THE TREATMENT OF ACUTE BRANCH VEIN OCCLUSION BY PHOTOCOAGULATION BY Paul C. Wetzig, MD INTRODUCTION
RETINAL BRANCH VEIN OCCLUSION WAS
FIRST OBSERVED AND
described by Leber in 1888.1 It has been well described in the literature over the past seven decades and the reports have been well summarized by Seitz.2 It continues to challenge therapeutic attempts at preservation and restoration of vision.3 Branch vein occlusion may be divided into two phases, acute and chronic. The acute phase may be characterized by a sudden onset associated with visual disturbances most often resulting from involvement of the macula. The clinical picture is that of venous obstruction. This obstructive vascular stage is associated with retinal hemorrhages, exudates, and edema in the area distal to the obstruction. Various degrees of obstruction may be seen. A few flame-shaped hemorrhages may occur with minimal retinal edema and exudates. With more extensive obstruction, there may be marked retinal elevation with extensive retinal hemorrhage obscuring all the retinal structures. The degree of macular involvement also may vary. The macula may be totally spared, moderately involved with edema, or totally obscured by retinal edema and hemorrhages. Fluorescein angiography demonstrates obstruction of the venous circulation at the site of the arterio-venous crossing as manifested by delayed emptying of the retinal veins distal to the occlusion. Perivenous leakage of fluorescein dye, and diffuse late leakage of dye into the adjacent tissue is observed. The angiographic picture may be totally obscured by the density of the overlying blood. Usually after six to twelve months depending on the extent of the obstruction, the hemorrhages and generalized retinal edema gradually disappear and the sequelae of the chronic phase comTR. AM. OPHTH. Soc., vol LXXVI, 1978
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mence with the development of new collateral circulation, cystoid edema ofthe macula and hard exudates. The new vessel formations may either occur in the plane of the retina or extend into the vitreous cavity. These new vessels may sometimes rupture with resultant hemorrhage into the vitreous cavity and retina. The visual loss at this stage is due to involvement of the macula by cystoid edema or hemorrhage from adjacent new vessels into the retina or vitreous. Pigmentary derangement in the macula also may develop at this time. Recovery of visual function, according to Wise, Dollery, and Henkind, is thought to be dependent on the small veins draining the macula. "In a major temporal branch vein occlusion where a patent venule lies between the obstructed branch and the fovea, an excellent prognosis can be given. In cases where the intervening patent venule only drains a part of the foveal area, some protection is afforded, but some degree of macular damage is likely, and the visual prognosis must be guarded."4 It has been shown that photocoagulation in the chronic phase in most instances, after six months - may be of value in obliterating new vessel formations associated with bleeding into the vitreous. Hard exudates and edema will disappear.527 For the purposes of this study, the acute phase is defined as that period during which visual symptoms have been present for not more than sixty days. It appears that in the acute phase of branch vein occlusion, there is a progressive venous congestion, retinal edema, and retinal hemorrhage - a vicious circle, each event compounding the other. Photocoagulation used during the acute phase may impede progression of the congested phase thereby reducing new vessel formation, cystoid edema, and hard exudates which develop in the chronic phase. BASIS
Treatment by photocoagulation in the acute phase of retinal branch vein occlusion is an attempt to preserve macular function and to prevent the sequelae associated with the chronic phase with its irreversible retinal damage. According to Wolfe, the fovea has a blood supply which is independent of the retinal circulation. "In the macular region the fovea, as is well known, shows a completely avascular area, varying from 0.4 to 0.5 mm. in diameter."N Intercapillary connections develop in the parafoveal region according to Wise, Dollery, and Henkind. "At the central macular area the capil-
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Wetzig Wti lary bed thins out and in the parafoveal region there is only a single
656
layer of capillaries. At the fovea itself, there is a lack of the inner retinal layers in which the vessels normally reside. The slope of the fovea is such that only a single layer of capillaries is found in the parafoveal region, but as the surrounding retina thickens, the capillary bed becomes multilayered."29 According to Gass, the fovea may be involved by edema arising from the adjacent structures. "Alterations in the permeability of the retinal capillaries in the macular region, whether due to intrinsic disease affecting the capillary bed directly or to venous obstruction, will result in outpouring of serous exudation into the retina."30 There are two possible mechanisms of action to prevent macular damage in branch vein occlusion. Firstly, the production of a scar between the fovea and the adjacent involved area provides a mechanical barrier preventing progression of edema and extravasation of blood into the fovea. Secondly, the massive destruction of the capillary bed reduces the input of the arterial blood supply thereby allowing the remaining intact capillary bed to drain into the adjacent less congested, intact capillary bed near the intercapillary communicating vessels, thereby reversing the vicious circle of events. Based on this rationale, a pilot study was done on 28 eyes with temporal branch vein occlusion that were treated by photocoagulation during the acute phase. SELECTION OF PATIENTS
Twenty-eight consecutive patients who presented with a complaint of visual loss and with occlusion of two or more branches of the central retinal vein were selected for treatment. Only one branch involved the temporal aspect. The onset of the visual symptoms was three to sixty days prior to treatment, with an average of 39 days. The clinical picture was that of acute congestion manifested by venous stasis, superficial retinal hemorrhages, and generalized retinal edema and cotton wool exudates in the involved areas. The site of obstruction was at the arteriovenous crossing nasal to the macula, and the fovea itself was involved to some degree. Fluorescein angiography showed no evidence of new vessel formation. The clinical history was evaluated and reinvestigated by the internist or family-care physician. The rationale of treatment was discussed with each patient. All patients who consented to treatment were included in this study.
