References

1.What is retinal detachment?

Retinal detachment (RD) is separation of the neurosensory retina from the underlying retinal pigment epithelium with accumulation of fluid in the potential space between the two layers. The types of retinal detachment include rhegmatogenous, tractional, and exudative.

•In rhegmatogenous retinal detachment (RRD), a break in the retina allows fluid from the vitreous cavity access to the potential space between the retina and the retinal pigment epithelium.

•Tractional retinal detachment occurs when epiretinal tissue forms and contracts, pulling the retina away from the pigment epithelial layer. Occasionally the severe traction caused by epiretinal membranes may cause a tear in the retina, creating a combined rhegmatogenous–tractional detachment.

•Exudative retinal detachment is produced by retinal and choroidal conditions that damage the blood–retina barrier and allow fluid to accumulate in the subretinal space (the potential space between the retina and the retinal pigment epithelium).

2.What are the major characteristics of each type of retinal detachment?

•Rhegmatogenous retinal detachments typically have a corrugated appearance caused by intraretinal edema (Fig. 48-1). Obviously, they are associated with a retinal break, although in a small percentage of cases the break is not easily identifiable. Decreased intraocular pressure, pigmented cells in the vitreous cavity, and vitreous hemorrhage are also associated with RRDs. Fixed folds and other signs of proliferative vitreoretinopathy (PVR) strongly suggest an RRD. Extension of fluid through the macula is a poor prognostic sign. The intraocular pressure is usually low.

•Tractional retinal detachments are characterized by a smooth and stiff-appearing retinal surface. In most cases the epiretinal membranes that cause the traction may be ophthalmoscopically observed. The detachment is usually concave toward the front of the eye. The most common location of the tractional membranes is in the postequatorial region; the traction detachment rarely extends to the ora serrata.

•Exudative retinal detachments are characterized by shifting subretinal fluid. The subretinal fluid accumulates according to gravitational forces and detaches the retina in the area where it accumulates. Thus, the fluid is noted to shift when the patient is viewed in an upright compared with a supine position. The surface of the retina is usually smooth in exudative detachments, compared with the corrugated appearance of an RRD. Occasionally the retina may be seen directly behind the lens in exudative detachments. This rarely occurs in RRDs, unless severe vitreoretinal traction is present.

Figure 48-1.  Bullous rhegmatogenous retinal detachment with mobile, corrugated appearance.

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3.What are the major causes of exudative retinal detachments?

The major causes of exudative RDs are intraocular tumors, intraocular inflammatory diseases, and congenital abnormalities. Intraocular neoplasms, such as choroidal melanomas, choroidal hemangiomas, and metastatic choroidal tumors, are most likely to produce serous RDs. Intraocular inflammation, such as posterior scleritis, Harada’s disease, severe posterior uveitis, and central serous chorioretinopathy, occasionally produce shifting subretinal fluid. The most common congenital abnormalities known to produce exudative RDs are optic pits, nanophthalmos, and the morning glory disc syndrome.

4.How does the retina remain attached?

The retinal photoreceptors and retinal pigment epithelial (RPE) cells are oriented with the apices of the cells in apposition. An interphotoreceptor matrix between the cells forms a “glue” that helps to maintain cellular apposition. It also has been postulated that the RPE functions as a cellular pump to remove ions and water from the interphotoreceptor matrix, providing a “suction force” that helps to keep the retina attached.

5.What are the major predisposing factors for rhegmatogenous retinal detachments?

The main predisposing factors for RRDs are previous cataract surgery, lattice degeneration, and myopia. The incidence of RRD after cataract surgery is approximately 2 in 1000. The incidence becomes much higher after complicated cataract surgery, including posterior capsule rupture, vitreous loss, and retained lens fragments. Some studies have shown an incidence of RRD after complicated cataract surgery as high as 15%. Currently, approximately half of all primary RRDs occur in patients with a history of cataract surgery.

Lattice degeneration (Fig. 48-2) is a peripheral retinal degeneration characterized by thinning of the retina with liquefaction of the overlying vitreous, which results in a high risk for retinal tears and breaks. Lattice degeneration is found in 6% to 7% of the population and is often bilateral. Lattice degeneration is the direct cause of primary RRD in approximately 25% of eyes.

