Management of Retinal Breaks and Detachment
Joseph Sowka, OD, FAAO, Diplomate
Retinal Break:
 Any full thickness disruption in the sensory retina providing a conduit for fluid to enter the
potential space between the sensory retina and RPE.
Major Complications:
 Potential for progression to rhegmatogenous retinal detachment.
 There are three types of retinal detachments
 Rhegmatogenous
 This is the only type caused by a retinal break
 Tractional
 Serous/exudative
 Success rate for retinal reattachment surgery: 95%
 Best to avoid RD altogether
 Prophylactic treatment for retinal breaks with laser photocoagulation or cryoretinopexy. The
goal is to create RPE hyperplastic scar around the break and seal the retina to the RPE, thus
preventing fluid from accumulating in the subretinal space.
Pathogenesis of Vitreous Detachment and Tractional Retinal Breaks:
 Vitreous cavity is composed of collagen fibrils supported by hyaluronic acid molecules
interspersed among the fibrils. The fibrils attach to the retina at specific areas resulting in
vitreoretinal adhesion
 Areas of vitreoretinal adhesion:
 Vitreous base
 Optic disc
 Macula
 Along areas of chorioretinal scarring
 Along retinal blood vessels
 Along the edges of lattice degeneration
 Vitreoretinal tufts
 As hyaluronic acid concentration decreases with age, collagen fibrils lose support, aggregate,
form pockets of liquefied vitreous, and the vitreous collapses resulting in a posterior vitreous
detachment (PVD). As the vitreous collapses, traction is exerted on areas of vitreoretinal
adhesion and a tear can result. Symptoms of retinal tears can include photopsia (flashes) and
floaters (PVD, vitreous inflammatory cells, blood in vitreous, liberated pigment - also known
as tobacco dust).
 In a study of 589 symptomatic patients, those presenting with:
 Diffuse spots:
52% had a retinal tear
 Vitreous cells:
65% had a retinal tear
 Vitreous blood: 91% had a retinal tear
 Atrophic retinal holes can develop without tractional forces due to cystic
erosion/degenerations within the retina. This is extremely common in retinal thinning
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conditions such as lattice degeneration.
When encountering a recent onset PVD, carefully evaluate the peripheral retina. An acute
PVD has a 15% likelihood of having a retinal tear at initial presentation. Of these, ½ will
have two or more tears. If there are no retinal defects seen, repeat examination in 6 weeks.
Statistically, most retinal complications from PVD occur within the first 6 weeks (about 35% will develop a late-onset retinal break). If no complications develop within 6 weeks,
routine yearly follow-up is indicated, unless symptoms change.
When encountering an acute PVD with vitreous or pre-retinal hemorrhage, but no discernible
break (examining with Goldmann fundus lens, non-contact lens, and scleral depression), reexamine every 2 weeks for 6 weeks. If no break is seen, re-examine at regular intervals until
the hemorrhage clears. The concern is that there is a retinal break that also tore a blood
vessel. If no break is ever found to account for the hemorrhage, then the likely cause is
rupture of superficial capillaries caused by the PVD.
When encountering a recent onset PVD and a retinal tractional break is seen associated with
the PVD, refer for therapeutic treatment, as the risk of detachment is 52%.
Clinical Pearl: Most floaters in patients under the age of 50 are due to benign vitreous
syneresis.
Clinical Pearl: A sudden onset of floaters could indicate posterior vitreous detachment,
vitreous hemorrhage secondary to a retinal tear, liberated pigment cells from a retinal
detachment, or vitreous cells from a posterior inflammation.
Clinical Pearl: PVD typically presents as a singular large floater.
Lattice Degeneration and Atrophic Holes:
 Lattice degeneration represents thinning of all 10 retinal layers due to dropout of peripheral
retinal capillaries and resulting ischemia with subsequent retinal collapse and glial fibrosis.
 Age and severity are unrelated.
 Lattice degeneration typically has an appearance of a white lattice-type of degeneration
representing glial tissue filling the degenerated lumen of the larger capillaries. A classic
appearance is "snail track" degeneration, where it appears as a discrete fibrotic trail across the
retina. Fibrotic appearance occurs in 12% of cases.