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FIGURE 1, CASE 11
A: Pretreatment 15 second fluorescein angiogram demonstrates obstruction at the site of the second and third arteriovenous crossing with congestion and dilation of the vein with venous stasis and perivascular fluorescein leakage. Dilation of the capillaries and diffuse leakage with areas of perfusion are seen above the macula at the obstruction site. B: Four weeks following xenon photocoagulation 15 second fluorescein angiogram demonstrates restoration of venous circulation in the superior temporal vein with disappearance of congestion and perivenous leakage. There is no sign of diffuse leakage throughout the smaller venules. C: Pretreatment fundus photograph demonstrates superior temporal branch vein occlusion at the site of the second and third arteriovenous crossing. Diffuse hemorrhages are scattered throughout the involved area, extending into the macula and fovea with fine exudates below the macula. D: Fundus photograph 17 months following xenon photocoagulation demonstrates no hemorrhages or exudates in the macula. Flame shaped hemorrhages in the superior temporal quadrant have disappeared. Xenon photocoagulation scars can be seen and a preretinal gliosis is seen along the vessels of the involved area.
This study included a total of 28 eyes (28 patients) (Table I). The patients varied in age from 41 to 85 years with an average age of
Branch Vein Occlusion
659
69.6 years, and median age of 71 years. There were 12 male and 16 female patients. Quadrants involved were the superotemporal, 19; inferotemporal, 7; inferotemporal and inferonasal, 1; superotemporal and superonasal, 1. The follow-up period ranged from 1.0 to 8 years, with an average of 3.3 years, and a median of 2.9 years. The concomitant diseases included hypertension, 13; cardiac insufficiency, 1; diabetes mellitus, 3 (no other evidence of diabetic retinopathy in either eye); generalized arteriosclerosis, 2. Macular hemorrhages and foveal edema were present in all of the eyes before treatment. EXAMINATION AND TREATMENT
Every effort was made to ensure objectivity during the examination. An initial careful refraction by the examiner was performed to determine the best correctable vision. All patients were examined in the same standard examination areas which included a Snellen chart projected with mirrors at a distance of 20 feet. Applanation tonometry, visual fields (in most cases) using the Goldmann perimeter, ophthalmoscopic examination with the indirect ophthalmoscope and the stereoscopic biomicroscope, stereoscopic fundus color phot'ography, and fluorescein angiography were conducted prior to treatment. Two instruments were used for treatment, the xenon photocoagulator manufactured by the firm of Carl Zeiss, Oberkochen, West Germany, or the argon laser photocoagularor manufactured by Coherent Radiation, Palo Alto, California. Each pupil was widely dilated with 0.25% scopolamine and 10%o phenylephrine solution. When the xenon photocoagulator was used, valium (Diazepam) was administered slowly intravenously, until the patient demonstrated a change in mental sensorium - usually 5 to 10 mg was sufficient. Following this, 3 cc. of 2% xylocaine (Lidocaine) was unjected retrobulbarly. Treatment was then directed to the geographic areas involved. Six-degree burns of moderate intensity, sufficient to produce yellow coagulation, were placed in a nonconfluent pattern along the course of the vascular arcades to cover the entire affected area. Three-degree bums of similar intensity were placed between the involved area and the fovea. When indicated, three-degree bums were extended in a crescentric pattern to encompass the temporal aspect. Approximately 40 to 50 such applications were made in the quadrant involved (Fig. 2B).
