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Discussion by John T. Thompson, MD
Byer 䡠 Subclinical RD Table 2. Prevalence of Subclinical Retinal Detachment (in United States (1990) Population of persons ⬎age 10 Prevalence of asymptomatic retinal breaks Prevalence of SCRD in patients with breaks Prevalence of SCRD in United States (⬎age 10) (1 in 200) Number of persons with SCRD (asymptomatic)
212,340,000 5.8% 8.5% 0.5% 1,061,700
adverse factor and has not been associated with dangerous progression. This is consistent with the observation that clinical detachments resulting from atrophic holes of lattice degeneration characteristically are not associated with PVD. In conclusion, SCRDs in phakic primary (nonfellow) eyes are not dangerous findings and should be managed with occasional observation and patient education regarding symptoms rather than by urgent remedial treatment.
SCRD ⫽ subclinical retinal detachment.
References office by the same examiner, the prevalence of asymptomatic retinal breaks in this age group is 5.8%. Of this group, among 196 patients followed for an average of 11 years, the incidence of SCRD was 8.5% (17 of 196). Therefore, the risk of SCRD among the U. S. population over age 10 is 0.5% (0.058 ⫻ 0.085) or 1 in every 200 persons. This means that it is found in more than 1 million persons. Fortunately, these persons do not realize the presence of SCRD, and the condition will only rarely be discovered by an ophthalmologist, another happy circumstance, permitting the involved persons to avoid unnecessary surgical procedures.
Conclusions In phakic primary (nonfellow) eyes, the prognosis of SCRD is decidedly nonthreatening. Almost all the total cases (and all that were associated with round, atrophic holes) originated from lesions of lattice degeneration. Almost half of the areas of detachment occurred before the age of 27 years. Most (59%) were located inferiorly, and 90.9% were in the temporal half of the fundus. Eight (36%) showed pigmented demarcation lines, all present before age 44 years. Three (13%) of the 22 areas have spontaneously gotten smaller in size, and then have completely disappeared; one has been followed for 9 more years without change, even in the presence of a PVD. The incidence rate for progression of SCRD to CRD and also the incidence rate for spontaneous regression and disappearance of this lesion have not been previously reported in the ophthalmic literature. It was notable and startling to find that the likelihood of these two opposite outcomes were identical. PVD was found in four eyes with SCRD and was not an
1. Byer NE. What happens to untreated asymptomatic retinal breaks, and are they affected by posterior vitreous detachment? Ophthalmology 1998;105:1045–9; discussion 1049 – 50. 2. Davis MD. The natural history of retinal breaks without detachment. Trans Am Ophthalmol Soc 1973;71:343–72. 3. Byer NE. Clinical study of retinal breaks. Trans Am Acad Ophthalmol Otolaryngol 1967;71:461–73. 4. Byer NE. The natural history of asymptomatic retinal breaks. Ophthalmology 1982;89:1033–9. 5. Byer NE. Spontaneous regression and disappearance of subclinical rhegmatogenous retinal detachment. Am J Ophthalmol 2001;131:269 –70. 6. Schepens CL. Subclinical retinal detachments. Arch Ophthalmol 1952;47:593– 606. 7. Schepens CL. Preventive treatment of idiopathic and secondary retinal detachment. Acta XVIII Concilium Ophthalmologicum Belgica 1958;vol 1:1019 –27. 8. Morse PH, Scheie HG. Prophylactic cryoretinopexy of retinal breaks. Arch Ophthalmol 1974;92:204 –7. 9. Tillery WV, Lucier AC. Round atrophic holes in lattice degeneration–an important cause of phakic retinal detachment. Trans Am Acad Ophthalmol Otolaryngol 1976;81:509 –18. 10. Folk JC, Arrindell EL, Klugman MR. The fellow eye of patients with phakic lattice retinal detachment. Ophthalmology 1989;96:72–9. 11. Davis MD, Segal PP, MacCormick A. The natural course followed by the fellow eye in patients with rhegmatogenous retinal detachment. In: Pruett RC, Regan CDJ, eds. Retina Congress. New York: Appleton-Century-Crofts, 1974;643– 59. 12. Brod RD, Flynn HW Jr, Lightman DA. Asymptomatic rhegmatogenous retinal detachments. Arch Ophthalmol 1995;113: 1030 –2. 13. Statistical. Abstract of the United States, U. S. Department of Commerce Bureau of the Census. Washington, DC: Government Printing Office, 1990.
