Ablasio Retina

2.3.1 Definisi
Adalah kelainan mata dimana lapisan sensori retina terlepas dari lapisan epitel pigmen retina.
Antara kedua lapisan tersebut tidak terdapat taut yang erat, sehingga terjadi akumulasi cairan
subretinal di antara kedua lapisan tersebut.1-3
2.3.2 Klasifikasi
Terdapat empat klasifikasi pada ablasio retina, antara lain yaitu:

(1) Rhegmatogenous

Etiologi
Faktor risiko lebih tinggi didapatkan pada kelompok orang-orang dengan miopia berat, afakia,
usia lanjut, dan trauma. Khususnya yang disebabkan oleh trauma sering terjadi pada individu
berusia 25-45 tahun. Miopia tinggi (>5-6 dioptri) berhubungan dengan 67 % kasus ablasio
retina dan cenderung terjadi lebih muda dari pasien non miopia. 15 % kemungkinan akan
berkembang pula pada mata yang lainnya. Risiko sekitar 25-30 % pada pasien yang telah
menjalani operasi katarak pada kedua mata.3,5,6
Klasifikasi
Ablasio retina regmatogenosa dapat diklasifikasikan berdasarkan patogenesis, morfologi dan
lokasi.
Berdasarkan patogenesisnya, dibagi menjadi; (1) Tears, disebabkan oleh traksi vitreoretina
dinamik dan memiliki predileksi di superior dan lebih sering di temporal daripada nasal.(2)
Holes, disebabkan oleh atrofi kronik dari lapisan sensori retina, dengan predileksi di daerah
temporal dan lebih sering di superior daripada inferior, dan lebih berbahaya dari tears.
Berdasarkan morfologi, dibagi menjadi; (1) U-tearsm, terdapat flap yang menempel pada
retina di bagian dasarnya, (2) incomplete U-tears, dapat berbentuk L atau J, (3) operculated
tears, seluruh flap robek dari retina, (4) dialyses: robekan sirkumferensial sepanjang ora serata,
(5) giant tears.
Gambar 4. Morfologi robekan pada ablasio retina regmatogenosa

Berdasarkan lokasi, dibagi menjadi; (1) oral, berlokasi pada vitreous base, (2) post oral,
berlokasi di antara batas posterior dari vitreous base dan equator, (3) equatorial, (4) post
equatorial: di belakang equator (5) macular, di fovea.2

Patogenesis2

Ablasio jenis ini terjadi akibat adanya rhegma atau robekan pada lapisan retina sensorik (full
thickness) sehingga cairan vitreus masuk ke dalam ruang subretina. Pada tipe ini, gaya yang
mencetuskan lepasnya perlekatan retina melebihi gaya yang mempertahankan perlekatan
retina. Tekanan yang mempertahankan perlekatan retina, antara lain tekanan hidrostatik,
tekanan onkotik, dan transpor aktif. Hal yang mempertahankan perlekatan retina yaitu (1)
Tekanan intraokular memiliki tekanan hidrostatik yang lebih tinggi pada vitreus dibandingkan
koroid. (2) Koroid memiliki tekanan onkotik yang lebih tinggi karena mengandung substansi
yang lebih dissolved dibandingkan vitreus. (3) Pompa pada sel epitel pigmen retina secara aktif
mentranspor larutan dari ruang subretina ke koroid. Robekan retina terjadi sebagai akibat dari
interaksi traksi dinamik vitreoretina dan adanya kelemahan di retina perifer dengan faktor
predisposisi nya yaitu degenerasi. synchysis, yaitu pada traksi vitreoretina dinamik, terjadi
likuefaksi dari badan vitreus yang akan berkembang menjadi lubang pada korteks vitreus
posterior yang tipis pada fovea. Cairan synchytic masuk melalui lubang ke ruang retrohialoid.
Akibatnya terjadi pelepasan permukaan vitreus posterior dari lapisan sensori retina. Badan
vitreus akan menjadi kolaps ke inferior dan ruang retrohialoid terisi oleh cairan synchitic.
Proses ini dinamakan acute rhegmatogenous PVD with collapse (acute PVD). Selain itu juga
dapat terjadi sebagai akibat dari komplikasi akut PVD (posterior vitreal detachment). Robekan
yang disebabkan oleh PVD biasanya berbentuk huruf U, berlokasi di superior fundus dan sering
berhubungan dengan perdarahan vitreus sebagai hasil dari ruptur pembuluh darah retina
perifer.
 Gambar 5. Vitreous syneresis 2

Kebanyakan robaekan terjadi di daerah perifer retina. Hal tersebut dapat berhubungan
dengan degenerasi retina perifer. Terdapat berbagai macam degenerasi, antara lain:

1. Degenerasi lattice
Biasa ditemukan pada pasien dengan sindrom Marfan, sindrom Stickler, sindrom Ehler-
Danlos. Ditandai dengan bentuk retina yang sharply demarcated, circumferentially
orientated spindle shaped areas. Biasanya terdapat bilateral dan lebih sering di daerah
temporal dan superior.

