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Chapter 135 – Retinal Breaks

Chapter 135 – Retinal Breaks

 

CRAIG M. GREVEN

 

 

 

 

 

DEFINITION

• A full-thickness defect in the neural retina.

 

KEY FEATURES

• A round, oval, or horseshoe-shaped defect.

• Typical location near the vitreous base, but can occur anywhere.

• Subcategories are holes, tears, or dialyses.

 

ASSOCIATED FEATURES

• Pigmented cells in the vitreous (tobacco dust).

• Vitreous traction.

• Vitreous hemorrhage.

• Pigmentary changes in the adjacent retina.

• Localized abnormal vitreoretinal interface (lattice degeneration).

 

 

 

INTRODUCTION

Retinal breaks are full-thickness defects in the neurosensory retina. Although they typically occur in the equatorial and ora serrata regions of the retina, such defects can develop more posteriorly. Peripheral retinal breaks alone do not cause loss of vision, but the associated conditions of vitreous hemorrhage and rhegmatogenous retinal detachment can culminate in severe visual loss. The first goal in the management of retinal breaks is to differentiate those that are not likely to cause severe visual sequelae from those that are more likely to lead to visual loss and retinal detachment. In this chapter the identification of “high-risk” retinal breaks is discussed and appropriate management strategies are suggested.

EPIDEMIOLOGY AND PATHOGENESIS

The pioneering works of ophthalmic giants such as deWecker, Leber, and Gonin pointed out the significance of retinal breaks in the pathophysiology of rhegmatogenous retinal detachment. The importance of prophylaxis of retinal breaks to help prevent detachments became popular after the introduction of the binocular indirect ophthalmoscope.

The incidence of retinal breaks at autopsy in individuals over 20 years of age is in the range 6–11%.[1] [2] The prevalence of retinal breaks in clinical series of routine patients aged 10 years or more with no known antecedent ocular disease is in the range 6–14%. [3] [4] The annual incidence of retinal detachment is approximately 12 per 100,000 population per year.[5] [6] From these data, it is intuitive that the majority of retinal breaks do not lead to retinal detachment. Therefore, it has been the goal of clinicians to determine which breaks may benefit from prophylaxis.

The occurrence of retinal breaks is age dependent, with increasing incidence accompanying increasing age. However, no statistical difference exists between men and women in the incidence of retinal breaks.[1] [3] The prevalence of retinal breaks in myopic eyes is similar to that in eyes of the general population, about 11%.[7] However, myopes account for 42% of all phakic retinal detachments, and, therefore, myopia is considered a risk factor for retinal breaks that lead to retinal detachment. [8]

Lattice degeneration of the retina is another risk factor for the development of a retinal break. Lattice degeneration is a condition in which peripheral retinal thinning is associated with liquefaction and separation of the overlying vitreous. A pronounced vitreoretinal adhesion occurs at the margin of lattice lesions. Lattice is present in 11% of autopsy cases, occurs equally in men and women, and increases in incidence with increasing age.[9] It is a bilateral condition in nearly 50% of cases, and approximately 25% of affected eyes have associated retinal breaks.

Ocular contusion and penetrating trauma also increase the risk for development of a retinal break. The most common type of retinal break after ocular contusion injuries is a retinal dialysis.[10] [11] Penetrating trauma may cause retinal breaks immediately at the time of impact, because of direct retinal trauma, or as a result of later vitreous traction on the peripheral retina.

OCULAR MANIFESTATIONS

Retinal Tears

Retinal tears are full-thickness breaks that occur secondary to vitreous traction. The most common inciting vitreous traction is spontaneous posterior vitreous detachment (PVD). These horseshoe or flap-shaped tears occur at sites of strong vitreoretinal adhesion, most commonly at the vitreous base. The posterior edge of the tear is its apex, and the anterior extensions are its base ( Figs. 135-1 and 135-2 ). Symptoms associated with acute retinal horseshoe tears include floaters secondary to vitreous debris (hemorrhage, retinal pigment epithelium cells) and flashes that result from persistent vitreous traction.

Firm vitreoretinal adhesions are present at the margins of lattice degeneration. When a PVD occurs, traction at the margin of the lattice degeneration can lead to retinal tears. These tears typically occur at the posterior margin or posterior lateral margin of a patch of lattice.

