Retinal detachment

RETINAL
DETACHMENT
Dr Nikhil R P

ANATOMY OF THE
PERIPHERAL RETINA
 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.
• 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.

Ora Serrata
• The ora serrata forms the junction between the retina
and ciliary body and is characterized by the following

1 Dentate processes are teeth-like extensions of retina onto
the pars plana; they are more marked nasally than temporally
and can have extreme variation in contour.
2 Oral bays are the scalloped edges of the pars plana
epithelium in between the dentate processes
3 A meridional fold is a small radial fold of thickened retinal
tissue in line with a dentate process, usually located in the
superonasal quadrant . A fold may occasionally exhibit a small
retinal hole at its apex.

Normal variants of the ora serrata. (A) Meridional fold with a small retinal
hole at its base; (B) enclosed oral bay; (C) granular tissue

4 An enclosed oral bay is a small island of pars plana
surrounded by retina as a result of meeting of two adjacent
dentate processes.
5 Granular tissue characterized by multiple white opacities
within the vitreous base can sometimes be mistaken for
small peripheral opercula.
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).

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.

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:

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.
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.

Vitreous adhesions
1 Normal. The peripheral cortical vitreous is loosely attached to the
internal limiting membrane (ILM) of the sensory retina. Stronger
adhesions occur at the following sites:
• Vitreous base, where they are very strong.
• Around the optic nerve head, where they are fairly strong.
• Around the fovea, where they are fairly weak, except in eyes
with vitreomacular traction and macular hole formation.
• Along peripheral blood vessels, where they are usually weak.

2 Abnormal adhesions at the following sites may be
associated with retinal tear formation as a result of
dynamic vitreoretinal traction associated with
acute PVD.
• Posterior border of islands of lattice
degeneration.
• Retinal pigment clumps.
• Peripheral paravascular condensations.
• Vitreous base anomalies such as tongue-like
extensions and posterior islands.
• ‘White with pressure’ and ‘white without
pressure’.

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

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.
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 the vitreous base.
Rhegmatogenous RD is usually associated with acute PVD;
tractional RD is associated with chronic, incomplete PVD;
exudative RD is unrelated to the presence of PVD.

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 (temporal
more than nasal).
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 (upper more than lower).

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. The tear itself consists of two anterior
extensions (horns) running forward from the apex.
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.
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..

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

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

• 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.

Head-mounted Indirect Ophthalmoscopy
1 Principles.
• Indirect ophthalmoscopy provides a stereoscopic view of
the fundus.
• The light emitted from the instrument is transmitted to
the fundus through a condensing lens held at the focal
point of the eye, which provides an inverted and laterally
reversed image of the fundus.
• AS THE POWER OF THE CONDENSING LENS DECREASES
THE WORKING DISTANCE AND THE MAGNIFICATION
INCREASE BUT THE FIELD OF VIEW IS REDUCED, AND
VICE VERSA.

(A) Principles of indirect ophthalmoscopy; (B) condensing
lenses

2 Condensing lenses of various powers and diameters are
available for indirect ophthalmoscopy.
• 20 D (magnifies ×3; field about 45°) is the most commonly
used for general examination of the fundus.
• 25 D (magnifies ×2.5; field is about 50°).
• 30 D (magnifies ×2; field is 60°) has a shorter working distance
and is useful when examining patients with small pupils.
• 40 D (magnifies ×1.5; field is about 65°) is used mainly to
examine small children.
• Panretinal 2.2 (magnifies ×3; field is about 55°).

• 3 Technique
a Both pupils are dilated with tropicamide 1% and, if necessary,
phenylephrine 2.5% so that they will not constrict when exposed to
a bright light during examination.
b The patient should be in the supine position with one pillow, on
a bed, reclining chair or couch and not sitting upright in a chair.
c The examination room is darkened.
d The eyepieces are set at the correct interpupillary distance and
the beam aligned so that it is located in the centre of the viewing
frame.

Position of patient during indirect ophthalmoscopy

e The patient is instructed to keep both eyes open at all times.
f The lens is taken into one hand with the flat surface facing the
patient and throughout the examination is kept parallel to the
patient's iris plane.
g If necessary, the patient's eyelids are gently separated with the
fingers.
h In order to enable the patient to adapt to the light he should be
asked to look up and the superior peripheral fundus should be
examined first.
i The patient is asked to move the eyes and head into optimal
positions for examination. For example, when examining the extreme
retinal periphery, the patient is asked to look away from the examiner.

Scleral indentation
1 Purposes.
Scleral indentation should be attempted only after the
art of indirect ophthalmoscopy has been mastered.
Its main function is to enhance visualization of the
peripheral retina anterior to the equator; it also
permits a kinetic evaluation of the retina.

Appearance of retinal breaks in detached
retina. (A) Without scleral indentation; (B) with
indentation

Technique of scleral
indentation.
(A) Insertion of indenter;
(B) indentation;
(C) mound created by
indentation

Goldmann Three-mirror Examination
1 Goldmann three-mirror lens consists of four parts; the central lens
and three mirrors set at different angles. Because the curvature of the
contact surface of the lens is steeper than that of the cornea, a viscous
coupling substance with the same refractive index as the cornea is
required to bridge the gap between the cornea and the goniolens. It is
important to be familiar with each part of the lens as follows :
• The central part provides a 30° upright view of the posterior
pole.
• The equatorial mirror (largest and oblong-shaped) enables
visualization from 30° to the equator.
•

The peripheral mirror (intermediate in size and square-
shaped) enables visualization between the equator and
the ora serrata.
• The gonioscopy mirror (smallest and dome-shaped)
may be used for visualizing the extreme retinal
periphery and pars plana.
• It is therefore apparent that the smaller the mirror,
the more peripheral the view obtained.

2 Mirror positioning
• The mirror should be positioned opposite the area of the
fundus to be examined; to examine the 12 o’clock position
the mirror should be positioned at 6 o’clock.
• When viewing the vertical meridian, the image is upside
down but not laterally reversed, in contrast to indirect
ophthalmoscopy. Lesions located to the left of 12 o’clock in
the retina will therefore also appear in the mirror on the
left-hand side
• When viewing the horizontal meridian, the image is
laterally reversed.

