveal effusion syndrome

63. Systemic diseases and exudative retinal detachment
include
 hypertensive retinopathy,
 retinopathy of nephropathy,
and exudative retinal detachment related to eye diseases,
such as
 Vogt-Koyanagi-Harada syndrome,
 central exudative chorioretinopathy,
 bullous retinal detachment,
 uveal effusion syndrome,
 posterior scleritis,
 sympathetic ophthalmia,
 acute posterior multifocal placoid pigment epitheliopathy,
and
 exudative retinal detachment secondary to central retinal
vein occlusion (CRVO).

64.  In the abscence of retinal break or traction
Accumulation of SRF
Overwhelmed RPE Decreased RPE activity
Pump
Exudative RD

65. Symptoms.
Depending on the cause, both eyes may be
involved simultaneously.
○ There is no vitreoretinal traction, so photopsia is
absent.
○ Floaters may be present if there is associated
vitritis.
○ A visual field defect may develop suddenly and
progress rapidly.

66. Signs
 ○ The RD has a convex
configuration, as with a
rhegmatogenous RD, but its
surface is smooth and not
corrugated.
 ○ The detached retina is very
mobile and exhibits the
henomenon of ‘shifting fluid’ in
which SRF detaches the area of
retina under which it
accumulates (Fig.). 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 SRF
shifts posteriorly, detaching the
superior retina.
SITTING
SUPINE

67.  ○ The cause of the RD, such as
a choroidal tumour (Fig.), may
be apparent when the fundus is
examined or on B-scan
ultrasonography, 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 (Fig.).