2. Degenerasi snailtrack
Degenerasi ini berbentuk snowflakes atau white frost like appearance.

3. Degenerasi retinoschisis
Pada degenerasi ini terjadi pemisahan antara lapisan sensori retina menjadi 2 lapisan, yaitu
lapisan koroidal dan lapisan vitreus. Kejadian ini banyak berhubungan dengan hipermetrop.

4. White-with-pressure, White-without-pressure.
 Gambar 6. Degenerasi vitreoretinal2

Gejala Klinis 1,2,3,5

Gejala utama yang ditimbulkan adalah fotopsia akibat stimulasi mekanik pada retina.
Fotopsia muncul dalam kurun waktu 24-48 jam setelah terjadinya robekan retina. Fotopsia
dapat diinduksi oleh gerakan bola mata. Pasien akan merasa dapat melihat lebih jelas pada
malam hari. Biasanya fotopsia terdapat di bagian temporal perifer dari lapangan penglihatan.
Pada ablasio bagian supratemporal yang menyebabkan terangkatnya macula, maka akan terjadi
penurunan tajam penglihatan yang mendadak. Keluhan lain yang khas adalah, floater, adanya
bayangan gelap pada vitreous akibat retina yang robek, darah dan sel epitel pigmen retina yang
masuk ke badan vitreus. Kekeruhan vitreus ini terbagi atas 3 tipe, yaitu; (1) Weiss ring, floater
yang soliter terdiri dari annulus yang terlepas dari vitreus. (2) Cobwebs, disebabkan oleh
kondensasi serat kolagen di korteks vitreus yang kolaps. (3) Pancaran seketika berupa titik
hitam atau merah yang biasanya mengindikasikan perdarahan vitreus akibat robekan pembuluh
darah retina. Black curtain, defek lapang penglihatan dirasakan oleh pasien mulai dari perifer
yang lama-lama hingga ke sentral. Keluhan ini dapat saja tidak muncul di pagi hari karena
cairan subretina diabsorbsi secara spontan pada saat malam hari. Arah munculnya defek
membantu dalam menentukan lokasi dari robekan retina. Hilangnya penglihatan sentral
mungkin dikarenakan keterlibatan fovea.
 Selanjutnya melalui pemeriksaan oftalmologis dapat ditemukan adanya Marcus Gunn
pupil, tekanan intraokular yang menurun, iritis ringan, adanya gambaran tobacco dust atau
Schaffer sign, robekan retina pada funduskopi. Pada pemeriksaan funduskopi akan terlihat
retina yang terangkat berwarna pucat dengan pembuluh darah di atasnya dan terlihat adanya
robekan retina berwarna merah. Bila bola mata bergerak akan terlihat retina yang terlepas
bergoyang.

Gambar 7. Tobacco dust 2

Tatalaksana 1-3
Prinsip penatalaksanaan dari ablasio retina adalah untuk melepaskan traksi vitreoretina
serta dapat menutup robekan retina yang ada. Penutupan robekan dilakukan dengan melakukan
adhesi korioretinal di sekitar robekan melalui diatermi, krioterapi, atau fotokoagulasi laser.
Pembedahan yang sering dilakukan adalah scleral buckling, pneumatic retinopexy dan
intraocular silicone oil tamponade. Kebanyakan praktisi lebih sering melakukan prosedur
scleral buckling. Penempatan implan diletakkan dalam kantung sklera yang sudah direseksi
yang akan mengeratkan sclera dengan retina

Prognosis
Prognosis ditentukan oleh tatalkasana yang dini, mekanisme yang mendasari terjadinya ablasio
retina, dan adanya keterlibatan makula.6