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FIGURE 2, CASE 18
A: Pretreatment fundus photograph demonstrates superior temporal branch vein occlusion with marked congestion of the veins and scattered hemorrhages and exudates throughout the superior temporal quadrant extending into the macula. B: Fundus photograph two weeks after photocoagulation demonstrates yellow xenon photocoagulation marks along the superior temporal vascular arcades. There is no hemorrhage or edema in the treated area. Retinal structures can be seen in the adjacent area. The hemorrhages in the macular region persist. c: Fundus photograph three months after treatment with xenon photocoagulation and argon laser photocoagulation shows no congestion ofthe veins and no hemorrhages or exudates. Light coagulation scars from xenon photocoagulation are seen along the superior temporal arcade. Faint argon laser photocoagulation marks can be seen temporal to the macula. D: Fundus photograph 52 months following photocoagulation shows increased pigmentation of the xenon photocoagulation marks. The macula continues to appear dry.
A similar technique was used with the argon laser photocoagulator with the exception that intravenous valium (Diazepam) and retrobulbar anesthesia were not used. In these eyes, 100 to 150 applications were made with the 100 to 200 microspot size at 3 to 5 milliwatts on the nonpulse setting. In the parafoveal region the 50 micro-spot size was used applying nonconfluent bums, avoiding the fovea, but otherwise completely covering the affected area, even extending beyond the horizontal raphe. Usually 50 to 60 bums were made with a 0.2 to 0.3 millivolt nonpulse setting.
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FIGURE 3, CASE 5
A: Pretreatment fundus photograph demonstrates an inferior temporal and nasal branch vein occlusion with marked segmentation of the veins. The occlusion presumably is on the inferior portion of the optic disc. Hemorrhages and exudates are scattered throughout the lower half of the retina extending into the macula. B: Fundus photograph three months after photocoagulation shows no sign of venous congestion; hemorrhages and exudates have cleared and the macula appears dry. There continues to be narrowing and segmentation in the inferior temporal retinal vessels. Vision has improved to 20/30. C: Fundus photograph 41 months after treatment with photocoagulation demonstrates recurrence of diffuse scattered hemorrhages in the treated area with involvement of the macular region. The veins, however, show no marked congestion and the small flame shaped hemorrhages are scattered diffusely throughout the lower half of the retina. Vision has slowly deteriorated to 10/300.
Twenty-two patients were treated with xenon arc only; four patients were treated with only argon photocoagulation, and two patients were treated with both xenon and argon photocoagulation. If there was no evidence of clearing in the foveal region in three to four months, further treatment was considered. Immediately following treatment, the patients did not experience any discomfort and they were not aware of any change in the visual acuity unless the parafoveal treatment technique was used. These patients were aware of round scotomas which they described as "black spots"
662
Wetzig which eventually turned gray after a few weeks, at which time the patient was no longer aware of them. Follow-up examination consisted of determining the best visual acuity utilizing identical techniques to those used for the initial examination. The visual acuity used in this study to evaluate the efficacy of treatment is that level of vision after the vision was stabilized at two consecutive visits and at least a thirty day interval. Applanation tension was taken on each return visit. The patient was first seen two weeks following treatment at which time color fundus photography and fluorescein angiography were repeated. The patient was seen again at three months and at six months following treatment, each time the color fundus photography was repeated. Thereafter, the patient was seen at six month intervals. Visual acuity usually was found to be stabilized after nine to twelve months. Thereafter, fluorescein angiography and color fundus photography were repeated on a yearly basis. In some patients visual fields were also repeated. Two weeks following treatment, there was usually a marked clearing of the edema and hemorrhage in the treated areas to such an extent that the previously obscurred retinal vessels could be seen. The coagulation marks subsequently began to show signs of pigmentation. The untreated foveal region appeared to clear more slowly (Fig. 2B). Fluorescein angiography four weeks posttreatment showed restoration of circulation in the previously occluded vessels. There was no evidence of perivenous leakage and a reduction in the diffuse leakage was noted (Fig. 1B). In most eyes, the macular edema and hemorrhage cleared after six months (Fig. 2c). Visual acuity gradually improved after three months. In some eyes, cystoid edema did not resolve and the vision remained static or worsened. There appeared to be occlusion of branches other than those in the treated areas, with subsequent deterioration of vision (Fig. 3c). Visual field patterns were variable. In the pretreatment visual field, the density of scotoma varied with the density of the obstruction, hemorrhage, and exudates. The post-treatment fields were also extremely variable. The only consistent finding was dense scotoma at the treatment site. When the treatment applications were placed in a nonconfluent pattern, the patient was not aware of the scotoma. Fluorescein angiography did not demonstrate new vessel formations in any of the treated areas and none of the eyes had hemorrhage into the vitreous cavity.