Round Holes with Opercula

Horseshoe or flap tears with persistent traction often avulse the base of the tear to leave a small, round defect in the neural retina with an overlying operculum of retinal tissue. This generally indicates complete relief of vitreoretinal traction in this area ( Fig. 135-3 ).

Round Holes without Opercula (Atrophic Holes)

Atrophic holes in the retina occur secondary to retinal thinning. Vitreous traction is not the pathogenic mechanism of atrophic retinal holes. Although these can occur in isolation, they often present within areas of lattice degeneration.

Traumatic Retinal Breaks

Blunt trauma to the globe can induce many varieties of retinal breaks, which include horseshoe tears, retinal dialysis, and macular

 

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Figure 135-1 Symptomatic acute, superotemporal horseshoe tear anterior to the equator in the right eye. A, At presentation. Note the hemorrhage at its margins. B, The same eye 1 week after cryopexy. Note the affectation of retinal pigment epithelium adjacent to the tear.

 

 

Figure 135-2 Symptomatic inferior horseshoe tear 6 weeks after cryopexy.

holes. The major mechanism of peripheral break formation is hypothesized to be compression of the globe with subsequent distortion and expansion at the area of the ora serrata and equator. This expansion produces an acute increase in vitreoretinal traction, which often results in a retinal dialysis.[11] Traumatic retinal dialyses most commonly occur inferotemporally and superonasally. [12] They can occur at the anterior margin of the vitreous base in the pars plana, at the junction of the ciliary epithelium and neural retina, or in the retina at the posterior margin of the vitreous base. Occasionally, a “ribbon” of avulsed vitreous base is seen adjacent to a dialysis. This finding is considered diagnostic of previous trauma. Direct contusion injury to the globe can lead to disruption of the retina and necrotic breaks. The retinal defects are typically irregular and located in the region of the vitreous base.

 

 

 

 

 

 

Figure 135-3 Symptomatic operculated hole. A, At presentation. B, Immediately after laser treatment. C, 1 month postoperatively. Operculum is best seen in C.

Macular Breaks

Macular holes occur secondary to tangential traction on the retina from the precortical vitreous. They also are well-recognized sequelae of blunt trauma. A more complete discussion of macular holes is presented in Chapter 128 .

DIAGNOSIS AND ANCILLARY TESTING

With clear media, the diagnosis of retinal break is straightforward. In the setting of cloudy media, ultrasonography helps to rule out associated retinal detachment. In some cases, experienced ultrasonographers are able to detect the presence of larger retinal breaks in attached retina when cloudy media prevents direct observation.

DIFFERENTIAL DIAGNOSIS

Many conditions exist in the peripheral fundus that can mimic full-thickness retinal breaks. Obstacles to an accurate diagnosis being made include inadequate pupillary dilatation, cataract, anterior and posterior capsular opacities in pseudophakic eyes,

 

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Differential Diagnosis of Retinal Breaks

 

 

Pars plana cysts

Paving-stone degeneration

Enclosed oral bays

Chorioretinal scars

Meridional folds/complexes

Peripheral cystoid degeneration

Ora pearls

White with/without pressure

Granular tags

Retinal erosions

 

 

 

 

 

vitreous opacities, and patient compliance. Binocular indirect ophthalmoscopy with scleral depression to see the retina in relief, supplemented by Goldmann three-mirror examination, remains the standard method by which to differentiate these lesions. The differential diagnosis of retinal breaks is given in Box 135-1 . (See Chapter 134 for a more detailed discussion.)

SYSTEMIC ASSOCIATIONS

The majority of retinal breaks occur in patients who have no predisposing systemic association. However, certain systemic conditions, such as Marfan’s syndrome, Ehlers-Danlos syndrome, and homocystinuria, as well as hereditary hyaloideoretinopathies such as Wagner’s syndrome and Stickler’s syndrome can predispose to retinal break formation (see Chapter 112 ).

TREATMENT

Upon the discovery of a retinal break, the initial decision is whether the benefits of treatment (to prevent retinal detachment) outweigh the risks and cost of treatment. In each case many factors should be considered and the risks and benefits of treatment discussed with the patient. The factors under consideration in each case include the presence or absence of symptoms; age and systemic health of the patient; refractive error of the eye; location, age, type, and size of the break; status of the fellow eye; and whether the patient is aphakic, pseudophakic, or will soon undergo cataract surgery.