High myopes have a high risk of RD for several reasons. First, the incidence of lattice degeneration is higher in myopes. Second, myopes tend to have a higher rate of posterior vitreous detachment. Of greater importance, myopic eyes have a higher rate of retinal breaks because of the thin peripheral retina. The rate of retinal breaks tends to be higher with increasing myopia.

6.What are the signs and symptoms of a retinal break?

Flashes and floaters are the classic symptoms. Pigmented cells or blood in the vitreous strongly suggests the possibility of a retinal break.

7.What are the types of retinal breaks?

•Horseshoe tear: A flap of retina created by vitreous traction gives the appearance of a horseshoe. The open end of the horseshoe is anterior. A retinal vessel may bridge the gap of the tear (Figs 48-3 and 48-4). The risk of subsequent RD is high, especially with acute tears.

•Operculated tear: When a piece of retina is completely torn away by vitreous traction, the fragment is seen floating over the retinal defect. The risk of RD is lower than with a horseshoe tear.

Figure 48-2.  Lattice degeneration.

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Figure 48-3.  Horseshoe retinal tear with a bridging vessel.

Figure 48-4.  Horseshoe retinal tear after laser photocoagulation.

•Atrophic hole: A round hole without evidence of retinal traction is often associated with lattice degeneration. The risk of RD is low.

•Dialysis (Fig. 48-5): A disinsertion of the retina at the ora serrata, this is most common in the inferotemporal quadrant. The second most common site is superonasal. A frequent cause is trauma.

KEY POINTS: SYMPTOMS AND SIGNS OF RHEGMATOGENOUS RETINAL DETACHMENT

1.Flashes

2.Floaters

3.Pigment in the vitreous

4.Posterior vitreous detachment (usually)

5.Elevated mobile retina

6.Corrugations

7.Loss of retinal transparency

8.Presence of a retinal break

9.Retinal pigment epithelial alterations under detachment, i.e., a demarcation line

10.Fixed folds

11.Peripheral visual field loss

12.Loss of central vision (with macular involvement)

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Figure 48-5.  Retinal detachment resulting from inferotemporal dialysis.

8.What are the signs of a chronic rhegmatogenous retinal detachment?

The retina is more transparent than in an acute RD, and the corrugations are minimal or absent. Pigmentary alterations are more prominent, including hyperpigmented demarcation lines (indicative of progression if multiple), RPE atrophy in the bed of the detachment, and abundant pigment in the vitreous. Retinal cysts, sometimes very large, may develop. The causative retinal break may be difficult to identify. PVR may also be present. The intraocular pressure may be low, normal, or high.

9.What is degenerative retinoschisis?

Sometimes called senile retinoschisis, this is a dome-shaped elevation of the inner retina caused by a splitting within the outer plexiform layer. In contrast to an RRD, this rarely progresses and is usually observed. Occasionally, outer wall holes will form and create a progressive retinoschisis-related RRD. The inferotemporal quadrant is most commonly affected, and 80% are bilateral.

KEY POINTS: SIGNS OF CHRONIC RETINAL DETACHMENT VERSUS RETINOSCHISIS

1. Presence of retinal break most reliable method to distinguish the two but is often difficult to find 2. Pigment in the vitreous

3. Pigment alterations in the retinal pigment epithelium

4. Retinal folds

5. Absence of schisis in the fellow eye

10.What are the options for repair of retinal detachment?

First, determining the type of RD is important before identifying the modality of treatment. Exudative RDs are approached differently compared to rhegmatogenous or traction detachments. Exudative detachments are repaired by treating the primary cause of the fluid extravasation into the subretinal space. For example, an RD associated with choroidal melanoma is addressed by treating the tumor with radiation, thermotherapy, or resection. Exudative RDs related to intraocular inflammatory conditions are generally treated by aggressive anti-inflammatory regimens. Rarely does an exudative detachment require primary surgical repair.

On the other hand, treatment of rhegmatogenous and tractional RD is primarily surgical. Tractional RDs caused by diabetes or proliferative vitreoretinopathy require relief of all traction membranes before the retina will remain reattached.