Discussion by John T. Thompson, MD The article presents important data that suggest that the risk of progression of subclinical retinal detachment (RD) to clinical RD is low for asymptomatic eyes. Dr. Byer followed 18 phakic eyes that were examined in a general ophthalmology practice for a
From Retina Specialists of Maryland, Towson, Maryland. Address correspondence to John T. Thompson, MD, 6569 North Charles Street, Suite 504, Towson, MD 21204.
mean of 13.5 years. These patients were examined by an ophthalmologist experienced with scleral depression, and detailed retinal drawings were performed on the patients with subclinical RD. The definition of subclinical RD was previously proposed by Davis1 and is a RD of at least one disc diameter from the retinal break but not more than two disc diameters posterior to the equator. His major findings were that only 2 of 18 eyes (11%) had progression from a subclinical RD to a clinical RD. Of these, one eye was treated with a scleral buckle, and one was followed. One additional
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Ophthalmology Volume 108, Number 8, August 2001 eye (5.6%) had an increase in the size of a subclinical RD (but not to a clinical RD) and was treated with a scleral buckle. Two eyes (11%) had spontaneous resolution of the RD during follow-up. The risk of progression of a subclinical RD was 0.8% per year of follow-up. Dr. Byer recommends that eyes with subclinical RD be followed regularly and treated only if the subclinical RD progresses to a RD. This recommendation applies to asymptomatic patients who have not had a RD in the fellow eye. Prior studies of fellow eyes have suggested that the risk of progression of subclinical RD is about 50% in this higher risk group.2 His data and conclusions need to be examined in the context of the risks, costs, and potential benefits of following versus treating the subclinical RD. Subclinical RD often developed early in adult life because 10 of 22 (45%) total areas of subclinical RD were present in patients under the age of 27 years. The risk of progression to a clinical RD is calculated by the author at 0.8% per year but could be as high as 1.2% per year, because one eye in his study with enlargement of a subclinical RD was treated with a scleral buckle and might have progressed to a clinical RD if treatment had not been performed. If an average of 1% risk of progression per year is applied to a 25-year-old, then the risk of progression of a subclinical RD to a clinical RD over an 80-year total life span would be 55%. There are always risks in extrapolating trends from a study with a mean follow-up duration of 13.5 years over the lifetime of a patient. No study, however, has provided data for subclinical RD in eyes followed 40 or 50 years, and these data are needed to determine the cumulative risk of RD for the life of the patient. Some subgroups of eyes may be at higher risk for progression of a subclinical RD, such as eyes with larger subclinical RD, high myopia, no demarcation line, superior retinal location, or eyes having cataract surgery. Furthermore, progression of a RD, although improbable, is unpredictable, and some patients might not be seen by their ophthalmologist until the macula is detached and vision is permanently lost in the eye. The published literature includes data helpful in evaluating the risk of treating versus following asymptomatic RDs. Brod and associates3 followed 31 eyes with asymptomatic RD for a mean of 3.4 years and found progression of the RD in only 2 of 31 eyes (6%). Greven and colleagues4 evaluated the results of treating asymptomatic RDs with a scleral buckle and reported retinal reattachment in 28 of 28 eyes (100%) with one surgery. One eye had a recurrent RD 14 months later because of a new tear.4 Visual acuity was stable or improved in 93% eyes.4 Hence, the risk of RD progression is low, and the risk of surgical treatment is also low. Some of the less-extensive subclinical RDs described in this study could be treated with laser indirect photocoagulation, which carries essentially no risk of adverse events from the laser procedure itself. Laser indirect photocoagulation would likely prevent progression