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TABLE II. CHANGE IN VISUAL STATUS OF EYES INCLUDED IN THIS STUDY COMPLETION OF TREATMENT BY PHOTOCOAGULATION
Change in Visual Status after Treatment Improved Static Worse Total
Number of Eyes Per Cent 12 43% 11 39% 5 18% 28 100%0
TABLE III. FINAL VISUAL ACUITY OF EYES TREATED WITH PHOTOCOAGULATION AND OF UNTREATED EYES
Untreated Eyes Michels and Gutman and Gass Series* Zegarra Series** Average follow-up (yrs.) 3.3 3.6 2.07 20/40 or better 11 ( 39%) 24 ( 60 %) 23 ( 53%) 20/50 through 20/100 4 ( 14%) 12 ( 28%) 7 ( 17.5%) 20/200 or worse 13 ( 46%) 8 ( 19%) 9 ( 22.5%) Total 28 (100%) 43 (100%o) 40 (100 %) 20/50 or better 13 ( 46%) 26 ( 60%) 26 ( 65 %) 20/25 or better 6 ( 21%) 13 ( 30%) 17 ( 42.5%) * Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:;166, 1974.31 ** Gutman F A, Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974.33
Treated Eyes (This Study)
TABLE IV. INITIAL VISUAL ACUITY OF EYES TREATED WITH PHOTOCOAGULATION AND OF UNTREATED EYES
20/40 or better 20/50 through 20/100 20/200 or worse
Unknown** Total
Untreated Series Treated Series Michels and Gutman and (This Study) Gass Series* Zegarra Series*** 6 (21 %) 17 (40%) 17 (42.5%) 7 (25 %) 13 (309%) 11 (27.5%) 15 (54 %) 12 (28%) 12 (30 %) 28
1 43
40
20/50 or better 8 (28.5%) 19 (44%) 20 (50 %) 2 (57 %) 20/25 or better 3 (57%) 9 (22.5%) * Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:166, 1974.31 ** Michels R G, and Gass, J D M: Personal Communication.32 * Gutman F A, and Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974.33
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TABLE V. CHANGE IN VISUAL STATUS OF EYES AFTER TREATMENT BY PHOTOCOAGULATION (THIS STUDY) AND UNTREATED EYES WITH INITIAL VISUAL ACUITY OF 20/200 OR LESS
Untreated Series Gutman and Michels and Treated Eyes Change in Zegarra Series** Gass Series* This Study Visual Status 6 ( 50%o) 8 ( 67%) 6 ( 40%) Improved 6 ( 50%) 4 ( 33%) 9 ( 60%) Unimproved or Worse 12 (100%o) 12 (100%) 15 (100%) Total * Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:166, 1974.31 ** Gutman F A, Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974.33 TABLE VI. CHANGE IN VISUAL STATUS AFTER TREATMENT WITH PHOTOCOAGULATION IN RESPECT TO QUADRANT INVOLVED
Quadrant Involved Superior Inferior Total
Improved 9 3 12
Static 9 2 11
Worse 2 3 5
RESULTS
The results of treatment are evaluated on the basis of visual improvement (Table I and II). A visual improvement is defined as an increase of two lines or more on the Snellen chart. Static is a change of less than two lines, and worsening is a decrease of two lines or more. In a total of 28 eyes, 12 (43%) were improved, 11 (39%) were static, and 5 (18%) were worse. The cause of worsening in three eyes was progression of cystoid edema and in one eye progression of the occlusive disease in vessels in other untreated areas of the retina. Those eyes that remained unchanged demonstrated cystoid edema or atrophy in the region of the macula. The final visual status achieved is shown in Table III. The relationship of change in visual status in regard to quadrant involved is shown in Table VI. Five patients (71%) in the age group under 65 showed improvement in visual acuity after photocoagulation. Seven patients (33%) in the age group of 65 or over demonstrated visual acuity improvement.