 There are many faces of lattice- pigmented lattice occurs as the retinal thinning is perceived
as damage to the retina, and this stimulates RPE hyperplasia. Pigmentation is present in 8090% of cases
 Lattice nearly always runs circumferentially around the eye.
 Retinal degeneration causes secondary effects on the vitreous
 Vitreous liquefaction (hyaluronic acid) overlying lattice lesion. Develops lacunae.
 Increased vitreoretinal adhesion along edges of lattice lesion
 Lattice degeneration is present in 8-11% of all eyes. Atrophic holes are present in 18-42% of
all lattice lesions. Occasionally, the hole encompasses the entirety of the lattice lesion.
 There is no traction on atrophic holes in lattice lesions due to overlying vitreous liquefaction
 Retinal detachment occurs when hyaluronic acid washes through the holes and accumulates
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as subretinal fluid. This usually is a result of the coalescing of several pockets of liquid
vitreous over a lattice hole. Approximately 30% of all rhegmatogenous retinal detachments
are caused by holes in lattice.
Less than 2% of atrophic holes in lattice progress to retinal detachment.
 Atrophic holes in lattice degeneration do not need prophylactic treatment. Monitor
The risk of retinal detachment occurring from a tear along the edge of lattice is 37%.
 This entity needs treatment.
Treatment of lattice lesions in eyes above -6.00D has no benefit.
Lattice lesions without tears require no prophylactic treatment: Monitor
The only instances where lattice lesions are treated prophylactically is if the patient
previously had a retinal detachment from lattice degeneration in the fellow eye, or
possibly if there is lattice in the eye of a monocular patient. Lattice lesions alone and
those with atrophic holes are not treated. Tears along the border of lattice lesions are
treated.
Flap Tears:
 Also known as horseshoe tears or tractional tears
 Retina is incompletely pulled away from RPE. This bridge between vitreous and retina
exerts traction.
 Base of tear is always toward vitreous base and apex of flap points towards posterior pole.
 Mechanical forces pulling on the retina produce symptoms. The same forces that pull on the
retina and cause symptoms exert force to further pull the retina off of the RPE. Traction may
avulse flap, releasing traction and creating operculum.
 Subclinical retinal detachment can occur with flap tear or any other break. Subclinical
detachment is defined as retinal detachment (or subretinal fluid) extending beyond 1DD from
the edge of the break, but not progressing more than 2DD posterior to the equator. The
presence of subretinal fluid is ominous.
 Davis 1974: 16 year study of natural history of 222 eyes with breaks:
 Symptomatic flap tear without fluid:
36% progressed to RD.
 Asymptomatic flap tear with fluid:
40% progressed to RD
 Asymptomatic flap tear without fluid:
10% progressed to RD
 Asymptomatic flap tear without fluid:
0% progressed (Byer)
Symptomatic flap tears and asymptomatic flap tears with subclinical retinal detachment
(fluid) need prophylactic therapy. An asymptomatic flap tear without fluid likely does
not need treatment.
Clinical Pearl: Most flap tears are initially symptomatic at the time of origin, but the
symptoms may have stopped by the time that the patient reaches the office.
Clinical Pearl: If a symptomatic retinal breaks stops being symptomatic for a period of
several months, then it is considered to be asymptomatic and thus safer.
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Operculated Break:
 Retinal tissue is completely pulled free of RPE. Traction may or may not remain on the
edges of the hole.
 Davis 1974:
 Symptomatic operculated breaks:
20% progressed to RD
 Asymptomatic operculated breaks with fluid:
23% progressed to RD
 Asymptomatic operculated breaks without fluid:
0% progressed to RD
Asymptomatic operculated breaks without fluid do not need treatment. Symptomatic
operculated breaks and those with sub-retinal fluid (either symptomatic or
asymptomatic) need prophylactic treatment.
Clinical Pearl: A subclinical retinal detachment is defined as retinal elevation (or the
presence of subretinal fluid) extending more than one disc diameter beyond the edge of
a break, but not more than 2 disc diameters posterior to the equator.