1504
of the RD in eyes with a smaller RD. Eyes with larger subclinical RD would need to be treated with a scleral buckle or pneumatic retinopexy if surgery is chosen, and these are certainly associated with higher risks of complications and costs than laser photocoagulation. Dr. Byer advocates that patients with subclinical RD be followed indefinitely for changes in the subclinical RD, but it is important to recall that there are costs to long-term follow-up by an ophthalmologist skilled with scleral depression and retinal drawings. This would usually mean annual examinations by a retina specialist, which would approach the cost of a surgical procedure for 55 additional years of life of the hypothetical 25-year-old patient. If treating the same patient with laser photocoagulation, a scleral buckle or pneumatic retinopexy would eliminate the need for follow-up by a retina specialist several years after surgery, then the cost of following the patient without treatment would approach that of laser or surgery. An analysis of subclinical RD using evidence-based medicine may help us to more precisely define the benefits and costs of following subclinical RD versus treatment. This study of eyes with subclinical RD makes a substantial contribution to the literature using long-term follow-up of patients that would not be readily available from a referral-based retina practice. His data confirm that the risk of progression from a subclinical RD to a clinical RD is small in asymptomatic patients without a history of RD in their fellow eye. This allows the physician to explain the 1% risk per year of progression to a clinical RD and encourage the patient to make the decision. The data convincingly demonstrate that the decision to treat or follow the subclinical RD is not urgent and can be made without pressuring our patients toward surgical intervention. One of our roles as physicians is to advise our patients about therapeutic options, and these data fill a gap in our knowledge that will help our patients make more knowledgeable decisions about treatment. References 1. Davis MD. The natural history of retinal breaks without detachment. Trans Am Ophthalmol Soc 1973;71:343–72. 2. Davis MD, Segal PP, MacCormick A. The natural course followed by the fellow eye in patients with rhegmatogenous retinal detachment. In: Pruett RC, Regan CDJ, eds. Retina Congress. New York: Appleton-Century-Crofts, 1974;643–59. 3. Brod RD, Flynn HW Jr, Lightman DA. Asymptomatic rhegmatogenous retinal detachments. Arch Ophthalmol 1995;113: 1030 –2. 4. Greven CM, Wall AB, Slusher MM. Anatomic and visual results in asymptomatic clinical rhegmatogenous retinal detachment repaired by scleral buckling. Am J Ophthalmol 1999;128: 618 –20.
212,340,000 5.8% 8.5% 0.5% 1,061,700
adverse factor and has not been associated with dangerous progression. This is consistent with the observation that clinical detachments resulting from atrophic holes of lattice degeneration characteristically are not associated with PVD. In conclusion, SCRDs in phakic primary (nonfellow) eyes are not dangerous findings and should be managed with occasional observation and patient education regarding symptoms rather than by urgent remedial treatment.
SCRD ⫽ subclinical retinal detachment.
References office by the same examiner, the prevalence of asymptomatic retinal breaks in this age group is 5.8%. Of this group, among 196 patients followed for an average of 11 years, the incidence of SCRD was 8.5% (17 of 196). Therefore, the risk of SCRD among the U. S. population over age 10 is 0.5% (0.058 ⫻ 0.085) or 1 in every 200 persons. This means that it is found in more than 1 million persons. Fortunately, these persons do not realize the presence of SCRD, and the condition will only rarely be discovered by an ophthalmologist, another happy circumstance, permitting the involved persons to avoid unnecessary surgical procedures.