1. Hardy RA,. Retina dan Tumor Intraokuler. In : Vaughan D.G, Asbury T., Riordan E.P,
editor. Oftalmologi Umum Edisi 14. Jakarta : Widya Medika. 2000.p. 38-43, 185-99.
 2. Kanski JJ, Bowling B, editors. Clinical Ophthalmology: a systemic approach. 7th ed.
Elsevier, 2011
3. Ilyas S. Ilmu Penyakit Mata. Edisi ketiga. 2004. Jakarta: Balai Penerbit FKUI.
4. Sidarta I,. Anatomi dan Fisiologi Mata. Dalam : Ilmu Penyakit Mata Edisi kedua.
Jakarta: BP-FKUI. 2002. p.10-5.
5. Larkin GL. Retinal Detachment. [series online] 2006 April 11 [cited on 2013 January
15]. Available from URL: http://www.emedicine.com/emerg/topic504.htm.
6. Gariano RF, Kim CH. Evaluation and Management of Suspected Retinal Detachment.
American Academy of Family Physicians. [series online] 2004 April 1 [cited on 2013
January 15]; vol. 69, no. 7. Available from URL:
http://www.aafp.org/afp/20040401/1691.html.
7. Wu L. Retinal Detachment Exudative. [series online] 2010 Agustus 2 [cited on 2013
January 15]. Available from URL: http://www.emedicine.com/oph/topic407.htm.

Peter A. Netland, Shizuo Mukai, Henry I. Covington, Elevated intraocular pressure secondary to
rhegmatogenous retinal detachment, In Survey of Ophthalmology, Volume 39, Issue 3, 1994, Pages
234-240, ISSN 0039-6257, https://doi.org/10.1016/0039-6257(94)90196-1.

(http://www.sciencedirect.com/science/article/pii/0039625794901961)

Abstract: Abstract

Elevated intraocular pressure secondary to rhegmatogenous retinal detachment was described by

Ariah Schwartz in 1972, an entity commonly known as Schwartz's syndrome. Photoreceptor outer
segments identified in the aqueous of patients with this syndrome are thought to play a role in the
elevation of the intraocular pressure. We present two patients with open angles and elevated
intraocular pressure associated with retinal detachment. Retinal reattachment surgery resulted in
normalization of the intraocular pressure. Electron microscopic examination of aqueous specimens
from our patients demonstrated a predominance of photoreceptor outer segments in varying stages
of degeneration. In these specimens, inflammatory cells, fibrin, and pigment granules were rarely
observed or were absent. We review the literature regarding the epidemiology, clinical
characteristics, and pathogenesis of Schwartz's syndrome.

Keywords: glaucoma; photoreceptor outer segments; retinal detachment; Schwartz's syndrome

 Klasifikasi ablasio retina berdasarkan etiologinya, terdiri atas :1
1. Ablasio retina regmatogenosa
Pada ablasio retina regmatogenosa dimana ablasio terjadi akibat adanya robekan pada retina
sehingga cairan masuk ke belakang antara sel pigmen epitel dengan retina. Terjadi pendorongan retina
oleh badan kaca cair (fluid vitreous) yang masuk melalui robekan atau lubang pada retina ke rongga
subretina sehingga mengapungkan retina dan terlepas dari lapis epitel pigmen koroid.
Ablasio retina akan memberikan gejala terdapatnya gangguan penglihatan yang kadang-kadang
terlihat sebagai tabir yang menutup. Terdapatnya riwayat adanya pijaran api (fotopsia) pada lapangan
penglihatan.
Ablasio retina yang berlokalisasi di daerah supratemporal sangat berbahaya karena dapat
mengangkat makula. Penglihatan akan turun secara akut pada ablasio retina bila dilepasnya retina
mengenai makula lutea.
Pada pemeriksaan funduskopi akan terlihat retina yang terangkat berwarna pucat dengan
pembuluh darah di atasnya dan terlihat adanya robekan retina berwarna merah.
Bila bola mata bergerak akan terlihat retina yang lepas (ablasio) bergoyang. Kadang-kadang terdapat
pigmen di dalam badan kaca. Pada pupil terlihat adanya defek aferen pupil akibat penglihatan menurun.
Tekanan bola mata rendah dan dapat meninggi bila telah terjadi neovaskular glaukoma pada ablasio yang
telah lama.
Ilyas S, dkk. Ablasio retina. In: Sari ilmu penyakit mata. Cetakan ke-4. Gaya Baru Penerbit Fakultas Kedokteran
Universitas Indonesia; 2004: 9,10,183-6.