(A) U-tear left of 12 o’clock and an island of lattice degeneration right of 12
o’clock; (B) the same lesions seen with the three-mirror lens positioned at 6 o’clock

3 Technique
a The pupils are dilated.
b The locking screw of the slit-lamp is unlocked to
allow the illumination column to be tilted.
c Anaesthetic drops are instilled.
d Coupling fluid (high viscosity methylcellulose or
equivalent) is inserted into the cup of the contact lens;
it should be no more than half full.

Preparation of the slit-lamp for fundus examination. (A) Unlocking the
screw; (B) tilting the illumination column

e The patient is asked to look up; the inferior rim
of the lens is inserted into the lower fornix and
quickly pressed against the cornea so that the
coupling fluid is retained.
f The illumination column should always be tilted
except when viewing the 12 o’clock position in the
fundus (i.e. with the mirror at 6 o’clock).

(A) Insertion of the three-mirror lens into the lower fornix
with the patient looking up; (B) three-mirror lens in

The illumination column is tilted and positioned right of centre to view the
oblique meridian at 1.30 and 7.30 o’clock

Fundus Drawing
• 1 Technique.
• The image seen with indirect ophthalmoscopy is vertically
inverted and laterally reversed.
• This phenomenon can be compensated for when viewing the
fundus if the top of the chart is placed towards the patient's
feet (i.e. upside down).

• In this way the inverted position of the chart in
relation to the patient's eye corresponds to the
image of the fundus obtained by the observer.
• For example, a U-tear at 11 o’clock in the patient's
right eye will correspond to the 11 o’clock position
on the chart; the same applies to the area of lattice
degeneration between 1 o’clock and 2 o’clock.

Technique of drawing retinal lesions. (A) Position of
the chart in relation to the eye;

• 2 Colour Code
a The boundaries of the RD are drawn by starting at the optic
nerve and then extending to the periphery.
b Detached retina is shaded blue and flat retina red.
c The course of retinal veins is indicated with blue. Retinal
arterioles are not usually drawn unless they serve as a
specific guide to an important lesion.
d Retinal breaks are drawn in red with blue outlines; the
flat part of a retinal tear is also drawn in blue.
e Thin retina is indicated by red hatching outlined in blue,
lattice degeneration is shown as blue hatching outlined in
blue, retinal pigment is blackk, retinal exudates yellow, and
vitreous opacities green.

(B) colour
coding for
documentin
g retinal
pathology

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.
• The upper temporal quadrant is therefore by far the
most common site for retinal break formation and
should be examined in great detail if a retinal break
cannot be detected initially.
• 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.

• 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 by Lincoff rules.

• 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.

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

• 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.

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 .

• 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.

RHEGMATOGENOUS
RETINAL DETACHMENT

• Pathogenesis
• Rhegmatogenous RD affects about 1 in 10 000 of the
population each year and both eyes may eventually be
involved in about 10% of patients.
• It is characterized by the presence of a retinal break held
open by vitreoretinal traction that allows accumulation of
liquefied vitreous under the NSR, separating it from the RPE.

• The retinal breaks responsible for RD are caused by
interplay between dynamic vitreoretinal traction
and an underlying weakness in the peripheral
retina referred to as predisposing degeneration.
• Even though a retinal break is present, a RD will not
occur if the vitreous is not at least partially
liquefied and if the necessary traction is not
present.

DYNAMIC VITREORETINAL TRACTION
1 Pathogenesis.
1. Syneresis defines liquefaction of the vitreous gel. Some eyes with
syneresis develop a hole in the posterior hyaloid membrane and
fluid from within the centre of the vitreous cavity passes through
this defect into the newly formed retrohyaloid space.
2. This process forcibly detaches the posterior vitreous and the posterior
hyaloid membrane from the ILM of the sensory retina as far as the
posterior border of the vitreous base.
3. The remaining solid vitreous gel collapses inferiorly and the
retrohyaloid space is occupied entirely by synchytic fluid.

2 Age at onset is typically 45–65 years in the
general population but may occur earlier in myopic
or otherwise predisposed individuals (e.g. trauma,
uveitis).
The fellow eye frequently becomes affected within 6
months to 2 years.

(A) Vitreous syneresis; (B) uncomplicated posterior
vitreous detachment

Complications Of Acute PVD
• Following PVD, the sensory retina is no longer protected
by the stable vitreous cortex, and can be directly affected
by dynamic vitreoretinal tractional forces. The vision-
threatening complications of acute PVD are dependent on
the strength and extent of pre-existing vitreoretinal
adhesions.
1 No complications occur in most eyes because
vitreoretinal attachments are weak so that the vitreous
cortex detaches completely without sequelae.

2 Retinal tears may develop as a result of
transmission of traction at sites of abnormally
strong vitreoretinal adhesion as previously
described .
3 Avulsion of a peripheral blood vessel resulting
in vitreous haemorrhage in the absence of retinal
tear formation may occur.

(A) U-tear and localized
subretinal fluid
associated with acute
posterior vitreous
detachment;
(B) the vitreous shows
syneresis, posterior
vitreous detachment
with partial collapse,
and retained
attachment of cortical
vitreous to the flap of
the tear

• About 60% of all breaks develop in areas of the peripheral
retina that show specific changes.
• These lesions may be associated with a spontaneous
breakdown of pathologically thin retinal tissue to cause a
retinal hole, or they may predispose to retinal tear formation
in eyes with acute PVD.
• Retinal holes are round or oval, usually smaller than tears
and carry a lower risk of RD.

PREDISPOSING
PERIPHERAL RETINAL
DEGENERATION

Lattice degeneration
1 Prevalence. Lattice degeneration is present in about 8% of the
population.
• It probably develops early in life, with a peak incidence during
the second and third decades.
• It is found more commonly in moderate myopes and is the most
important degeneration directly related to RD. It is usually
bilateral and most frequently located in the temporal rather than
the nasal fundus, and superiorly rather than inferiorly.
• Lattice is present in about 40% of eyes with RD.