Clinical Pearl: Subclinical detachments, especially those associated with atrophic holes in
lattice, tend to be asymptomatic.
Clinical Pearl: Flap tears are difficult to identify as the retinal flap frequently covers the
break, thus hiding the disturbed retina.
Retinoschisis:
 The splitting of the retina into an inner and outer layer.
 Results from the coalescence of microcystoid degeneration of the peripheral retina.
 Etiology is inadequate nutrition from the choroid causing retinal cellular degeneration of the
peripheral retina.
 Can appear as a shallow or bullous elevation of the inner layers of the retina from the ora
serrata to the equator
 Inner layer is thin and transparent and contains retinal blood vessels. Shadows cast on the
outer retina by the vessels are diagnostic of schisis.
 Inner surface has Gunn dots: insertion of footplate of Muller cells into ILM.
 Present in 3.5% of general population
 72% are in the inferiotemporal quadrant while 28% are superiotemporal. It does not (seem
to) occur anywhere else. Bilaterality in 82% of cases.
 Retina immediately outside schisis is normal. Results in a sharp border field defect whereas
detachment has more gradual border
 Inner layer holes are present in nearly all cases, but only 3% show double layer breaks.
Danger of detachment occurs in double layer breaks because liquid vitreous can gain access
to schisis cavity and then wash beneath retina.
 Risk of detachment in retinoschisis with double layer holes: 0.25%-1.4%
 Risk of detachment in eyes with schisis: 0.024%
 Progression rate of retinoschisis is very slow.
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Do not treat retinoschisis unless progressive retinal detachment is present simultaneously
or macula is threatened.
Differential Diagnosis: Retinal Detachment vs. Retinoschisis
 Schisis has sharp border field defect- RD has graduated border
 Schisis has transparent inner layer- RD is translucent
 RD has demarcation line- schisis doesn't
 RD is undulated and uneven- schisis is smooth
 Rhegmatogenous retinal detachment often has fixed folds
 Fixed folds only occurs in rhegmatogenous retinal detachment
Management of Rhegmatogenous Retinal Detachment:
1. Scleral buckling procedure- most common
 Primary procedure
 Inciting break is treated with cryoretinopexy
 Subretinal fluid is drained through small incision
 Soft silicone sponge or hard silicone band is utilized to indent the eye at the point of
detachment and sutured into place (subtenon’s) in order to reestablish the adhesion
between the sensory retina and RPE
2. Pneumatic retinopexy
 Injection of intravitreal expansive gas bubble (perfluoropropane, C3F8) to achieve reattachment of the retina following cryoretinopexy of the inciting break. Works best for
smaller, superiorly located detachments and requires strict head positioning as forces of
gravity are employed. Main advantage: Office procedure using only local anesthesia
3. Intraocular silicone oil tamponade
 Similar to pneumatic retinopexy except that silicone oil is used rather than expansive gas.
Application is limited and is not frequently used. It is the procedure of choice in
detachments secondary to AIDS-related cytomegalovirus infection.
Clinical Pearl: A retinal detachment with threatens the macula is considered an emergency.
A retinal detachment that already involves the macula is not an emergency and is
barely an urgency. These patients will be treated at the surgeon’s convenience.
Risk Factors and Special Considerations:
Symptomatic vs. Asymptomatic Breaks:
 Photopsia indicates vitreoretinal traction and active forces to wash liquid vitreous (hyaluronic
acid) under break and cause detachment. The presence of photopsia in phakic eyes is the most
significant risk factor for progression.
 Davis 1974:
 Asymptomatic breaks in phakic eyes:
5% progressed
 Symptomatic breaks in phakic eyes:
46% progressed
 Byer 1974:
 Asymptomatic breaks in phakic eyes:
0% progressed
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All symptomatic breaks must be treated.
Location of Breaks:
 Historically, it has always been believed that superiorly located breaks are more dangerous
and have a higher rate of progression to detachment due to gravitational effects.
Unfortunately, this belief is incorrect
 No difference in progression rate for a superiorly or inferiorly located break.
 Superiorly located detachments are, however, more troublesome due to gravitational effects.