Retinal detachment (RD). RD refers to separation of the

neurosensory retina (NSR) from the RPE. This results in the
accumulation of SRF in the potential space between the NSR
and RPE.
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. RRD, as opposed to the
presence merely of a cuff of SRF surrounding a retinal break,
is said to be present when fluid extends further than one
optic disc diameter from the edge of the break.

Pathogenesis
Rhegmatogenous RD affects about 1 in 10 000 of the population
each year, with both eyes eventually affected in about 10%. In most
cases it is characterized by the presence of a retinal break in concert
with vitreoretinal traction that allows accumulation of liquefied
vitreous under the neurosensory retina, separating it from the
RPE. Even though a retinal break is present, a RD will almost never
occur if the vitreous is not at least partially liquefied and traction
is absent. Over 40% of RDs occur in myopic eyes; the higher the
refractive error the greater the risk of RD. Vitreous degeneration
and PVD, and predisposing lesions such as lattice and snailtrack
degeneration, are more common in myopia. Highly myopic eyes
are also at risk from RD due to small round holes in chorioretinal
atrophy and from macular holes. Vitreous loss during cataract
surgery, and laser capsulotomy, also carry a higher risk of RD in
highly myopic eyes.
Identification of retinal breaks
Distribution of breaks in eyes with RD is approximately as
follows: 60% superotemporal quadrant, 15% superonasal,
15% inferotemporal and 10% inferonasal. The upper
temporal region should therefore be examined in detail if a
break cannot be detected initially. It should also be
remembered that about 50% of eyes with RD have more
than one break, often within 90 of each other.
Configuration of SRF. SRF spread is governed by gravity, 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 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 (modified from Lincoffs
rules):
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. 16.27A).
A primary break located at 6 oclock will cause an inferior
RD with equal fluid levels (Fig. 16.27B).
In a bullous inferior RD the primary break usually lies
above the horizontal meridian (Fig. 16.27C).
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. 16.27D).
A subtotal RD with a superior wedge of attached retina
points to a primary break located in the periphery nearest
its highest border (Fig. 16.27E).
When the SRF crosses the vertical midline above, the
primary break is near to 12 oclock, the lower edge of the
RD corresponding to the side of the break (Fig. 16.27F).
Symptoms
The classic premonitory symptoms reported in about 60% of
patients with spontaneous rhegmatogenous RD are flashing lights
and floaters associated with acute PVD. After a variable period of
time a curtain-like relative peripheral visual field defect may ensue,
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. A lower field defect is usually appreciated more quickly
by the patient than an upper 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; the location of photopsia is of no value in
predicting the site of the primary break; flashes are virtually always
temporal. 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.
Signs

General
Relative afferent pupillary defect (Marcus Gunn pupil) is
present in an eye with an extensive RD.
 Intraocular pressure (IOP) is often lower by about 5 mmHg
compared with the normal eye. If the intraocular pressure is
extremely low, an associated choroidal detachment may be
present. It may be raised, characteristically in Schwartz
Matsuo syndrome in which RRD is associated with an
apparent mild anterior uveitis, often due to a dialysis due to
prior blunt trauma in a young man; the aqueous cells are
believed in most cases actually to be displaced photoreceptor
outer segments that compromise trabecular outflow. Both
the aqueous cells and the elevated IOP typically resolve
following repair of the RD.
Iritis is very common but usually mild and should be
differentiated from SchwartzMatsuo syndrome (above).Occasionally it may be severe enough to cause posterior

synechiae; the underlying RD may be overlooked.

Tobacco dust consisting of pigment cells is commonly seen
in the anterior vitreous (Fig. 16.28); substantial vitreous
blood or inflammatory cells are also highly specific.

Retinal breaks (see Fig. 16.24) 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 (e.g.
high myopia), the colour contrast is decreased and small
breaks may be overlooked.
Retinal signs depend on the duration of RD and the
presence or absence of proliferative vitreoretinopathy (PVR)
as described below.

Fresh retinal detachment

The RD has a convex configuration and a slightly opaque
and corrugated appearance as a result of retinal oedema
(Figs 16.29AD). There is loss of the underlying choroidal
pattern and retinal blood vessels appear darker than in flat
retina.