2 Pathology. There is discontinuity of the internal
limiting membrane with variable atrophy of the
underlying NSR.
• The vitreous overlying an area of lattice is synchytic
but the vitreous attachments around the margins
are exaggerated.

Vitreous changes associated with lattice degeneration

3 Signs
• Spindle-shaped areas of retinal thinning, commonly
located between the equator and the posterior border of the
vitreous base.
• A characteristic feature is an arborizing network of white
lines within the islands.
• Some lattice lesions may be 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.

Clinical features of
lattice
degeneration.
(A) Small island of
lattice with an
arborizing network
of white lines;
(B) lattice associated
with ‘snowflakes’;
(C) lattice associated
with RPE changes;
(D) small holes within
lattice seen on
scleral indentation

• 4 Complications
a No complications are encountered in most patients.
b Tears may occasionally develop in eyes with acute PVD.
They typically occur in myopes over the age of 50 years and the
SRF progresses more rapidly than in RD caused by small round
holes.
c Atrophic holes may rarely lead to RD, particularly in young
myopes.

Complications of
lattice
degeneration.
(A) Atypical radial
lattice without
breaks;
(B) two U-tears, the
larger one of
which shows a
small patch of
lattice on its flap
and is surrounded
by a small puddle
of subretinal fluid;
(C) linear tear along
the posterior
margin of lattice;
(D) multiple small
holes within
islands of lattice

Snailtrack degeneration
• Snailtrack degeneration is characterized by sharply
demarcated bands of tightly packed ‘snowflakes’ which
give the peripheral retina a white frost-like appearance.
• The islands are usually longer than in lattice
degeneration and may be associated with overlying
vitreous liquefaction.
• However, marked vitreous traction at the posterior
border of the lesions is seldom present so that tractional
U-tears rarely occur, although round holes within the
snailtracks may be present.

Islands of snailtrack
degeneration, some of
which contain holes

Degenerative retinoschisis
• 1 Prevalence. Degenerative retinoschisis is present in
about 5% of the population over the age of 20 years
and is particularly prevalent in Hypermetropes (70% of
patients are hypermetropic).
• Both eyes are frequently involved.

2 Pathology. There is coalescence of cystic lesions as a
result of degeneration of neuroretinal and glial
supporting elements within areas of peripheral cystoid
degeneration.
• This eventually results in separation or splitting of the
NSR into an inner (vitreous) layer and an outer
(choroidal) layer with severing of neurones and
complete loss of visual function in the affected area.
• In typical retinoschisis the split is in the outer plexiform
layer, and in reticular retinoschisis, which is less
common, splitting occurs at the level of the nerve fibre
layer.

3 Signs
• Early retinoschisis usually involves the extreme inferotemporal
periphery of both fundi, appearing as an exaggeration of microcystoid
degeneration with a smooth immobile elevation of the retina.
• The lesion may progress circumferentially until it has involved the
entire fundus periphery. The typical form usually remains anterior to
the equator although the reticular type may spread beyond the
equator.
• The surface of the inner layer may show snowflakes as well as
sheathing or ‘silver-wiring’ of blood vessels and the schisis cavity may
be bridged by rows of torn grey-white tissue.

Microcystoid
degeneration.
(A) Histology shows
spaces in the nerve
fibre layer
delineated by
delicate vertical
columns of Müller
cells;
(B) circumferential
microcystoid
degeneration and
mild retinoschisis in
the inferotemporal
and superotemporal
quadrants

• 4 Complications
a No complications occur in most cases and the
condition is asymptomatic and innocuous.
b Breaks. Inner layer breaks are small and round, whilst
the less common outer layer breaks are usually larger, with
rolled edges and located behind the equator.

C.) RD may occasionally develop in eyes with breaks in
both layers, especially in the presence of PVD.
Eyes with only outer layer breaks do not as a rule
develop RD because the fluid within the schisis cavity
is viscous and does not pass readily into the
subretinal space.
However, occasionally the schisis fluid loses its
viscosity and passes through the break into the
subretinal space, giving rise to a localized detachment
of the outer retinal layer which is usually confined to
the area of retinoschisis
D.) Vitreous haemorrhage is uncommon.

Retinoschisis.
(A) Large
breaks in
both layers
but absence
of retinal
detachment;
(B) linear
break in the
outer layer
associated
with
localized
subretinal
fluid

Diffuse chorioretinal atrophy
• Diffuse chorioretinal atrophy is characterized by
choroidal depigmentation and thinning of the overlying
retina in the equatorial area of highly myopic eyes.
• Retinal holes developing in the atrophic retina may
lead to RD.
• Because of lack of contrast between the depigmented
choroid and sensory retina, small holes may be very
difficult to visualize without the help of slit-lamp
biomicroscopy.

Diffuse
chorioretinal
atrophy with
holes and
localized
subretinal
fluid

White withpressure’ and ‘whitewithout pressure’
1 ‘White with pressure’
Translucent grey appearance of the retina, induced by
indenting the sclera.
Each area has a fixed configuration which does not change
when the scleral indenter is moved to an adjacent area.
It is frequently seen in normal eyes and may be associated
with abnormally strong attachment of the vitreous gel.
It is also observed along the posterior border of islands of
lattice degeneration, snailtrack degeneration and the outer
layer of acquired retinoschisis.

• 2 ‘White without pressure’
• same appearance but is present without scleral
indentation.
• 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
performed.

(A) ‘White with
pressure’;
(B) extensive vitreous
syneresis and strong
attachment of
condensed vitreous gel
to an area of ‘white
without pressure’

(A) Pseudoholes
within an area
of ‘white
without
pressure’;
(B) total retinal
detachment
caused by a
giant tear

• PIGMENT CLUMPS
• Small,localised,irregular patches of pigmentation
often associated with vitreoretinal traction tufts.
• Paravascular vitreoretinal attachments.

Significance of myopia
• Although myopes make up to 10% of the general
population, over 40% of all RDs occur in myopic eyes; the
higher the refractive error the greater is the risk of RD.
The following interrelated factors predispose a myopic
eye to RD:
1 Lattice degeneration is more common in moderate
myopes and may give rise to either tears or atrophic
holes. Giant retinal tears may also develop along the
posterior edge of long lattice islands.
2 Snailtrack degeneration is common in myopic eyes and
may be associated with atrophic holes.