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SELECTED REPRESENTATIVE CASE HISTORIES CASE 11
A 64-year-old white woman was referred for evaluation of branch vein occlusion. She had noted blurring of vision in the left eye for two months. She was known to have had essential hypertension of "several years"
duration. Ophthalmoscopic examination: best corrected vision, right eye 20/20, left eye 3/300. Applanation pressure, right eye 14, left eye 17. The right eye was normal. Ophthalmoscopic examination of the left eye revealed flame hemorrhages scattered throughout the superior temporal quadrant with hemorrhages extending into the fovea and beneath it. There was marked constriction at the first arterio-venous crossing, the presumed site of the occlusion. Yellow exudates were noted below the macula (Fig. lc). Fluorescein angiography demonstrated obstruction distal to the first arteriovenous crossing with delayed emptying of dye, perivenous leakage, and diffuse leakage into the adjacent structures (Fig. IA). Xenon photocoagulation with 6° aperture was applied along the course of the superior temporal vessels and marks were made immediately above the macula. These marks are best demonstrated in the late follow-up pictures as they are not readily demonstrable in the presence of hemorrhages and exudates (Fig. 1D). Repeat fluorescein angiography four weeks after treatment (Fig. 1B) showed apparent resolution of the obstruction as demonstrated by the absence of delayed leakage from the superior temporal vein, reduction in caliber of vessels, and the absence of perivenous leakage and diffuse leakage. The vision was 20/40+ 17 months after treatment. The macula appeared to be flat, dry, and uninvolved. Light coagulation scars could be seen immediately above the macula. Above the visualized scars no marks could be seen because of the preretinal gliosis (Fig. 1D). CASE 18
A 68-year-old white man was first seen because of a "blood clot" in the left eye. The patient was aware of blurred vision in the left eye of about 21 day's duration. He had been on treatment for essential hypertension for one and one-half years. Ophthalmoscopic examination: vision, right eye, 20/25. Left eye, best corrected vision, 20/400. Applanation pressure, right eye 14, left eye 17. The right eye was normal. In the left eye there were scattered hemorrhages and edema involving the entire superior temporal quadrant of the retina. There was marked congestion of the veins and scattered hemorrhages extended into the fovea (Fig. 2A). Xenon photocoagulation was applied along the course of the superior temporal vessels in a nonconfluent pattern with a 60 aperture (Fig. 2B). These marks are obscurred somewhat by the
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associated hemorrhage and edema. Four weeks following treatment, there appeared to be marked clearing of the hemorrhages and edema in the treated area. The vessels are more visible. The hemorrhage in the macular region persisted after three months and argon laser photocoagulation was applied to the perimacular region. Following treatment, there was a gradual resorption of the hemorrhages and the macula appeared flat and dry (Fig. 2c and 2D). The best corrected vision 68 months after treatment was 20/200. CASE 5
A 70-year-old white woman was seen because of blurred vision and visual distortion of four day's duration. Ophthalmoscopic examination: best corrected vision, right eye 20/40, left eye 20/40-. Examination showed occlusion of the inferior temporal and inferior nasal veins in the right eye with hemorrhages and exudates (Fig. 3A). Xenon photocoagulation was applied to the inferior nasal and inferior temporal vascular arcades. Three months after treatment there was absorption of hemorrhages with light coagulation scars in the treated areas (Fig. 3B). Vision improved to 20/30. Forty-one months after treatment the patient complained of increased blurred vision in the right eye. The corrected vision in the right eye was 20/60 with additional hemorrhages in the inferior half of the retina (Fig. 3c). Eighty-four months following treatment, vision deteriorated to 10/300. DISCUSSION
The fact that 43% of eyes with branch vein occlusion had an improved visual acuity appears impressive and seems to support the basic concept of protecting the macula from secondary involvement. However, one must compare these results with the natural course of the disease. Unfortunately, only limited data appear in the literature at the present time. The only studies in the literature to date on the natural course of the disease are those of Michels and Gass31'32 and Gutman and Zegarra3 (Table 3). This paper has made an attempt to compare the results of the treatment by photocoagulation as compared with the observations of Michels and Gass and of Gutman and Zegarra (Tables 3,4 and 5). The initial visual acuity in the Michels and Gass series, and the Gutman and Zegarra series is given in Table 4 and is compared with the initial visual acuity of cases in this study before photocoagulation. It is to be expected that in this study there are relatively few patients in the group with better visual acuity, since those with near normal vision were excluded and those with worse visual acuity were specifically con-