SRF extends up to the ora serrata, except in the rare cases

caused by a macular hole in which fluid is initially confined
to the posterior pole (Fig. 16.29E).
Macular pseudohole. Because of the thinness of the foveal
retina, the impression of a macular hole may be given 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 trauma.
B-scan ultrasonography shows good mobility of the retina
and vitreous (see Fig. 16.10).
Long-standing retinal detachment
Retinal thinning secondary to atrophy is a characteristic
finding, and should not lead to a misdiagnosis of
retinoschisis.
Intraretinal cysts (Fig. 16.30AC) may develop if the RD has
been present for about 1 year; these tend to disappear after
retinal reattachment.
Subretinal demarcation lines (high water or tide marks)
caused by proliferation of RPE cells at the junction of flat

and detached retina (Fig. 16.30D and E) are common, taking

about 3 months to develop. Pigmentation tends to decrease
over time. Although representing sites of increased adhesion,
they do not invariably limit the spread of SRF.
Proliferative vitreoretinopathy
Proliferative vitreoretinopathy (PVR) is caused by epiretinal and
subretinal membrane formation, contraction of which leads
to tangential retinal traction and fixed retinal fold formation
(Fig. 16.31). Usually, PVR occurs following surgery for rhegmatogenous
RD or penetrating injury, though it may also occur in eyes
with rhegmatogenous RD that have not had previous retinal
surgery. The main features are retinal folds and rigidity so that
retinal mobility induced by eye movements or scleral indentation
is decreased. Progression from one stage to the next is not
inevitable.
Grade A (minimal) PVR is characterized by diffuse vitreous
haze and tobacco dust. There may also be pigmented clumps

on the inferior surface of the retina. Although these findings

occur in many eyes with RD, they are particularly severe in
eyes with early PVR.
Grade B (moderate) PVR is characterized by wrinkling of
the inner retinal surface (Fig. 16.32A), decreased mobility of
vitreous gel, rolled edges of retinal breaks, tortuosity of
blood vessels and retinal stiffness (Fig. 16.32B). The epiretinal
membranes responsible for these findings typically cannot be
identified clinically.
Grade C (marked) PVR is characterized by rigid fullthickness
retinal folds (often star-shaped) with heavy
vitreous condensation and strands (Fig. 16.32C and D). It
can be either anterior (A) or posterior (P), the approximate
dividing line being the equator of the globe. The severity of
proliferation in each area is expressed by the number of
clock hours of retina involved although proliferations need
not be contiguous.
Advanced disease shows gross reduction of retinal mobility
with retinal shortening and a characteristic funnel-like
triangular conformation (see Fig. 16.31D).

Differential diagnosis
The tractional and exudative forms of RD are described later in
the chapter.
Degenerative retinoschisis
See above.
Choroidal detachment
Causes of choroidal detachment (also known as ciliochoroidal
or choroidal effusion) include hypotony, particularly following
glaucoma drainage surgery (see Ch. 10), sulfa drugs such as acetazolamide
and topiramate, uveitis, posterior scleritis, choroidal
tumours and a cyclodialysis cleft following trauma (including
surgical); occasionally it occurs secondary to retinal detachment.
Idiopathic cases are generally labelled as uveal effusion syndrome
(see below).
Symptoms. Photopsia and floaters are absent because
there is no vitreoretinal traction. A visual field defect may be noticed if the choroidal detachment is
extensive.
Signs
Low intraocular pressure is common as a result of the
cause and of concomitant detachment of the ciliary body.
The anterior chamber may be shallow in eyes with
extensive choroidal detachments; non-pupillary block
angle closure can occur.
The elevations are brown, convex, smooth and relatively
immobile (Fig. 16.33A). Four lobes are typically present;
temporal and nasal bullae tend to be most prominent.
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 vortex veins entering their
scleral canals (Fig. 16.33B); however, in contrast to retinal
detachments they extend anteriorly beyond the ora
serrata.
Treatment is directed at the cause; drainage via partialthickness
sclerectomies is occasionally required.