3 Diffuse chorioretinal atrophy may give rise to small
round holes in highly myopic eyes
4 Macular holes may give rise to RD in highly myopic
eyes
5 Vitreous degeneration and PVD are more common
6 Vitreous loss during cataract surgery, particularly if
inappropriately managed, is associated with an
increased risk of subsequent RD, particularly in highly
myopic eyes

Inferior retinal
detachment in a
highly myopic eye
caused by a giant
tear which
developed along
the posterior
border of
extensive lattice
degeneration; also
note lattice in the
superotemporal
quadrant

Macular hole
surrounded
by shallow
subretinal
fluid
confined to
the
posterior
pole

SIGNIFICANCE OF APHAKIA
• About 30% of all RD’s occur in aphakic eyes.
• MECHANISM-Loss of hyaluronic acid from vitreous
gel causes synchysis and PVD which may result in
retinal tear.
• Vitreous loss if inappropriately managed is
associated with a 7% risk of RD.

SIGNIFICANCE OF BLUNT TRAUMA
• Severe blunt traumaAP length
decreasesSimultaneous expansion at equatorial
plane-Relatively inelastic vitreous causes traction
along the posterior border of vitreous base-
Traumatic retinal dialysis,RD develops months
later.
• Upper nasal quadrant is the most common site.

SIGNIFICANCE OF PENETRATING
TRAUMA
• It may be rhegmatogenous,due to retinal tears
caused by foreign bodies or tractional.

INNOCUOUS PERIPHERAL RETINAL
DEGENERATIONS
• The peripheral retina extends from the equator to the ora serrata and
may show the following innocuous lesions.
1 Microcystoid degeneration consists of tiny vesicles with indistinct
boundaries on a greyish-white background which make the retina appear
thickened and less transparent. The degeneration always starts adjacent
to the ora serrata and extends circumferentially and posteriorly with a
smooth undulating posterior border.
Microcystoid degeneration is present in all adult eyes, increasing in severity
with age, and is not in itself causally related to RD, although it may give
rise to retinoschisis.

2 Pavingstone degeneration is characterized by
discrete yellow-white patches of focal
chorioretinal atrophy which is present to some
extent in 25% of normal eyes.
3. Honeycomb (reticular) degeneration is an age-
related change characterized by a fine network of
perivascular pigmentation which may extend
posterior to the equator.
4 Peripheral drusen are characterized by clusters
of small pale lesions which may have
hyperpigmented borders. They are similar to
drusen at the posterior pole and usually occur in
the eyes of elderly individuals.

Innocuous
peripheral
retinal
degenerations.
(A) Microcystoi
d seen on scleral
indentation;
(B) pavingstone;
(C) honeycomb
(reticular);
(D) drusen

Symptoms
• The classic premonitory symptoms reported in
about 60% of patients with spontaneous
rhegmatogenous RD are flashing lights and vitreous
floaters caused by acute PVD with collapse.
• After a variable period of time the patient notices
a relative peripheral visual field defect which may
progress to involve central vision.

• 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.

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. Its presence
does not necessarily indicate total PVD, nor does its absence
confirm absence of PVD since it may be destroyed during the
process of separation.

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.

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

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.

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.
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.

‘Tobacco
dust’ in
the
anterior
vitreous

Fresh retinal detachment
• Convex configuration
• Mobile
• Slightly opaque and corrugated appearance as a result of retinal
oedema.
• 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.
• 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.

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

Long-standing retinal detachment
• The following are the main features of a long-standing
rhegmatogenous RD:
1 Retinal thinning and surface appears smooth 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.

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.

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

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.
• Classification is as follows although it should be emphasized
that progression from one stage to the next is not
inevitable.

B-scan ultrasonography in advanced disease shows
gross reduction of retinal mobility with retinal
shortening and the characteristic triangular sign

Differential Diagnosis
• Retinoschisis
• 1 Symptoms.
• Photopsia and floaters are absent because there is
no vitreoretinal traction.
• A visual field defect is seldom observed because
spread posterior to the equator is rare. If present it is
absolute and not relative as in RD.
• Occasionally symptoms occur as a result of either
vitreous haemorrhage or the development of
progressive RD.

•
2 Signs
• Breaks may be present in one or both layers.
• The elevation is convex, smooth, thin and relatively
immobile, unlike the opaque and corrugated appearance
of a rhegmatogenous RD.
• The thin inner leaf of the schisis cavity may be
mistaken, on cursory examination, for an atrophic long-
standing rhegmatogenous RD but demarcation lines and
secondary cysts in the inner leaf are absent.

(A) Degenerative
retinoschisis
showing
peripheral
vascular
sheathing and
‘snowflakes’;
(B) uveal effusion
characterized by
choroidal
detachment and
exudative retinal
detachment

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.
• Utilises high frequency sound waves ranging from 8-10
MHz.
• B stands for bright echoes.

Types of frequency
• Low frequency: orbital tissue
• Medium frequency: ( 7 – 10 mhz ) Retinal , vitreous , optic
nerve
• High frequency: ( 30 – 50 mhz) : ant chamber upto 5 mm

Examination technique
The patient is either
reclining on a chair or
lying on a couch.
The probe can be
placed directly over
the conjunctiva or the
lids.

Probe positions
• Transverse : Lateral extent, 6 clock hours
• Longitudinal : radial ,1 clock hours
• Axial : lesion in relation to lens and optic nerve .

• Gain adjusts the amplification of the echo signal,
similar to volume control of a radio.
• Higher gain increases the sensitivity of the instrument
in displaying weak echoes such as vitreous opacities.
•
• Lower gain only allows display of strong echoes such as
the retina and sclera, though improves resolution
because it narrows the beam.