Small, localized RRDs are usually treated by cryotherapy or barrier laser photocoagulation. Rarely, an asymptomatic localized detachment may be treated with close observation only. If significant vitreous traction is present on the retinal tear, especially if the tear is superior in location, or if a large amount of subretinal fluid is found, more definitive treatment is usually indicated. Options include pneumatic retinopexy, Lincoff balloon, scleral buckling, and pars plana vitrectomy. Scleral buckling surgery is the time-honored approach and has been applied routinely since the 1950s. Pars plana

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vitrectomy was first performed in the late 1960s and has become the operation of choice for some surgeons. Pneumatic retinopexy has gained popularity since the early 1980s.

11.What is pneumatic retinopexy?

To perform a pneumatic retinopexy, an inert gas or sterile air is injected into the vitreous cavity. Strict positioning is required to place the gas bubble in contact with the retinal break. If the break is closed by the surface tension from the gas bubble, the retinal pigment epithelium can pump the subretinal fluid back into the choroid and allow the retina to reattach. The break is sealed either with cryotherapy at the time of gas injection or with laser photocoagulation after the retina is flattened.

12.Which patients are the best candidates for pneumatic retinopexy?

The ideal candidates are patients with a detachment caused by a single retinal break in the superior eight clock hours or multiple breaks if all of the tears are within one to two clock hours of one another. Obviously the patient must not have a systemic disease or mechanical problem that precludes the positioning requirements. Phakic patients tend to fare slightly better than patients with a history of cataract surgery.

13.Which patients are poor candidates for pneumatic retinopexy?

Patients with RDs caused by multiple tears in several locations are poor candidates, as well as patients with a detachment resulting from a single tear but with tears in other areas of attached retina. Proliferative vitreoretinopathy, especially if fixed folds are present, lessens the chances for reattachment with pneumatic retinopexy. And, as previously stated, patients who are unable to obey the strict postoperative positioning requirements are poor candidates.

KEY POINTS: FACTORS THAT INFLUENCE THE DECISION TO TREAT RETINAL BREAKS PROPHYLACTICALLY

1. Type of break.

2. Presence of symptoms of vitreoretinal traction.

3. Horseshoe tears are usually treated, especially if symptomatic. 4. Operculated tears are generally not treated unless symptomatic. 5. History of retinal detachment in the fellow eye.

6. Family history of retinal detachment.

7. Anticipated prolonged inaccessibility to care.

14.What are the advantages of scleral buckling and pars plana vitrectomy?

Scleral buckling and pars plana vitrectomy reduce vitreous traction mechanically. Scleral buckling involves the surgical placement of a silicone band or sponge, either sewn to the sclera as an exoplant or implanted in the sclera after a partial-thickness scleral bed is surgically created (Fig. 48-6). Scleral buckles provide smooth, broad relief of vitreous traction. Subretinal fluid may be drained at the time of placement of the scleral buckle via an external sclerostomy, and intraocular gas may be injected into the vitreous cavity as an adjunct to aid in retinal reattachment. Scleral buckles are especially effective in anterior retinal breaks. This is the most common site for postcataract retinal breaks. Another advantage of scleral buckling is the opportunity to repair the RD from a purely external approach with no intraocular invasion.

With vitrectomy, it is possible to relieve vitreous traction directly with the vitrectomy cutter. This technique is especially useful in cases with very posterior breaks. Vitrectomy is advantageous in cases of RD with vitreous hemorrhage or vitreous opacities that obscure a view of the retinal breaks. Vitrectomy also allows the surgeon to remove epiretinal membranes when proliferative vitreoretinopathy is present. When vitrectomy is performed, the vitreous cavity must be filled with gas to reattach the retina. The presence of intravitreal gas hastens the development of cataract in phakic patients.

15.What are the major risks and complications with scleral buckling and pars plana vitrectomy?

Risks of infection and hemorrhage are found with any invasive ocular procedure. The risk of an infection with a scleral buckle is less than 3%. Other risks and complications from scleral buckles include angle-closure glaucoma, acute glaucoma from intraocular gas injection, intraocular hemorrhage from

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perforation during drainage of subretinal fluid, and anterior-segment ischemia and necrosis. The surgically placed buckles may cause extrusion or intrusion over time, and, if the buckle is placed under an extraocular muscle, strabismus may result.

Vitrectomy involves the risks of endophthalmitis, iatrogenic retinal breaks, retinal or vitreous incarceration in the sclerostomy sites, and glaucoma from the use of intraocular gases.

16.What intraoperative findings should be confirmed at the time of scleral buckle placement?