Uveal effusion syndrome

The uveal effusion syndrome is a rare idiopathic, often bilateral,
condition that most frequently affects middle-aged hypermetropic
men but can occur in association with nanophthalmos. The cause
is thought to be impairment of normal fluid drainage from the
choroid via the sclera (which is sometimes of abnormal thickness
and composition) or vortex veins.
Signs
Inflammation is absent or mild.
Ciliochoroidal detachment followed by exudative RD.
Following resolution, the RPE frequently shows a
characteristic residual leopard spot mottling caused by
degenerative changes in the RPE associated with a high
concentration of protein in the SRF.
Differential diagnosis includes uveal effusion secondary to
other causes (see above), choroidal haemorrhage and ring
melanoma of the anterior choroid.
Treatment is usually with full-thickness sclerectomies; pars
plana vitrectomy alone may also be successful, but
sclerectomies are usually first-line in nanophthalmos.
Surgery
Indications for urgent surgery
In general, an acutely symptomatic RD should be operatively
repaired urgently, particularly if the macula is as yet uninvolved
(Fig. 16.34). Other factors that may increase the urgency of intervention
include the presence of a superior or large break, from
which SRF is likely to spread more rapidly, and advanced syneresis
as in myopia. Patients with dense fresh vitreous haemorrhage in
whom visualization of the fundus is impossible should also be
operated on as soon as possible if B-scan ultrasonography shows an underlying RD. When an RD likely to require an urgent
operation
is diagnosed or suspected, it is important that the patient does
not eat or drink in the hours before assessment so that surgery is
not delayed. Minimizing activity may be helpful, and some
authorities advocate bed rest with the head turned so that the
retinal break is in the most dependent position, which may lessen
the amount of SRF and facilitate surgery.
Pneumatic retinopexy
Pneumatic retinopexy (Fig. 16.35) is an outpatient procedure in
which an intravitreal gas bubble together with cryotherapy or laser
are used to seal a retinal break and reattach the retina without
scleral buckling. The most frequently used gases are sulfur hexafluoride
(SF6) and the longer-acting perfluoropropane (C3F8). It
has the advantage of being a relatively quick, minimally invasive,
office-based procedure. However, success rates are usually worse
than those achievable with conventional scleral buckling. The procedure
is usually reserved for treatment of uncomplicated RD with
a small retinal break or a cluster of breaks extending over an area
of less than two clock hours in the upper two-thirds of the peripheral
retina.
Principles of scleral buckling
Scleral buckling, sometimes referred to as conventional or external
RD surgery as opposed to the internal approach of pars plana
vitrectomy (see below), is a surgical procedure in which material
sutured onto the sclera (explant Fig. 16.36A) creates an inward
indentation (buckle Figs 16.36B and C). Its purposes are to close
retinal breaks by apposing the RPE to the sensory retina, and to
reduce dynamic vitreoretinal traction at sites of local vitreoretinal
adhesion.
Explants are made from soft or hard silicone. The entire
break should ideally be surrounded by about 2 mm of
buckle. It is also important for the buckle to involve the area
of the vitreous base anterior to the tear in order to prevent
the possibility of subsequent reopening of the tear and
anterior leakage of SRF. The dimensions of the retinal break
can be assessed by comparing it with the diameter of the
optic disc.
Buckle configuration can be radial, segmental,
circumferential or encircling, depending on the size,
configuration and number of breaks.
Technique. The conjunctiva is incised (peritomy) to
facilitate access, following which retinal breaks are localized
and cryotherapy applied. An explant of appropriate
dimensions and orientation is then sutured to the sclera
and the position of the buckle checked in relation to the
break.
Drainage of subretinal fluid
Drainage of SRF via the sclera (e.g. the D-ACE: Drainage-Air-
Cryotherapy-Explant) surgical technique (Fig. 16.37A) is advocated
by many practitioners, citing more rapid retinal reattachment in the presence of deep or long-standing viscous SRF; other
authorities prefer to avoid external drainage due to its potential
complications such as retinal perforation or incarceration in the
drainage site (Fig. 16.37B) and choroidal haemorrhage, and would
perform a pars plana vitrectomy in such cases.
Complications of scleral buckling
Diplopia due to the mechanical effect of the buckle is very
common. Early spontaneous resolution is typical, though
intervention is sometimes necessary.
Cystoid macular oedema occurs in up to 25%, but usually
responds to treatment. Other macular complications include
epiretinal membrane (around 15%), persistent subfoveal
fluid and foveal structural disruption, usually in macular-off
detachments.
Anterior segment ischaemia due to vascular compromise. This
is a particular risk with an encircling band, and with predisposing
systemic conditions such as sickle haemoglobinopathies.
Buckle extrusion, intrusion or infection (Figs 16.38A and
B). Removal is usually required, with aggressive antibacterial
therapy as indicated. Elevated IOP. Early IOP spikes usually resolve rapidly, but B
occasionally persist. Angle closure can occur.
Choroidal detachment usually resolves spontaneously,
presumably as scleral oedema settles and allows improved
vortex vein function.
Surgical failure
Missed breaks. A thorough search should always be made
for the presence of multiple breaks, particularly if the configuration of the RD does not correspond to the
position of the primary break.
Buckle failure may occur due to inadequate size, incorrect
positioning (Fig. 16.38C), or inadequate height; the
explant may have to be replaced or repositioned to
address the first two, but drainage of SRF or intravitreal
gas injection may suffice for the latter, though pars plana
vitrectomy (PPV) may be preferred as a more definitive
measure. Fish-mouthing (Fig. 16.38D) describes the
phenomenon of a tear, typically a large superior
equatorial U-tear in a bullous RD, to open widely
following scleral buckling, requiring further operative
treatment.