Appearance of Normal Ocular
Structures
• LENS: oval highly reflective structure with intralesional
echoes with none to highly reflective echoes.
• Vitreous is echolucent.
• Retina, choroid and sclera: single reflective high
structure.
• OPTIC NERVE : Wedge shaped acoustic void in the
retrobulbar region.
• EXTRA OCULAR MUSCLES : Echolucent
to low reflective fusiform structures. The SR- LPS
complex is the thickest. IR is the thinnest. IO is
generally not seen except in pathological conditions.

• ORBIT -highly reflective
due to orbital fat.
• Always examine the
other eye before coming
to a conclusion regarding
the lesion .
• Opacities produce dots or
short lines
• Membranous lesions
produce an echogenic
line

USES
• Vitreous haemorrhage
• Vitreous exudation
• Retinal detachment (type / extent)
• Posterior vitreous detachment (extent)
• Tumour (size/ site/ post treatment follow up)
• Retinal detachment (solid / exudative)

ULTRASONOGRAPHIC
CHARACTERISTICS

VITREOUS HAEMORRHAGE
To detect extent,
density, location and
cause
Fresh haemorrhage
shows dots or lines
Old haemorrhage the
dots gets brighter

POSTERIOR VITREOUS
DETACHMENT
membranous lesion
with no/some
attachments to the
optic disc

POSTERIOR VITREOUS
DETACHMENT
Mobility of PVD is
more than RD.
The spike of RD is
more than PVD.
PVD becomes more
prominent in higher
gain settings

RETINAL DETACHMENT
The detachment
produces a bright
continuous, folded
appearance with
insertion into the disc
and ora serrata.
It is to determine the
configuration of the
detachment as shallow,
flat or bullous

CLOSED FUNNEL RD
WITH RETINAL CYST
Retinal Tear

Appears as RD but it is a PVD
Clues: non uniform thickness of membrane
very thin attachment to the disc.

(C) B-scan image showing vitreous haemorrhage and
flat retina; (D) B-scan image showing vitreous
haemorrhage and funnel-shaped retinal
detachment

• The main causes of tractional RD are
(a) proliferative retinopathy due to diabetes
(b) penetrating posterior segment trauma

Pathogenesis of diabetic tractional
retinal detachment
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.

• 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.

Tractional retinal
detachment
associated with
anteroposterior
and bridging
traction

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).

(A) Tractional
retinal
detachment in
severe
proliferative
diabetic
retinopathy;
(B) B-scan image
of another
patient shows a
shallow
tractional
retinal
detachment

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

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 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.

Diagnosis
1 Symptoms.
Photopsia is absent
Floaters may be present if there is associated vitritis.
The visual field defect may develop suddenly and progress rapidly.
2 Signs
• The RD has a convex configuration, just like a
rhegmatogenous RD, but its surface is smooth and not corrugated.
• The detached retina is very mobile
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.

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

Exudative retinal
detachment
caused by a
choroidal
melanoma

‘Leopard spot’
pigmentation
following
resolution of
exudative retinal
detachment

Choroidal detachment
1 Symptoms. Photopsia and floaters are absent
A visual field defect may be noticed if the choroidal
detachment is extensive.
2 Signs
• Low intraocular pressure is common as a result of
concomitant detachment of the ciliary body.
• The anterior chamber may be shallow in eyes with
extensive choroidal detachments.
• The elevations are brown, convex, smooth and
relatively immobile.

• • Large ‘kissing’ choroidal detachments may
obscure the view of the fundus.
• The elevations do not extend to the posterior
pole because they are limited by the firm adhesion
between the suprachoroidal lamellae where the
vortex veins enter their scleral canals.

(A) Choroidal
detachment.
(B) B-scan
image of
extensive
choroidal
detachment
almost
touching in
the middle of
the vitreous
cavity

TREATMENT
• The choice of treatment to resolve the secondary
subretinal accumulation of fluid should be
directed toward the primary pathology.
• Laser treatment may be effective to treat focal
breakdown of the blood-retina barrier, as seen in
central serous chorioretinopathy, exudative
diabetic retinopathy, Coats’ disease, or vascular
malformations.

PROPHYLACTIC TREATMENT
• Criteria for selection
• Characteristics of break
• Tear is more dangerous than a hole
• Large break is more dangerous than a small break
• Location-Superior tears,Upper temporal
tears,equatorial breaks are more dangerous.
• A retinal break in an aphakic eye,myopia.

• Family history of RD.
• If patient cannot be relied upon to report new
synptoms indicative of RD.
• In patients with Marfan’s syndrome,Stickler’s
syndrome or Ehlers danlos syndrome.

• In the absence of breaks, neither of predisposing
degeneration is treated prophylactically unless
associated with following risk factors
• 1.RD in fellow eye
• 2.Aphakia
• 3.High myopia
• 4.Strong family history of RD.
• 5. Marfan’s syndrome,Stickler’s syndrome or Ehlers
danlos syndrome.

TREATMENT MODALITIES
• Cryotherapy v/s Photocoagulation
• 1.Location of lesion
 Equatorial lesions-cryo or Photocoagulation
 Postequatorial lesions-Photocoagulation
 Peripheral lesions-Cryotherapy

• Clarity of media-In hazy media cryotherapy
preferred.
• Pupil size-Small pupils easier to treat with
cryotherapy.

Laser photocoagulation
200 microns spot size,duration of 0.1-0.2 seconds.
Two rows of confluent burns surrounding the lesion.
LASER used- Argon Green, Krypton Red, Diode Laser

• Cornea-Burns,endothelial damage.
• Iritis,iris atrophy
• Anterior capsular opacities
• Cystoid macular edema
• Exudative RD
• New retinal tears
• Retinal haemorrhage.
Complications

Cryotherapy
• PRINCIPLE
• The normal microvillous interdigitations seen between
retina and RPE are missing.
• If both the RPE and overlying retina are frozen, the
adhesion that results after reattachment demonstrates
cellular connections between the NSR and RPE consisting
of desmosome formation between retinal glia and RPE or
direct contact between retinal glia and Bruch’s membrane.

• Current cryotherapy instrumentation employs expansion of
high-pressure nitrous oxide at the tip of a probe generating
temperatures as low as −89°C.
• Temperature effect is confined to the tip of the probe by an
insulating sleeve.
• A probe 2.0 to 2.5 mm in diameter usually is used for retinal
work.
• Treatment of retinal breaks & pathologic conditions requires
accurate placement of the cryoprobe tip.