Vitreous Hemorrhage Breaks Due to Trauma, and Acute (New) Breaks:
 Vitreous hemorrhage and breaks due to trauma are considered fresh, or of recent origin.
When we see a retinal break on routine fundus examination, we know that the break has
existed for some time without detaching, thus has a "track record” for remaining attached. A
recent onset break has no such "track record" for staying attached and popular thinking
dictates that these breaks be treated immediately. Acute retinal breaks typically progress to
detachment within 6 weeks.
 Byer (1998)
 Total risk of retinal detachment following occurrence of acute retinal tear: 52%- needs
treatment
Treat all breaks associated with hemorrhage and of recent origin.
Pigment Demarcation Lines and RPE Hyperplasia:
 Retinal breaks and detachment damage the retina and may affect RPE
 In reaction to the damage, the RPE becomes hyperplastic and invades the retina surrounding
the break, thus creating a seal preventing liquid vitreous from washing under the retina and
causing detachment.
 Pigment surrounding a break or detachment indicates a long-standing condition (> 3 months)
 Pigment reduces the risk of progression
Clinical Pearl: The presence of pigment surrounding a retinal break makes the break
inherently less dangerous.
Clinical Pearl: Symptoms in the form of photopsia is the most significant risk factor for the
progression to rhegmatogenous retinal detachment.
Vitreoretinal Tufts:
 Vitreoretinal adhesion of unknown origin
 Grayish white mounds of tissue in peripheral retina, most commonly in inferior-temporal
region; cause of peripheral opercula
 Risk of tuft detachment from vitreoretinal: < 1%: no treatment
Fellow eyes:
 Fellow eye: undetached counterpart of any eye that has previously undergone a retinal
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detachment.
11 % of fellow eyes experience a retinal detachment. Prophylactic treatment of fellow eyes
reduces the incidence of detachment to 3%
Treatment of all breaks in fellow eyes is indicated.
Miotics:
 Popular thinking states that those eyes that are using miotics for glaucoma are undergoing
unusual stretching and traction. It is felt that breaks in eyes that are on miotics should be
treated promptly, regardless of other factors. Miotics have been implicated in the
development of breaks and detachment in previously normal eyes.
Myopia:
 Lifetime risk for RD > (-) 5.00: 2.4% (Overall average: 0.06%)
 Weak consideration
Complications of Prophylactic Therapy
 Only 95-98% successful in preventing detachment. Untreated, many breaks have better
prognosis. Also, breaks have been seen to form in areas that are considered "normal". Thus,
treatment would not prevent those breaks and detachments.
 Macular pucker/ epiretinal membrane formation - 3%
 Tears and detachments in and posterior to treated areas
 Detachment due to inadequate sealing
 Treatment induces vitreous shrinkage which induces tears and detachment
 Penetration of the globe during anesthesia for cryoretinopexy
Clinical Pearl: Complication and success rate are equal for both cryoretinopexy and laser
photocoagulation. Choice of modality depends upon the location of the break.
Anteriorly located breaks are more easily reached with cryoretinopexy while
posteriorly located breaks are more easily reached with laser.
Clinical Pearl: When encountering retinal breaks and degenerations that have a potential
for progression to retinal detachment, the patient should be educated about the signs
(flashes, floaters) and symptoms (vision loss, onset of floaters). However, be aware that
atrophic holes often are asymptomatic when they progress to retinal detachment, as
there is no traction exerted.
Do Not Treat:
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Lattice degeneration (without a history of lattice-related RD)
Atrophic holes in or out of lattice degeneration
Asymptomatic flap tears without fluid
Asymptomatic flap tears without PVD
Asymptomatic operculated breaks without fluid
Retinoschisis (unless macula is threatened)
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Atrophic holes in lattice with fluid (unless the fellow eye has detached for this reason)
Treat:
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Any symptomatic break
Any break with an associated subclinical detachment (fluid), except atrophic holes in lattice
unless it is also in a fellow eye which detached for this reason
Breaks in fellow eyes (except atrophic holes in lattice without fluid)
Breaks planned cataract extraction eyes
Any break associated with trauma
Any break with vitreous hemorrhage
Any tractional break of recent origin
Any break in eyes on miotic therapy
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