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was not reported. The literature regarding the value of treating round holes unassociated with lattice lesions is not clear. Treatment can be expected to prevent retinal detachment resulting from the identified break but not detachment resulting from breaks in other areas of the retina. Treatment of asymptomatic horseshoeshaped tears in aphakic fellow eyes and in fellow eyes scheduled to undergo cataract extraction is usually recommended, despite the absence of supportive data.

Asymptomatic nonphakic eyes with a history of giant retinal tear in the fellow eye

Aphakic fellow eyes in nontraumatic giant retinal tear cases have a high risk of retinal detachment. Prophylactic therapy has been recommended for fellow eyes of these patients, particularly if significant vitreous liquefaction and progressive “white-with-pressure” are observed.

TREATMENT TO PREVENT RETINAL DETACHMENT

Photocoagulation, cryotherapy, diathermy, and, in certain rare instances, scleral buckling have all been used for prophylactic treatment of retinal breaks without detachment. The choice of treatment technique depends on the surgeon’s experience and the availability of equipment. The laser indirect ophthalmoscope (LIO) with scleral indentation has become a frequent choice where this equipment is available. Alternatively, far anterior tears can be treated with cryotherapy, and more posterior tears can be treated with photocoagulation using a slit-lamp laser with a mirrored contact lens. Diathermy is infrequently used at present because of the need for conjunctival peritomy, but good results can be obtained with it.

CRYOTHERAPY

Tanks of compressed gas are connected to a pressure regulator, and tubing directs the gas under pressure to the cryoprobe. The gas is allowed to expand at the tip of the cryo probe, which causes the probe to freeze. When the probe is pressed onto the scleral wall, the freeze will extend into the interior of the eye and achieve the desired thermal burn in the retina and retinal pigment epithelium. Cryotherapy can also be applied directly to the retina through the interior of the eye during vitrectomy, although this practice has rarely been employed since the development of contemporary laser equipment and techniques.

Good anesthesia is obtained by supplementing topical 4% lidocaine with an injection of subconjunctival 1% or 2% lidocaine in the involved quadrants. Retrobulbar anesthesia may be necessary in some patients, but the patient then loses the ability to position the eye in accordance with the surgeon’s instructions.

To apply cryotherapy for a retinal break near the ora, the surgeon instructs the patient to move the eye in the direction of the break. Breaks near the equator are most easily indented with the cryoprobe when the eye is approximately in the primary position. Breaks posterior to the equator can often be reached with the cryoprobe if the patient is instructed to move the eye away from the meridian of the

Figure 6–5. Prophylactic treatment should be limited to flat retina and extend only to the margin of the subretinal fluid.

break and slightly toward the surgeon, who is positioned in the meridian opposite that of the break. More posterior lesions can be reached by a small incision in the conjunctiva but are more easily treated by laser.

A number of applications should be used to surround the break completely with an adequate margin, and treatment of horseshoe tears should extend anteriorly into the vitreous base (Figure 6–5). Treatment should be limited to flat retina and extend only to the margin of the subretinal fluid. Freezing of the exposed pigment epithelium within the tear should particularly be avoided, because this will encourage the migration of retinal pigment epithelial cells into the vitreous cavity. In a patient with lattice degeneration, the treatment should include not only the lattice patch but also adjacent normal retina on all sides of the patch.

If there is significant subretinal fluid associated with the break(s), the patient is generally restricted in activities until some pigmentation appears around the focal detachment; this generally occurs within 7 to 10 days. Extension of subretinal fluid before an effective chorioretinal adhesion develops may be more common following cryotherapy than after laser photocoagulation, because the adhesion forms more quickly after laser.