The typical symptoms associated with an acute retinal break are new floaters and flashes. These symptoms occur secondary to an acute PVD. Studies have shown that the presence or absence of symptoms in association with the onset of the break is the most important prognostic criterion for progression to retinal detachment.[13] [14] In a prospective follow-up study of 359 asymptomatic retinal breaks in 231 phakic eyes of 196 patients, no clinical retinal detachment had occurred after a minimum of 1 year follow-up.[13] Included in this study were 276 round atrophic holes, 50 tears with attached flaps, and 33 tears with free opercula. In phakic patients who have no previous history of retinal disease or of high myopia and who develop asymptomatic horseshoe tears, atrophic holes, or holes with opercula, prophylactic treatment is rarely indicated. In each case, the patient should be made aware of the symptoms of vitreous traction and retinal detachment and should be instructed on how to assess the peripheral visual field.

In contrast, the rate of retinal detachment in phakic patients who have symptomatic breaks is 35%.[14] Therefore, it is recommended that nearly all acute, symptomatic retinal breaks be treated prophylactically to prevent retinal detachment.

Age and systemic health status of the patient are other variables to be considered in the management of a retinal break. As an example, a superotemporal horseshoe tear in a 27-year-old patient is more likely to cause a subsequent retinal detachment than is one in an 80-year-old patient who has metastatic lung cancer.

Refractive error is another variable to consider in the management of retinal breaks. The increased incidence of retinal detachment in patients who have greater than 6D of myopia may increase the likelihood for treatment of an asymptomatic retinal tear.

The age, location, and size of a retinal break are also considered when its management is determined. Long-standing tears often have retinal pigment epithelial changes adjacent to them. These changes indicate to the clinician the decreased likelihood of retinal detachment. Although no increased incidence of retinal detachment occurs with a retinal break in any particular quadrant, a greater likelihood of a macula-off retinal detachment is present as a result of superotemporal breaks than of either inferior breaks or nasal breaks. Although small retinal breaks can lead to retinal detachment, most ophthalmologists agree that in general larger breaks are more likely to cause a retinal detachment.

The type of break should also be a consideration in whether prophylactic treatment is offered. A horseshoe tear with persistent traction or a retinal dialysis is much more likely to result in a detachment than is an atrophic hole.

Some controversy exists about the management of asymptomatic horseshoe tears in patients who need cataract surgery, in aphakic or pseudophakic patients, and in patients who have retinal detachments in their fellow eye.[15] [16] In general, because of the increased incidence of detachment in these scenarios, strong consideration should be given to prophylaxis in these cases.

Retinal dialyses, whether traumatic or idiopathic, have a high association with the development of retinal detachment. In these cases, prophylaxis is usually indicated.

Asymptomatic holes in lattice degeneration rarely lead to detachment and usually receive no prophylaxis.[17] However, retinal tears at the margin of lattice degeneration, particularly in symptomatic eyes, are more likely to result in the development of a retinal detachment and require prophylactic therapy.

Retinopexy

Two main modalities are utilized in the treatment of retinal breaks—cryopexy and laser photocoagulation. Cryotherapy is delivered transconjunctivally. It destroys the choriocapillaris, retinal pigment epithelium (RPE), and outer retina to provide a chorioretinal adhesion between the tear and the adjacent retina, which prevents liquid vitreous access through the hole and into the subretinal space. The adhesion with cryotherapy is not immediate; 1 week is required to achieve partial adhesion and up to 3 weeks for the full adhesive effects to occur.

Laser photocoagulation treatment of retinal breaks typically utilizes the argon green, argon blue-green, krypton red, or diode laser. No evidence exists that one wavelength is better than another. Two main delivery systems are used, the slit lamp and the indirect ophthalmoscope. In contrast to cryotherapy, chorioretinal adhesion occurs the instant that the laser photocoagulation is applied, but maximal adhesion occurs 7–10 days later.

Often, either of the techniques can be used for successful prophylaxis of retinal breaks. However, certain circumstances dictate which modality is easiest and has the best chance of success. Cryopexy has the advantage of not requiring a perfectly clear media; it can be delivered adequately despite the presence of extensive cataract, anterior or posterior capsular opacity, or relatively dense vitreous hemorrhage. Media opacity can make adequate treatment of retinal breaks by laser nearly impossible.