Proliferative vitreoretinopathy is the most common cause

of late failure. The tractional forces associated with PVR
can occasionally open old breaks and create new ones.
Presentation is typically several weeks postoperatively
with re-detachment.
Reopening of a retinal break in the absence of PVR can
occur as a result of inadequate cryotherapy or scleral
buckling, or sometimes when buckle height decreases
either with time or following late surgical removal.
Fig. 16.38
Pars plana vitrectomy
Pars plana vitrectomy (PPV) is discussed later in this chapter.

Ablatio retina e (retinai detachment) adalah pemisahan retina

sensorik, yakni lapisan fotoreseptor dan jaringan bagian
dalam, dari epitel pigmen retina di bawahnya' Terdapat
tiga jenis utama: ablasi regmatogenosa, ablasi traksi, dan
ablasi serosa atau hemoragik.

RD refers to separation of the

neurosensory retina (NSR) from the RPE. This results in the
accumulation of SRF in the potential space between the NSR
and RPE.
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. RRD, as opposed to the
presence merely of a cuff of SRF surrounding a retinal break,
is said to be present when fluid extends further than one
optic disc diameter from the edge of the break.

Ablatio Retinae Regmatogenosa

Bentuk tersering ablatio retinae, ablatio retinae regmatogenosa,
ditandai dengan pemutusan (suatu "regma") total
(full-thickness) retina sensorik, traksi vitreus dengan derajat
bervariasi, dan mengalirnya vitreus cair melalui robekan
ke dalam ruang subretina. Ablatio retinae regmatogenosa
spontan biasanya didahului atau disertai oieh pelepasan
vitreus posterior dan berhubungan dengan miopia, afakia,
degenerasi lattice, dan trauma mata. Oftalmoskopi indirek
binokular dengan depresi sklera (Gambat 2-15 dan 2-17)
mernperlihatkan peninggian retina sensorik yang lepas
dan berwarna translusen denlan satu atau lebih pemutusan
retina sensorik total, misalnya robekan berbentuk
tapal kuda, lubang atrofik bundar, atau robekan sirkumferensial
anterior (dialisis retina). Letak pemutusan retina
bervariasi sesuai dengan jenisnya; robekan tapal kuda
paling sering terjadi di kuadran superotemporal, lubang
atrofik di kuadran temporal, dan dialisis retina di kuadran
inferotemporal. Bila terdapat robekan retina multipel,
defek-defek tersebut biasanya terletak 90 derajat satu
sama lain.
Terapi
Tujuan utama bedah ablasi adalah untuk menemukan dan
memperbaiki semua robekan retina; digunakan krioterapi
atau laser untuk menimbulkan adhesi antara epitel
pigmen dan retina sensorik sehingga mencegah influks
cairan lebih lanjut ke dalam ruang subretina, mengalirkan
cairan subretina ke dalam dan ke luar, dan meredakan
traksi vitreoretina. Diterapkan berbagai teknik bedah.
Pada retinopeksi pneumatik, udara atau gas yang
dapat memuai disuntikkan ke dalam vitreus untuk mempertahankan
retina pada posisinya, sementara adhesi korioretina
yang diinduksi oleh laser atau cryoterapi menutup
robekan retina secarh permanen. Teknik ini memiliki
angka keberhasilan yang lebih rendah dibandingkan cara
lain dan hanya digunakan pada robekan retina tunggal
kecil yang mudah dicapai, cairan subretina yang minimal,
dan tidak adanya traksi vitreoretina.
Scleral buckling mempertahankan retina di posisinya
sementara adhesi korioretinanya terbentuk, dengan rnelekukkan
sklera menggunakan eksplan yan$ dijahitkan
pada daerah robekan retina. Teknik ini juga mengatasi
traksi vitreoretina dan menyingkirkan cairan subretina
dari robekan retina. Angka keberhasilannya adalah92-94%
pada kasus-kasus tertentu yang sesuai. Komplikasinya
antara lain perubahan kelainan refraksi, diplopia akibat
fibrosis atau terganggunya otot-otot ekstraokular oleh
eksplan, ekstrusi eksplan, dan kemungkinan peningkatan
risiko vitreoretinopati proli{eratif .
Vitrektomi pars plana memungkinkan pelepasan
traksi vitreo-retina, drainase internal cairan subretinajika
diperlukan dengan penyuntikan perfluorocarbon atau
cairan berat, dan penyuntikan udara atau gas yang dapat
memuai untuk mempertahankan retina pada posisinya,
atau penyuntikan dengan minyak jika dibutuhkan tamponade
retina yang lebih lama. Teknik ini digunakan
bila terdapat robekan retina multipel, di superior, atau di
posterior; bila visualisasi retina terhalang, misalnya oleh
perdarahan vitreus; dan bila ada vitreoretinopati proliferal:,
l yang bermakna. Vitrektomi menginduksi pembentukan
katarak dan mungkin dikontraindikasikan pada
mata fakik. Mungkin diperlukan pengaturan posisi pasien
pascaoperasi.
Hasil-akhir penglihatan pascabedah ablatio retinae
regmatogenosa terutama tergantung dari status praoperasi
makula. Apabila makula terlepas, pengembalian penglihatan
sentral biasanya tidak sempurna. OIeh karena itu,
tindakan bedah harus segera dilakukan selagi makula
masih melekat. Bila makula sudah terlepas, penundaan tindakan bedah hingga 1 minggu tidak mengubah
hasilakhir
penglihatan.