LASER PHOTOCOAGULATION

For various reasons (including the more rapid development of an adhesive reaction and avoiding any liberation of viable retinal pigment epithelial cells), laser therapy has become a more popular means of creating an adhesion. A laser photocoagulator provides an excellent viewing system, with either the laser indirect ophthalmoscope (LIO) or the binocular biomicroscope and slit lamp used in association with

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Figure 6–6. Laser burns surrounding a retinal tear and focal retinal detachment.

the Goldmann three-mirror or panfunduscopic contact lens. The appropriate end point for these lesions is the development of a dull white reaction within the retina (Figure 6–6). The entire retinal break should be surrounded by a series of photocoagulation lesions, and treatment should be extended into the vitreous base with flap tears.

RESULTS OF TREATMENT

The efficacy of prophylactic treatment obviously depends on the relative risk of detachment before and after treatment. If a retinal detachment ensues within a few days of a prophylactic procedure, it might be argued that the treatment actually precipitated the detachment. But the detachment could very well be due to progression of the disease despite treatment. If the detachment develops several weeks later, it is more likely due to the ongoing, progressive nature of the basic vitreoretinal disease, and is not to be regarded as an iatrogenic complication. While some detachments are caused by the treated breaks, in most cases detachment subsequent to treatment is due to a new break in a different meridian.

Reports of prophylactic therapy results are all somewhat incomplete, as most do not describe information about important variables, including the refractive error, the status of the crystalline lens, the status of the posterior vitreous surface, the type of retinal breaks, and whether there had been a detachment in the fellow eye. In addition, long-term follow-up information is lacking in most reports. In one important study, it was demonstrated that new retinal breaks continued to occur long after the initial prophylactic therapy. In symptomatic eyes that were treated, new retinal breaks were observed in 13% of cases after 3 months, and in 21% of cases 2 years postoperatively. The outcomes in this report were not stratified as a function of the type of retinal break. Another study demonstrated that most detachments that occurred after prophylactic therapy were associated with progression of an incomplete initial PVD.

Flap tears

Horseshoe-shaped tears are most responsible for clinical retinal detachment. Symptomatic horseshoe-shaped tears are much more likely to cause retinal detachment than are asymptomatic tears, but many studies have not distinguished between these groups. However, failure of treatment appears to be more common following therapy of symptomatic cases. Early failures usually are due to vitreoretinal traction forces that cause an accumulation of subretinal fluid before the establishment of an adequate chorioretinal adhesion, or are due to incomplete or inadequate therapy. Treatment should be placed in flat retina immediately adjacent to the location of subretinal fluid, and treatment should extend well anterior to the “horns” of the tear and into the vitreous base.

Lattice degeneration

There are many difficulties in analyzing results of treatment of lattice degeneration, as mentioned earlier. Most new tears following therapy occur in areas not previously treated.

Retinal holes

The prognosis for round holes after treatment is substantially better than that for flap tears with persistent vitreoretinal traction. As noted earlier, round holes unassociated with persistent vitreoretinal traction or with lattice degeneration are usually not treated.

Patients with previous retinal detachment in the fellow eye

Fellow eyes of patients with retinal detachment in a first eye have a substantial risk of retinal detachment, and the risk is even higher after cataract extraction. Aphakia and pseudophakia appear to be statistically significant risk factors for failure after prophylactic therapy for retinal breaks, and treatment of the visible lesions in these cases does not appear to prevent many retinal detachments.

COMPLICATIONS OF TREATMENT

Retinal detachments that occur despite prophylactic therapy are a result of either inadequate adhesion around a retinal break or a new retinal break. Extension of the detachment is considered a complication of therapy if the treatment is inadequate in extent or intensity, and a particularly common cause of failure in treating horseshoe-shaped tears is the absence of an adequate chorioretinal adhesion surrounding the anterior margins of the break, where vitreoretinal traction persists.

New retinal breaks are a complication of prophylactic therapy if the treatment causes excessive damage to the retina, resulting in a break at that location, or if it aggravates vitreous degenerative changes and vitreoretinal traction, causing a tear elsewhere.

Epiretinal proliferation that causes macular pucker has been considered a potential complication of prophylactic therapy, but the association between treatment and membrane formation is uncertain. Symptomatic retinal tears are almost always due to a posterior vitreous detachment, and a PVD is present in more than