In general, retinal cryopexy and indirect ophthalmoscopic laser photocoagulation are preferred for anterior retinal breaks because of difficulty in treatment of the anterior margin at the slit lamp. Similarly, posterior breaks are difficult to reach with the cryoprobe unless a conjunctival incision is made. These breaks can be managed more easily with the slit lamp or an indirect laser delivery system. Occasionally, breaks with a large anteroposterior extent require both cryopexy to the anterior and photocoagulation to the posterior margins of the break.

Patients who have a retinal tear and no detachment may have an avulsed retinal vessel with persistent traction and recurrent vitreous hemorrhage. In these cases, scleral buckling or vitrectomy may be necessary to relieve traction and prevent further hemorrhage.[18]

 

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Anesthesia

Eyes that undergo laser photocoagulation with the slit-lamp delivery system can often be treated with topical anesthesia alone. If multiple large breaks are present and the patient is unable to tolerate the treatment, retrobulbar anesthesia may facilitate completion of the procedure.

In patients treated with transconjunctival cryotherapy or indirect laser photocoagulation with scleral depression, topical anesthesia supplemented with cotton-tipped applicators soaked in 4% lidocaine (lignocaine) or 10% cocaine placed on the conjunctiva that overlies the retinal breaks is usually adequate. In some cases, 2% lidocaine injection subconjunctivally via a 30 gauge needle may be necessary. Approximately 0.2?cm3 of anesthetic is necessary per quadrant.

Cryopexy

Under indirect ophthalmoscopic visualization, the cryoprobe is placed on the conjunctiva that overlies the break and cryotherapy is delivered until the retina adjacent to the tear becomes gray-white. Approximately 2?mm of retinal whitening should be obtained around the entire break. Multiple applications are placed until the break is surrounded completely with confluent treatment (see Figs. 135-1 and 135-2 ). An attempt should be made not to treat the choroid and RPE directly beneath the break, especially in large tears, because of disruption and displacement of RPE cells into the vitreous cavity and concerns of macular pucker and proliferative vitreoretinopathy. In horseshoe tears, the anterior retina between the tear and the ora serrata should be treated, as anterior extension of the tear secondary to continuous vitreous traction can lead to retinal detachment.

Photocoagulation

The Goldmann three-mirror lens or panfundoscope lens is used when treatment is with the slit-lamp delivery system. The tear should be surrounded completely by three to four rows of laser burns. Although the spots need not be confluent, there should be no more than half a spot size of untreated retina between burns. Typically, the settings are 200–500?µm spot size and 0.1–0.2 seconds application at the power necessary to generate a gray-white burn.

The indirect laser delivery system can also be used to treat retinal breaks. An advantage of this technique is that simultaneous scleral depression allows treatment of anterior tears and even dialysis.

As with cryopexy, care should be taken to treat thoroughly the anterior margin of horseshoe tears to prevent anterior traction that reopens the break.

COURSE AND OUTCOMES

The eye may be patched for a few hours after treatment. If a subconjunctival injection has been utilized, a topical antibiotic corticosteroid preparation may be used for the first 2–3 days. Subsequently, the eye is reexamined after approximately 7 days. Although vigorous patient activity is often discouraged initially, no clinical study has suggested that diminished activity improves treatment results. A firm chorioretinal adhesion is present by 3 weeks after either technique.

Failure rates for prophylactically treated retinal breaks depend on many factors, which include the type of retinal break, indications for treatment, length of follow-up, and definition of failure. Reported failure rates are in the range 0–22%.[19] [20] In one large series of prophylactically treated retinal breaks, 22% of eyes required an additional procedure to prevent or repair a retinal detachment.[20] Retinal detachment occurred in 9% of treated eyes, 4% from the original break and 5% from a new retinal break. A new break without detachment or an inadequate chorioretinal adhesion around the original break that required additional treatment occurred in 14% of eyes. Risk factors for failure in this series included aphakic or pseudophakic status, acute symptoms, retinal detachment in the fellow eye, and male gender. Nearly 90% of eyes treated in this series had a final visual acuity of 20/50 (6/17) or better.