• The goal is to surround all retinal breaks with 1 to 2 mm of
contiguous treatment.
• Treatment should include freezing of overlying retina,
because this results in a stronger adhesion than does
treatment of RPE alone.
• To avoid damage of refreezing, treatment should not
significantly overlap.

• The treatment end point is retinal whitening
without ice crystal formation.
•
• Cryoprobe should not be removed until it has
defrosted completely because premature removal
may crack the choroid and give rise to choroidal
haemorrhage.

COMPLICATIONS
• Chemosis
• Diplopia if rectus muscle is frozen.
• Vitritis if treatment is excessively heavy.
CAUSES OF FAILURE
• Failure to surround the entire lesion
• Failure to release vitreoretinal traction
• New breaks within or adjacent to treated area due
to excessively heavy treatment.

Cryotherapy vs LASER Retinopexy
Cryotherapy
• Use of external probe &
IDO
• Can be used with
moderate media
opacities
• Promotes dispersion of
viable RPE cells
• CME, wrinkling of ILM
• Increased Postoperative
flare, extensive retinal
oedema, necrosis
LASER Retinopexy
• Endolaser/ IDO with
laser
• Difficult in moderate
media opacities
• Ideal for posteriorly
located breaks

Retinal Reattachment Surgery
• Scleral Buckling Surgery with or without drainage
• Encircling
• Segmental
• Temporary scleral buckle
• Lincoff balloon
• Absorbable material
• Vitrectomy
• Classical
• Sutureless
• Pneumoretinopexy
• Routine
• With drainage of SRF/intravitreal liquid

INDICATIONS FOR BED REST
• To prevent macular involvement by subretinal fluid.
• To promote resorption of SRF.
• To unroll mobile flap of giant retinal tear.

• INSPECTION OF SCLERA
• To detect areas of thinning-It may be associated
with problems such as
• penetration of choroid and retina during insertion
of scleral sutures,
• cutting of sutures,
• scleral rupture during localisation or cryotherapy

Retinopexy
• The indent from the explant closes retinal breaks but
retinopexy is required to produce an enduring bond
between the retina & retinal pigment epithelium that
will persist even if the indent disappears.
• Retinopexy was initially achieved using diathermy in
association with lamellar scleral dissection and scleral
implants.
• Cryotherapy has supplanted diathermy because it can
be performed without scleral dissection .
• Intraoperative cryopexy remains a quick and simple
technique.

• Cryopexy remains the choice of most retinal
surgeons for the intraoperative treatment of
retinal breaks during scleral buckling

Scleral Buckling Surgery
• AIM
• Is to close retinal breaks by indenting eye wall, preventing
the passage of liquefied vitreous into the subretinal space.

How scleral buckle works???
• Gold standard for
uncomplicated RD
• Relieves vitreous traction
along the surface of the
buckle
• The buckle displaces the
retinal break centrally,
where the break becomes
tamponaded by cortical
vitreous
• It displaces SRF away from
the break & alters the
shape of eyewall, thus
reducing the effects of the
intraocular fluid currents

• EXPLANT-Material sutured directly onto the sclera
to create a buckle.
• IMPLANT-Material placed within the sclera to
create a buckle.

Scleral Buckles
• EXPLANT MATERIAL
• Soft silicone(silastic)sponge
• Hard silicone straps
• Hard silicone tyre

Buckle configuration
• Radial explants- right
angle to limbus- to seal
U tears/posterior
breaks
• Segmental
circumferential- parallel
to limbus
• Encircling- entire
circumference of globe
for 360˚ buckle

INDICATIONS
• Radial buckling
• Large U shaped tears
• Posterior breaks because sutures are easier to
insert.
Segmental circumferential buckling
• Multiple breaks
• Anterior breaks
• Wide breaks such as dialysis and giant tears.

ENCIRCLING BUCKLE
• Breaks involving three or more quadrants.
• Extensive RD without detectable breaks.
• PVR Grade C
• Failed local procedures.

• Complications
• Scleral perforation
• Choroidal Haemorrhage
• Buckle infection, migration, extrusion
• Failed retinal reattachment
• Redetachment- PVR
• Anterior segment ischemia
• Choroidal edema, detachment
• Secondary Glaucoma
• Suboptimal visual recovery- CME, persistent subfoveal SRF
• Diplopia and motility disturbances

Fish mouth Retinal Tears
• Typically large U shaped equatorial tears located
superiorly in a bullous RD open widely following scleral
buckling and drainage of SRF.
• Management-
• Prevented by using a radial buckle instead of
circumferential
• Extra radially oriented buckling material can be added.
• Air can be injected into the vitreous cavity so that
bubble will close the tear.

Radial retinal folds
• If encircling buckle is too tight,radial folds form
over the retina.
• Prevents retinal reattachment
• Management
• Loosen the buckle,if too tight
• Air injection into the vitreous cavity.

Lincoff’s balloon
• Can be inserted under LA
• Minimal surgical trauma
• No scleral suturing
• No changes in refractive status of the eye

DRAINAGE OF SUBRETINAL FLUID
INDICATIONS
• Difficulty in localization of retinal breaks in highly
elevated bullous RDs.
• In immobile retina due to PVR, eye is first softened
by draining SRF to achieve a high buckle.
• Long standing RD as they tend to have viscous SRF.
• Inferior tears.
• Coexisting glaucoma

• Technique
• Fundus examined to make sure SRF has not
shifted.
• Radial Sclerotomy, beneath the area of
deepest SRF, 4mm long, sufficient depth to
allow herniation of small dark knuckle of
choroid.
• Insert a 5-0 dacron mattress suture across
the lips of the sclerotomy.

• If large vessel is present, suture the sclerotomy
and choose another site
• Gentle low-heat cautery to the knuckle
• 27 G hypodermic needle bent at 2mm from tip,
full thickness perforation.
• Sclerotomy site inspected-Presence of small
pigment granules means all the SRF has been
drained.