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sidered for this study. The follow-up of the treated patients and the nontreated patients demonstrated some improvement in visual acuity in both groups. In analyzing the final results of patients with visual acuity of 20/200 or less (Table 5), it is obvious that treatment was to no avail, as compared to the natural course of the disease. Although the basic concept of a protective barrier and reduction in overall circulation protecting the fovea from secondary involvement following branch vein occlusion may be rational, it appears not to have influenced the course of the final result as compared to the untreated cases. We must conclude from this data that the use of photocoagulation in the proposed manner is not of obvious major benefit. The findings are inconclusive since this is a retrospective study. Patients were not treated in the same stage of the disease nor in an identical manner. If there were massive hemorrhages and exudates in the perifoveal region and underlying structures, caution was taken to avoid coming too close to the fovea. Only when the obstruction was partial and the landmarks could be seen clearly, could photocoagulation marks be placed more accurately in an attempt to barricade the fovea from the advancement of blood and edema in the adjacent area. Also, the numbers are admittedly small, making statistical evaluation difficult. Also, stricter criteria must be imposed to ensure proper evaluation of the natural course of the disease. In an attempt to find if the age of the patient plays a role in visual recovery, the results of the patients below the age of 65 and above the age of 65 are compared. Of the five patients under the age of 65, 71% had improvement, whereas of the seven patients over the age of 65, 33% had visual improvement. This would indicate that the younger age group had a better prognosis for visual improvement after treatment by photocoagulation. In analyzing the possible importance of the location of the branch vein occlusion, the difference between superior and inferior involvement is not significantly different (Table 6). CONCLUSION
This study of tIe potential protective value of photocoagulation in the treatment of acute branch vein occlusion did not demonstrate significant differences between the natural course of the disease and treatment. The shortcomings of a retrospective study in uncontrolled conditions are obvious. The basic concept of the use of
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photocoagulation in attempting to spare macular function remains intriguing and deserves further evaluation. This study also demonstrates the difficulty of evaluating the efficacy of a treatment modality in individual clinical practice. More conclusive evaluation can be obtained only when a prospective study on a large number of patients with a more similar pretreatment status, treated under controlled conditions and evaluated by unbiased observers is made as was done in the cooperative study of photocoagulation in the treatment of diabetic retinopathy.34
1.
2. 3. 4.
5. 6. 7. 8. 9.
10. 11. 12. 13. 14.
15. 16. 17.
REFERENCES Leber T: Die Kronkheiten der Netzhaut und der Sehnerven. Hbd Ges Ophthalmol Graefe-Saemisch, 1877. Seitz R: The Retinal Vessels. St Louis, C V Mosby 1964, p 750. Duff I F, Falls H F, Linman J: Anticoagulant therapy in occlusive vascular disease of the retina. Arch Ophthalmol 46:601, 1951. Wise G N, Dollery C T, Henkind P: The Retinal Circulation. New York, Harper & Row, 1971, p 352. Meyer-Schwickerath G: Light-coagulation. St Louis, C V Mosby, 1960. Shimizu K, Tobari J: Treatment of retinal vein obstruction by photocoagulation. Jpn J Clin Ophthalmol 25:1529, 1971. Krill A, Archer D, Newell F: Photocoagulation in complications secondary to branch vein occlusion. Arch Ophthalmol 85:48, 1971. Wetzig P, Thatcher D B: The treatment of acute and longstanding venous occlusion by photocoagulation. Modern Problems in Ophthalmology. Vol. 10. Basel, Karger, 1972. Blankenship G, Okun E: Retinal tributary vein occlusion. Arch Ophthalmol 89:363, 1973. Campbell J, Wise G N: Photocoagulation therapy of branch vein obstruction. Am J Ophthalmol 75:28, 1973. Suga K, Nagata M: Treatment of retinal venous branch occlusion by photocoagulation. Technique and effect of photocoagulation. Jpn J Clin Ophthalmol 27:1021, 1973. Archer D B, Ernest J T, Newell F W: Classification of branch retinal vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:148, 1974. Gitter K, Rosen E S: Angiographic analysis of patterns treated by photocoagulation for venous occlusive disease, In Schimizu K (ed): Fluorescein Angiography. Tokyo, Igaku Shoin Ltd, 1974 p 422. Asayama T, Fukuchi S: Experimental studies in the effectual mechanism of photocoagulation for retinal venous occlusion. 1. Histopathological changes in experimental retinal venous occlusion. Acta Soc OphthalmolJpn 77:1567, 1973. Bonnet M: Advantages - disadvantages of the use of photocoagulation in the treatment of the macular sequelae of retinal venous thrombosis. Bull Soc Ophtalmol Fr 73:719, 1973. Mosquera J M: Results of photocoagulation in the treatment of retinal venous branch occlusions. Arch Optalmol B Aires 49:171, 1974. Suga K, Nagata M: Treatment of retinal branch venous occlusion by photocoagulation. 2. Three types of fluorescein angiographic features and new mechanisms of photocoagulation. Jpn Clin Ophthalmol 27:1403, 1973.