Conclusions In phakic primary (nonfellow) eyes, the prognosis of SCRD is decidedly nonthreatening. Almost all the total cases (and all that were associated with round, atrophic holes) originated from lesions of lattice degeneration. Almost half of the areas of detachment occurred before the age of 27 years. Most (59%) were located inferiorly, and 90.9% were in the temporal half of the fundus. Eight (36%) showed pigmented demarcation lines, all present before age 44 years. Three (13%) of the 22 areas have spontaneously gotten smaller in size, and then have completely disappeared; one has been followed for 9 more years without change, even in the presence of a PVD. The incidence rate for progression of SCRD to CRD and also the incidence rate for spontaneous regression and disappearance of this lesion have not been previously reported in the ophthalmic literature. It was notable and startling to find that the likelihood of these two opposite outcomes were identical. PVD was found in four eyes with SCRD and was not an
1. Byer NE. What happens to untreated asymptomatic retinal breaks, and are they affected by posterior vitreous detachment? Ophthalmology 1998;105:1045–9; discussion 1049 – 50. 2. Davis MD. The natural history of retinal breaks without detachment. Trans Am Ophthalmol Soc 1973;71:343–72. 3. Byer NE. Clinical study of retinal breaks. Trans Am Acad Ophthalmol Otolaryngol 1967;71:461–73. 4. Byer NE. The natural history of asymptomatic retinal breaks. Ophthalmology 1982;89:1033–9. 5. Byer NE. Spontaneous regression and disappearance of subclinical rhegmatogenous retinal detachment. Am J Ophthalmol 2001;131:269 –70. 6. Schepens CL. Subclinical retinal detachments. Arch Ophthalmol 1952;47:593– 606. 7. Schepens CL. Preventive treatment of idiopathic and secondary retinal detachment. Acta XVIII Concilium Ophthalmologicum Belgica 1958;vol 1:1019 –27. 8. Morse PH, Scheie HG. Prophylactic cryoretinopexy of retinal breaks. Arch Ophthalmol 1974;92:204 –7. 9. Tillery WV, Lucier AC. Round atrophic holes in lattice degeneration–an important cause of phakic retinal detachment. Trans Am Acad Ophthalmol Otolaryngol 1976;81:509 –18. 10. Folk JC, Arrindell EL, Klugman MR. The fellow eye of patients with phakic lattice retinal detachment. Ophthalmology 1989;96:72–9. 11. Davis MD, Segal PP, MacCormick A. The natural course followed by the fellow eye in patients with rhegmatogenous retinal detachment. In: Pruett RC, Regan CDJ, eds. Retina Congress. New York: Appleton-Century-Crofts, 1974;643– 59. 12. Brod RD, Flynn HW Jr, Lightman DA. Asymptomatic rhegmatogenous retinal detachments. Arch Ophthalmol 1995;113: 1030 –2. 13. Statistical. Abstract of the United States, U. S. Department of Commerce Bureau of the Census. Washington, DC: Government Printing Office, 1990.
Discussion by John T. Thompson, MD The article presents important data that suggest that the risk of progression of subclinical retinal detachment (RD) to clinical RD is low for asymptomatic eyes. Dr. Byer followed 18 phakic eyes that were examined in a general ophthalmology practice for a
From Retina Specialists of Maryland, Towson, Maryland. Address correspondence to John T. Thompson, MD, 6569 North Charles Street, Suite 504, Towson, MD 21204.
mean of 13.5 years. These patients were examined by an ophthalmologist experienced with scleral depression, and detailed retinal drawings were performed on the patients with subclinical RD. The definition of subclinical RD was previously proposed by Davis1 and is a RD of at least one disc diameter from the retinal break but not more than two disc diameters posterior to the equator. His major findings were that only 2 of 18 eyes (11%) had progression from a subclinical RD to a clinical RD. Of these, one eye was treated with a scleral buckle, and one was followed. One additional
1503
Ophthalmology Volume 108, Number 8, August 2001 eye (5.6%) had an increase in the size of a subclinical RD (but not to a clinical RD) and was treated with a scleral buckle. Two eyes (11%) had spontaneous resolution of the RD during follow-up. The risk of progression of a subclinical RD was 0.8% per year of follow-up. Dr. Byer recommends that eyes with subclinical RD be followed regularly and treated only if the subclinical RD progresses to a RD. This recommendation applies to asymptomatic patients who have not had a RD in the fellow eye. Prior studies of fellow eyes have suggested that the risk of progression of subclinical RD is about 50% in this higher risk group.2 His data and conclusions need to be examined in the context of the risks, costs, and potential benefits of following versus treating the subclinical RD. Subclinical RD often developed early in adult life because 10 of 22 (45%) total areas of subclinical RD were present in patients under the age of 27 years. The risk of progression to a clinical