Vitreoretinal traction is responsible for the occurrence of most RRD. As the vitreous
becomes more syneretic (liquefied) with age, a posterior vitreous detachment (PVD)
occurs. In most eyes, the vitreous gel separates from the retina without any
sequelae. However, in certain eyes, strong vitreoretinal adhesions are present and
the occurrence of a PVD can lead to a retinal tear formation; then, fluid from the
liquefied vitreous can seep under the tear, leading to a retinal detachment.
A number of conditions exist that predispose to a PVD by prematurely accelerating
the liquefaction of the vitreous gel. Myopia, aphakia or pseudophakia, familial
conditions, and inflammation are among the common causes. In other cases, retinal
necrosis with a retinal break formation occurs; then, fluid from the vitreous cavity can
flow through the breaks and detach the retina without there being overt vitreoretinal
traction present. This commonly occurs in acute retinal necrosis syndrome and in
cytomegalovirus (CMV) retinitis in AIDS patients.
A given amount of vitreoretinal traction will cause retinal tears if the retina is thinner,
as in lattice degeneration of the retina.

Traksi Vitreoretinal bertanggung jawab atas terjadinya RRD yang paling banyak. Sebagai vitreous
menjadi lebih sinergis (dicairkan) dengan usia, sebuah pelepasan vitreous posterior (PVD) terjadi.
Pada kebanyakan mata, gel vitreous memisahkan dari retina tanpa sekuele apapun. Namun, pada
mata tertentu, adhesi vitreoretinal yang kuat hadir dan terjadinya PVD dapat menyebabkan
pembentukan robekan retina; Kemudian, cairan dari vitreous yang dicairkan bisa merembes di
bawah air mata, menyebabkan ablasio retina.

Sejumlah kondisi ada yang menjadi predisposisi PVD dengan mempercepat percepatan liquefaksi gel
vitreous secara dini. Miopia, aphakia atau pseudophakia, kondisi keluarga, dan pembengkakan
adalah penyebab umum. Dalam kasus lain, nekrosis retina dengan formasi istirahat retina terjadi;
Kemudian, cairan dari rongga vitreous dapat mengalir melalui jeda dan melepaskan retina tanpa
adanya traksi vitreoretinum yang terbuka. Hal ini biasanya terjadi pada sindrom nekrosis retina akut
dan pada retinitis sitomegalovirus (CMV) pada pasien AIDS.

Jumlah traksi vitreoretinal tertentu akan menyebabkan robekan retina jika retina lebih tipis, seperti
pada degenerasi kisi retina.