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18. Theodossiadis G, Charamis J, Velissaropoulos P: Photocoagulation in branch and total retinal venous occlusion. Klin Monatsbl Augenheilkd 164:713, 1974. 19. Cairns J D: Photocoagulation in the treatment of retinal branch vein occlusion. Aust J Ophthalmol 2:5, 1974. 20. Greyler H, Nichorlis S: Photocoagulation of retinal venous thrombosis. Klin Monatsbl Augenheilkd 165:750, 1974. 21. Heydenreich A: Late complications of retinal venous occlusions and their treatment by photocoagulation. Klin Monatsbl Augenheilkd. 165:259, 1974. 22. Oosterhuis J A, Sedney S C: Photocoagulation in retinal venous thrombosis. Ophthalmologica 171:365, 1975. 23. Sedney S C: Photocoagulation in retinal vein occlusion. Doc Ophthalmol 40 241, 1976. 24. Krasnov M M: Fluorescein angiography in laser therapy for retinal venous thrombosis. Vestn Ophthalmol 92:56, 1976. 25. Coscas G, Gavdric A: Laser and argon photocoagulation of retinal branch vein occlusions. Bull Soc Ophtalmol Fr 76:823, 1976. 26. Laatikainen L: Photocoagulation in retinal venous occlusion. Acta Ophthalmol (Kbh) 55:478, 1977. 27. Francois J: Argon laser photocoagulation in retinal branch vein occlusions. In L'Esperance F A (ed.) Current Diagnosis and Management of Chorioretinal Diseases. St Louis, C V Mosby, 1977, p 522. 28. Last R J: Wolffs Anatomy of the Eye and Orbit. Philadelphia and London, W B Saunders Company, 1968, p 154. 29. Wise G N, Dollery C T, Henkind P: The Retinal Circulation New York, Harper & Row, 1971, p 25. 30. Gass J D M: Stereoscopic Atlas of Macular Disease. St Louis, C V Mosby, 1970, p 148. 31. Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:166, 1974. 32. Michels R G, Gass J D M: Personal Communications. 33. Gutman F A, Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974. 34. The Diabetic Retinopathy Study Research Group: Preliminary Report on effects of photocoagulation therapy. Am J Ophthalmol 81:383-396, 1976.
RETINAL BRANCH VEIN OCCLUSION WAS
FIRST OBSERVED AND
described by Leber in 1888.1 It has been well described in the literature over the past seven decades and the reports have been well summarized by Seitz.2 It continues to challenge therapeutic attempts at preservation and restoration of vision.3 Branch vein occlusion may be divided into two phases, acute and chronic. The acute phase may be characterized by a sudden onset associated with visual disturbances most often resulting from involvement of the macula. The clinical picture is that of venous obstruction. This obstructive vascular stage is associated with retinal hemorrhages, exudates, and edema in the area distal to the obstruction. Various degrees of obstruction may be seen. A few flame-shaped hemorrhages may occur with minimal retinal edema and exudates. With more extensive obstruction, there may be marked retinal elevation with extensive retinal hemorrhage obscuring all the retinal structures. The degree of macular involvement also may vary. The macula may be totally spared, moderately involved with edema, or totally obscured by retinal edema and hemorrhages. Fluorescein angiography demonstrates obstruction of the venous circulation at the site of the arterio-venous crossing as manifested by delayed emptying of the retinal veins distal to the occlusion. Perivenous leakage of fluorescein dye, and diffuse late leakage of dye into the adjacent tissue is observed. The angiographic picture may be totally obscured by the density of the overlying blood. Usually after six to twelve months depending on the extent of the obstruction, the hemorrhages and generalized retinal edema gradually disappear and the sequelae of the chronic phase comTR. AM. OPHTH. Soc., vol LXXVI, 1978
Branch Vein Occlusion
655
mence with the development of new collateral circulation, cystoid edema ofthe macula and hard exudates. The new vessel formations may either occur in the plane of the retina or extend into the vitreous cavity. These new vessels may sometimes rupture with resultant hemorrhage into the vitreous cavity and retina. The visual loss at this stage is due to involvement of the macula by cystoid edema or hemorrhage from adjacent new vessels into the retina or vitreous. Pigmentary derangement in the macula also may develop at this time. Recovery of visual function, according to Wise, Dollery, and Henkind, is thought to be dependent on the small veins draining the macula. "In a major temporal branch vein occlusion where a patent venule lies between the obstructed branch and the fovea, an excellent prognosis can be given. In cases where the intervening patent venule only drains a part of the foveal area, some protection is afforded, but some degree of macular damage is likely, and the visual prognosis must be guarded."4 It has been shown that photocoagulation in the chronic phase in most instances, after six months - may be of value in obliterating new vessel formations associated with bleeding into the vitreous. Hard exudates and edema will disappear.527 For the purposes of this study, the acute phase is defined as that period during which visual symptoms have been present for not more than sixty days. It appears that in the acute phase of branch vein occlusion, there is a progressive venous congestion, retinal edema, and retinal hemorrhage - a vicious circle, each event compounding the other. Photocoagulation used during the acute phase may impede progression of the congested phase thereby reducing new vessel formation, cystoid edema, and hard exudates which develop in the chronic phase. BASIS