RD is calculated by the author at 0.8% per year but could be as high as 1.2% per year, because one eye in his study with enlargement of a subclinical RD was treated with a scleral buckle and might have progressed to a clinical RD if treatment had not been performed. If an average of 1% risk of progression per year is applied to a 25-year-old, then the risk of progression of a subclinical RD to a clinical RD over an 80-year total life span would be 55%. There are always risks in extrapolating trends from a study with a mean follow-up duration of 13.5 years over the lifetime of a patient. No study, however, has provided data for subclinical RD in eyes followed 40 or 50 years, and these data are needed to determine the cumulative risk of RD for the life of the patient. Some subgroups of eyes may be at higher risk for progression of a subclinical RD, such as eyes with larger subclinical RD, high myopia, no demarcation line, superior retinal location, or eyes having cataract surgery. Furthermore, progression of a RD, although improbable, is unpredictable, and some patients might not be seen by their ophthalmologist until the macula is detached and vision is permanently lost in the eye. The published literature includes data helpful in evaluating the risk of treating versus following asymptomatic RDs. Brod and associates3 followed 31 eyes with asymptomatic RD for a mean of 3.4 years and found progression of the RD in only 2 of 31 eyes (6%). Greven and colleagues4 evaluated the results of treating asymptomatic RDs with a scleral buckle and reported retinal reattachment in 28 of 28 eyes (100%) with one surgery. One eye had a recurrent RD 14 months later because of a new tear.4 Visual acuity was stable or improved in 93% eyes.4 Hence, the risk of RD progression is low, and the risk of surgical treatment is also low. Some of the less-extensive subclinical RDs described in this study could be treated with laser indirect photocoagulation, which carries essentially no risk of adverse events from the laser procedure itself. Laser indirect photocoagulation would likely prevent progression
1504
of the RD in eyes with a smaller RD. Eyes with larger subclinical RD would need to be treated with a scleral buckle or pneumatic retinopexy if surgery is chosen, and these are certainly associated with higher risks of complications and costs than laser photocoagulation. Dr. Byer advocates that patients with subclinical RD be followed indefinitely for changes in the subclinical RD, but it is important to recall that there are costs to long-term follow-up by an ophthalmologist skilled with scleral depression and retinal drawings. This would usually mean annual examinations by a retina specialist, which would approach the cost of a surgical procedure for 55 additional years of life of the hypothetical 25-year-old patient. If treating the same patient with laser photocoagulation, a scleral buckle or pneumatic retinopexy would eliminate the need for follow-up by a retina specialist several years after surgery, then the cost of following the patient without treatment would approach that of laser or surgery. An analysis of subclinical RD using evidence-based medicine may help us to more precisely define the benefits and costs of following subclinical RD versus treatment. This study of eyes with subclinical RD makes a substantial contribution to the literature using long-term follow-up of patients that would not be readily available from a referral-based retina practice. His data confirm that the risk of progression from a subclinical RD to a clinical RD is small in asymptomatic patients without a history of RD in their fellow eye. This allows the physician to explain the 1% risk per year of progression to a clinical RD and encourage the patient to make the decision. The data convincingly demonstrate that the decision to treat or follow the subclinical RD is not urgent and can be made without pressuring our patients toward surgical intervention. One of our roles as physicians is to advise our patients about therapeutic options, and these data fill a gap in our knowledge that will help our patients make more knowledgeable decisions about treatment. References 1. Davis MD. The natural history of retinal breaks without detachment. Trans Am Ophthalmol Soc 1973;71:343–72. 2. Davis MD, Segal PP, MacCormick A. The natural course followed by the fellow eye in patients with rhegmatogenous retinal detachment. In: Pruett RC, Regan CDJ, eds. Retina Congress. New York: Appleton-Century-Crofts, 1974;643–59. 3. Brod RD, Flynn HW Jr, Lightman DA. Asymptomatic rhegmatogenous retinal detachments. Arch Ophthalmol 1995;113: 1030 –2. 4. Greven CM, Wall AB, Slusher MM. Anatomic and visual results in asymptomatic clinical rhegmatogenous retinal detachment repaired by scleral buckling. Am J Ophthalmol 1999;128: 618 –20.