• Complications
• Failure of drainage- dry tap
• Retinal perforation
• Intraocular haemorrhage
• Ocular hypotony
• Vitreous loss
• Retinal incarceration(star shaped puckering at the
drainage site)
• Endophthalmitis

PNEUMATIC RETINOPEXY
• Sulfur hexaﬂuoride (SF6) and perﬂuoropropane (C3F8)
are the gases most frequently used with PR. Success
also has been reported with sterile room air.
• The value of the intraocular bubble is based on three
features: buoyancy, surface tension, and isolation of
retinal tears from intraocular currents.

• Buoyancy applies upward pressure on the detached
retina.
• The surface tension of the bubble closes the retinal
break and prevents the bubble from passing into
the subretinal space.
• With the break closed, the retinal pigment
epithelial pump removes the subretinal ﬂuid.

• Because of their low solubility in water, SF6 and C3F8 tend to
diffuse from the eye very slowly.
• But, the nitrogen and oxygen that are in solution in surrounding
tissues of the eye are much more soluble and pass relatively
quickly into the gas bubble, following the law of partial
pressures.
• The net result is the initial expansion of a bubble of pure SF6 or
C3F8 within the vitreous, followed by gradual resorption.

• Short, minimally invasive, OPD procedure
• Indications
• Retinal break smaller than one clock hour
• Multiple breaks within one clock hour
• All breaks in superior 8 clock hours
• Hypotony following drainage of SRF.
• Fishmouthing of large retinal tear
• Radial retinal folds
• Macular hole giving rise to RD.

Gases tried in vitreoretinal surgery
Non-expansile Expansile
Air SF6
Nitrogen C4F10
Helium CF4
Oxygen C2F6
Argon C3F8
Xenon C4F10
Krypton C5F12

Properties of intraocular gases
Gas Average
Duration
Largest size of
the bubble
(duration)
Average
expansion
Nonexpansile
concentration
Typical Dose
Air 3 days Immediate No expansion -- 0.8ml
SF6 12 days 36 hours 2 times 18% 0.5ml
C3F8 38 days 72 hours 4 times 14% 0.3ml

• Procedure
• Anaesthesia- Topical/LA
• Needle is inserted 4mm behind the limbus to avoid the
vitreous base.
• Aimed at the center of the globe, stopped when the tip
of needle is just visible through the pupil.
• Single, expansile gas bubble injected in vitreous cavity
through pars plana using sterile 30 G needle
• Paracentesis
• Positioning- to ensure max. tamponade, retinal break
should remain at the top

CASE SELECTION AVOIDED IN
• 1. Breaks larger than 1 clock-hour or multiple breaks
extending over more than 1 clock-hour of the retina.
• 2. Breaks in the inferior 4 clock-hours retina.
• 3. Presence of PVR grade C or D .
• 4. Disability precluding maintenance of the required
positioning.
• 5. Severe or uncontrolled glaucoma.
• 6. Cloudy media precluding full assessment of the retina.

PR presents a advantage IN
• 1. Macular breaks and other posterior retinal breaks.
Posterior retinal breaks are difﬁcult to treat with SB,
optic pits with macular detachment.
• 2. Redetachment or persistent detachment after SB .

• 3. Isolated tears under the superior rectus. Placing a
segmental buckle under a vertically acting muscle runs
the risk of iatrogenic diplopia; this is eliminated with
PR.
• 4. Filtering blebs. If a functioning ﬁltering bleb is
present, or if a ﬁltering procedure may be necessary in
future, PR should be considered.

• 5. Impending macular detachment.
• 6. Bullous detachment. When RD is highly bullous, retinal
tears can be difﬁcult to localize and treat with SB, a problem
which is avoided by two-session PR.

One-session / two-session procedure
• PR can be done in one session, with cryopexy applied to the
retinal breaks just before gas injection, or as a two-session
procedure, with initial gas injection followed by laser 1 or 2
days later, when the retina is reattached.
• One-session procedures always involve cryopexy, since laser
cannot be applied to detached retina.
• Two-session procedures are usually, but not always, done
with the laser.

Disadvantages
• Poor visualisation due to formation of minute air
bubbles in the vitreous.
• Excessive elevation of IOP.

Silicone Oil in RD Repair
• FDA approved for VR surgery in 1994
• Highly viscous, transparent liquid with high surface
tension, lighter than water
• Viscosity 1000-5000 centistokes
• Indications
• Detachment with inferior breaks
• Extensive PVR
• One eyed patient with need of early visual recovery
• Giant retinal tears

• Advantages
• Prolonged tamponading
effect
• Less strict requirement of
post-operative positioning
• Early visual rehabilitation
• No restriction on air travel
• Hypotony less common
• Disadvantages
• Needs repeat surgery for
removal
• Cataract, raised IOP,band
shaped keratopathy
• Inadequate tamponading
for inferior breaks
• Post-operative change in
refraction
• Perisilicone oil membrane
& macular pucker
• Redetachment after oil
removal (15-20%)

• Advantages of intraocular gases vs use of silicon
oil
• No need of repeat surgery for removal
• Absence of complications related to long-term presence of
silicone oil
• Disadvantages of intraocular gases
• Requirement of strict postoperative positioning
• Risk of postoperative rise in IOP
• Restriction of air travel
• Delayed visual rehabilitation
• Short duration of tamponading effect

Primary Vitrectomy in
Rhegmatogenous RD

Pars Plana Vitrectomy
• Indicated in
• Media opacities- cataract , VH & advanced PVR
• Posteriorly located breaks
• RD with giant retinal tear or macular hole
• Tractional RD
• Relative contraindications
• Relatively simple phakic RD

PRINCIPLES OF VITRECTOMY
• The principles of vitrectomy to treat RRD are release of
tractional forces that precipitated the retinal break,
and the closure and reattachment of breaks to the
underlying RPE .
• The surgical procedure requires: (1) removal of the vitreous
gel and preretinal tractional membrane; (2) intraoperative
ﬂattening of the detached retina; (3) application of
retinopexy; and (4) placement of a tamponade in vitreous
cavity.