The most important intraoperative decisions at the time of scleral buckling procedures are to find and treat all retinal tears and place the scleral buckle in a position to support all retinal breaks. After the buckle has been temporarily placed, the surgeon should confirm that the tears are flat on the buckle. If the tears are not flat, the placement of the buckle should be checked with scleral depression. If the buckle is in the appropriate position but fluid still exists between the retina and the buckle, the decision to drain subretinal fluid or to inject an intravitreal gas bubble should be made. If the detachment is primarily inferior in location, most surgeons prefer to have the retina completely attached before leaving the operating room. Superior detachments may flatten with gas injection and postoperative positioning; the decision to drain subretinal fluid adds potential complications.

17.What three factors should be confirmed with indirect ophthalmoscopy at the conclusion of scleral buckling surgery?

Apposition of the scleral buckle to the retinal breaks, absence of complications at the drainage site, and absence of central retinal artery pulsations should be confirmed before final closure. If pulsations are present, the intraocular pressure is high enough to cause a central retinal artery obstruction. The pressure should be lowered by loosening the buckle, removing intraocular fluid or gas until pulsations are no longer seen.

18.How should cases of rhegmatogenous retinal detachment be approached if pars plana vitrectomy is the chosen treatment?

Vitreous traction on all retinal breaks should be relieved if possible. Care must be taken to avoid damaging retinal blood vessels if they are coursing across the retinal tears. A complete posterior vitreous detachment and meticulous removal of peripheral vitreous should be ensured using wide-field illumination. All retinal tears should be treated completely with laser.

19.Which gases may be used inside the eye? In what concentrations?

The inert gases sulfur hexafluoride (SF6) and perfluoropropane (C3F8), along with sterile air, are the most commonly used intraocular gases. Nonexpansile mixtures are composed of approximately 20% sulfur hexafluoride and 14% perfluoropropane. These are the most commonly used mixtures when the vitreous cavity is filled with gas, as in vitrectomy. Pure 100% gas injection allows a larger bubble to form with a smaller volume of injection. This technique is advantageous in patients with pneumatic retinopexy and scleral buckles. Typically, sulfur hexafluoride expands to two to three times its initial volume, and perfluoropropane expands to approximately four times its initial volume. Thus, injection of 0.4 mL of each gas produces a 20% to 40% intravitreal gas bubble when they are injected as a pure concentration.

A B

Figure 48-6.  Placement of a scleral buckle. A, Rhegmatogenous retinal detachment. B, The retina is attached after placement­ of a scleral buckle supenaly.

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Figure 48-7.  Severe proliferative vitreoretinopathy with total retinal detachment.

Figure 48-8.  Proliferative diabetic retinopathy causing localized tractional retinal detachment.

20.What are the primary causes of failure of initial retinal detachment repair?

Except for cases of severe PVR, in which epiretinal membranes cause traction retinal detachments (Fig. 48-7), failures of RD repair are caused by an open retinal break. With pneumatic retinopexy, the most common reasons for failure include poor patient compliance with positioning requirements, inadequate identification of all retinal breaks, and development of new retinal tears from vitreous traction related to intravitreal gas. After scleral buckling surgery, failure to flatten the retina or to keep it attached results most often from undetected retinal breaks; continued vitreous traction with new, extended, or reopened retinal breaks; or a misplaced scleral buckle. Inadequate photocoagulation, continued vitreous traction, and new or missed breaks are the most common reasons for failure after pars plana vitrectomy. Ten percent of retinal reattachments have evidence of PVR. However, only 10% to 25% of these progress to require treatment for detachment.

21.What are the major objectives in repair of tractional retinal detachment?

When tractional retinal detachments are caused by proliferative diabetic retinopathy (Fig. 48-8), one of the major aims is to relieve all anteroposterior traction. A complete posterior vitreous separation must be created to remove or segment all retinal traction. Segmentation of diabetic tractional membranes is effective if no anterior traction remains (Fig. 48-9). Delamination of traction membranes is accomplished by carefully identifying the plane between the epiretinal tissue and the retina and by lysing all adhesions. In advanced PVR, retinal traction may be so severe that the retina must be cut to relieve all retinal traction. In cases with such severe traction, especially when a retinotomy must be created, silicone oil is often useful as a long-acting tamponade. The silicone oil is usually removed after 3 to 6 months but may be left in place longer if the retina appears unstable.