Epiretinal membrane and macular pucker are the most frequent visually significant complications associated with prophylactic treatment of a retinal break; they occur in 1–5% of treated eyes.[20] [21] As epiretinal membranes occur in eyes that have retinal breaks and receive no treatment, it is not entirely clear whether the macular pucker is exacerbated by the treatment modality or is solely a result of the disease process itself.

Additional, more rare, complications that can occur include Adie’s pupil, subretinal and vitreous hemorrhage, and breaks in Bruch’s membrane. An exceedingly rare, but potentially devastating, complication in patients who have staphylomatous sclera and eyes treated with cryotherapy is scleral rupture.

In eyes that fail prophylactic therapy, retinal detachment repair by pneumatic retinopexy, scleral buckling, or vitrectomy is usually successful in the anatomic reattachment of the retina.

 

 

REFERENCES

 

1. Okun E. Gross and microscopic pathology in autopsy eyes. Part III. Retinal breaks without detachment. Am J Ophthalmol. 1961;51: 369–91.

 

2. Foos RY, Allen RA. Retinal tears and lesser lesions of the peripheral retina in autopsy eyes. Am J Ophthalmol. 1967;64:643–55.

 

3. Byer NE. Clinical study of retinal breaks. Trans Am Acad Ophthalmol Otolaryngol. 1967;71:461–73.

 

4. Rutnin U, Schepens CL. Fundus appearance in normal eyes. IV. Retinal breaks and other findings. Am J Ophthalmol. 1967;64:1063–78.

 

5. Haiman MH, Burton TC, Brown CK. Epidemiology of retinal detachment. Arch Ophthalmol. 1982;100:289–92.

 

6. Wilkes SR, Beard CM, Kurland LT, et al. The incidence of retinal detachment in Rochester Minnesota, 1970–1978. Am J Ophthalmol. 1982;94:670–3.

 

7. Hyams SW, Neumann E. Peripheral retina in myopia with particular reference to retinal breaks. Br J Ophthalmol. 1969;53:300–6.

 

8. Ashrafadeh MT, Schepens CL, Elzeneiny II, et al. Aphakic and phakic retinal detachment. I. Preoperative findings. Arch Ophthalmol. 1973;89:476–83.

 

9. Straatsma BR, Zeegan PD, Foos RY, et al. Lattice degeneration of the retina. XXX Edward Jackson Memorial Lecture. Am J Ophthalmol. 1974;77:619–49.

 

10. Cox MS, Schepens CL, Freeman HM. Retinal detachment due to ocular contusion. Arch Ophthalmol. 1966;76:678–85.

 

11. Cox MS. Retinal breaks caused by blunt nonperforating trauma at the point of impact. Trans Am Ophthalmol. Soc. 1980;78:414–66.

 

12. Hagler WS, North AW. Retinal dialyses and retinal detachment. Arch Ophthalmol. 1968;79:376–88.

 

13. Byer NE. The natural history of asymptomatic retinal breaks. Ophthalmology. 1982;89:1033–9.

 

14. Davis MD. Natural history of retinal breaks without detachment. Arch Ophthalmol. 1974;92:183–94.

 

15. Benson WE, Grand MG, Okun E. Aphakic retinal detachments. Management of the fellow eye. Arch Ophthalmol. 1975;93:245–9.

 

16. McPherson A, O’Malley R, Beltangady SS. Management of the fellow eyes of patients with rhegmatogenous retinal detachment. Ophthalmology. 1981;88:922–34.

 

17. Byer NE. Long-term natural history of lattice degeneration of the retina. Ophthalmology. 1989;96:1396–402.

 

18. Robertson DM, Curtin VT, Norton EWD. Avulsed retinal vessels with retinal breaks. Arch Ophthalmol. 1971;85:669–72.

 

19. Morse PH, Scheie HG. Prophylactic cryoretinopexy of retinal breaks. Arch Ophthalmol. 1974;92:204–7.

 

20. Smiddy WE, Flynn HW, Nicholson DH, et al. Results and complications in treated retinal breaks. Am J Ophthalmol. 1991;112:623–31.

 

21. Robertson DM, Norton EWD. Long-term follow-up of treated retinal breaks. Am J Ophthalmol. 1973;75:395–404.

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