PPV
• Compared to SB, PPV offers several advantages.
• The view of the retinal periphery is enhanced,
• Identiﬁcation of retinal breaks is rendered easier,
• Achievement of complete intraoperative retinal attachment is
possible, the risks of hemorrhage or retinal incarceration
inherent to external drainage procedure applied during SB is
eliminated, and the technique is less likely to cause a
refractive change.

Sutureless Microincision
Vitrectomy
• Transconjunctival sutureless MIVS using 23G/
25G instrumentation
• Advantages
• Shorter surgical time
• Less surgically induced astigmatism
• Reduced risk of post-operative corneal astigmatism
• Greater rigidity, better illumination, improved fluidics
with 23 G
• IOP compensation via direct control of infusion
pressure
• Wide angle viewing systems

Management of Tractional Retinal
Detachment
• TRD progresses very slowly, may reattach
spontaneously
• Localized TRD away from macula- observation
• Indications for surgery
• Macular threatened or detached
• Vitreous haemorrhage
• Retinal holes
• Surgical Principles
• To relax the vitreoretinal traction
• Closure of retinal holes
• Drainage of SRF

• PPV- to clear media, release of AP & tangential
traction
• ERM- peeling/ segmentation/ delamination
• Enblock excision of traction membranes
• Retinotomy with internal drainage of SRF, internal
tamponade with gas/silicone oil injection
• Endodiathermy & endophotocoagulation- new
vessels & retinopexy

Comparison of various surgical techniques
Method Reattachment Rate Limitations/Complications Benefits
Scleral Buckling 94% Morbidity, infection, buckle
extrusion, ocular motility
disturbances
Excellent long term
anatomic success, good
visual outcome
Pars Plana Vitrectomy 71-92% (1˚ success
rate)
94% (2˚ success rate)
Iatrogenic retinal breaks, PVR,
lens trauma, cataract
progression
Visualization of all
breaks, removal of
opacities/synechiae,
anatomic success in
complicated
detachments
Pneumatic Retinopexy 64% (1˚ success rate)
91% (2˚ success rate)
Limited use only in
uncomplicated RRD with
superior breaks
Post-op positioning,
iatrogenic breaks
In-office procedure,
minimally invasive,
↓ Recovery time, better
post-op VA

SB / PR / PPV
• Complicated detachments are usually managed with PPV ,
whereas localized, relatively simple cases are usually
managed with a “walling-off” (demarcating) procedure
employing laser or cryotherapy, with PR, or with a small
and localized scleral buckling procedure.

• Pneumatic retinopexy versus scleral buckle for repairing
simple rhegmatogenous retinal detachments.
• Hatef E et al
• The objectives of this review were to assess the
effectiveness and safety of pneumatic retinopexy versus
scleral buckle or pneumatic retinopexy versus a combination
treatment of scleral buckle and vitrectomy for people with
RRD.

• The evidence suggests that pneumatic retinopexy may
result in lower rates of reattachment and higher rates of
recurrence than scleral buckle for eyes with RRD, but does
not rule out no difference between procedures.
• The relative safety of the procedures is uncertain and the
relative effects of these procedures in terms of other
patient-important outcomes, such as visual acuity and
quality of life, is unknown.

• Outcomes after Failed Pneumatic Retinopexy for Retinal
Detachment.
• Anaya et al
• Abstract
• PURPOSE:
• To provide visual and anatomic outcomes for patients with
retinal detachment (RD) in whom
primary pneumatic retinopexy (PR) failed.
• DESIGN:
• Retrospective, single-center, consecutive case series.
• PARTICIPANTS:
• Eyes with RD that failed a primary PR.

• METHODS:
• Anatomic and functional outcomes were evaluated for
patients receiving treatment for failed PR. Three secondary
procedures were compared, including repeat PR, pars plana
vitrectomy (PPV), and combined scleral buckle (SB) plus PPV
(SB+PPV).
• MAIN OUTCOME MEASURES:
• Anatomic reattachment and visual acuity (VA) at 1 year.
• Anatomic success rates for secondary PR, PPV, and
SB+PPV after failed PR were lower than published
success rates for their use in primary RD.

• Macular choroidal thickness after vitreoretinal surgery:
Long-term effect of pars plana vitrectomy with and
without encircling scleral buckling surgery.
• Gama et al.
• PURPOSE:
• To evaluate the macular choroidal thickness (CT) of eyes
subjected to pars plana vitrectomy (PPV) whether or not
combined with encircling scleral buckling (ESB) surgery for
primary rhegmatogenous retinal detachment repair at 6
months or more after surgery.

• The CT of the eyes subjected to combined ESB and PPV was
significantly increased at 6 months or more after surgery
compared to the CT of their FE and to the CT of the eyes
subjected to PPV alone, which could be explained by a
venous engorgement caused by the ESB.

• Scleral buckling in phakic uncomplicated primary
rhegmatogenous retinal detachment: long-term
outcomes.
• Quijano C et al
• The aim of this study was to report the long-term
anatomical and functional outcomes of SB surgery
in phakic patients with uncomplicated primary
rhegmatogenous retinal detachment (PRRD).

• Retrospective studyof 90 phakic eyes with PRRD
treated with SB surgery that had a minimum of 5
years follow-up.
• High single operation success rate over time in
phakic PRRD, repaired through SB surgery.
Functional and anatomical success was maintained
throughout the follow-up without complications.

• Anatomical and Functional Results Following 23-Gauge
Primary Pars Plana Vitrectomy for Rhegmatogenous
Retinal Detachment: Superior versus Inferior Breaks
• Panagiotis Stavrakas et al
• In this retrospective study, they evaluated the anatomical
and functional outcomes of patients with rhegmatogenous
retinal detachment primarily treated with pars plana
vitrectomy in regard to the location of the breaks.

• Conclusion
• This study supports that acceptable reattachment
rates can be achieved using PPV for uncomplicated
RRD irrespective of the breaks location and inferior
breaks do not constitute an independent risk factor
for worse anatomical or functional outcome.

REFERENCES
• RETINAL DETACHMENT-JACK KANSKI
• RETINAL DETACHMENT SURGERY-CHIGNELL
• AAO
• YANOFF

Retinal detachment

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