Treatment by photocoagulation in the acute phase of retinal branch vein occlusion is an attempt to preserve macular function and to prevent the sequelae associated with the chronic phase with its irreversible retinal damage. According to Wolfe, the fovea has a blood supply which is independent of the retinal circulation. "In the macular region the fovea, as is well known, shows a completely avascular area, varying from 0.4 to 0.5 mm. in diameter."N Intercapillary connections develop in the parafoveal region according to Wise, Dollery, and Henkind. "At the central macular area the capil-
656
Wetzig Wti lary bed thins out and in the parafoveal region there is only a single
656
layer of capillaries. At the fovea itself, there is a lack of the inner retinal layers in which the vessels normally reside. The slope of the fovea is such that only a single layer of capillaries is found in the parafoveal region, but as the surrounding retina thickens, the capillary bed becomes multilayered."29 According to Gass, the fovea may be involved by edema arising from the adjacent structures. "Alterations in the permeability of the retinal capillaries in the macular region, whether due to intrinsic disease affecting the capillary bed directly or to venous obstruction, will result in outpouring of serous exudation into the retina."30 There are two possible mechanisms of action to prevent macular damage in branch vein occlusion. Firstly, the production of a scar between the fovea and the adjacent involved area provides a mechanical barrier preventing progression of edema and extravasation of blood into the fovea. Secondly, the massive destruction of the capillary bed reduces the input of the arterial blood supply thereby allowing the remaining intact capillary bed to drain into the adjacent less congested, intact capillary bed near the intercapillary communicating vessels, thereby reversing the vicious circle of events. Based on this rationale, a pilot study was done on 28 eyes with temporal branch vein occlusion that were treated by photocoagulation during the acute phase. SELECTION OF PATIENTS
Twenty-eight consecutive patients who presented with a complaint of visual loss and with occlusion of two or more branches of the central retinal vein were selected for treatment. Only one branch involved the temporal aspect. The onset of the visual symptoms was three to sixty days prior to treatment, with an average of 39 days. The clinical picture was that of acute congestion manifested by venous stasis, superficial retinal hemorrhages, and generalized retinal edema and cotton wool exudates in the involved areas. The site of obstruction was at the arteriovenous crossing nasal to the macula, and the fovea itself was involved to some degree. Fluorescein angiography showed no evidence of new vessel formation. The clinical history was evaluated and reinvestigated by the internist or family-care physician. The rationale of treatment was discussed with each patient. All patients who consented to treatment were included in this study.
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658
Wetzig
FIGURE 1, CASE 11
A: Pretreatment 15 second fluorescein angiogram demonstrates obstruction at the site of the second and third arteriovenous crossing with congestion and dilation of the vein with venous stasis and perivascular fluorescein leakage. Dilation of the capillaries and diffuse leakage with areas of perfusion are seen above the macula at the obstruction site. B: Four weeks following xenon photocoagulation 15 second fluorescein angiogram demonstrates restoration of venous circulation in the superior temporal vein with disappearance of congestion and perivenous leakage. There is no sign of diffuse leakage throughout the smaller venules. C: Pretreatment fundus photograph demonstrates superior temporal branch vein occlusion at the site of the second and third arteriovenous crossing. Diffuse hemorrhages are scattered throughout the involved area, extending into the macula and fovea with fine exudates below the macula. D: Fundus photograph 17 months following xenon photocoagulation demonstrates no hemorrhages or exudates in the macula. Flame shaped hemorrhages in the superior temporal quadrant have disappeared. Xenon photocoagulation scars can be seen and a preretinal gliosis is seen along the vessels of the involved area.
This study included a total of 28 eyes (28 patients) (Table I). The patients varied in age from 41 to 85 years with an average age of
Branch Vein Occlusion
659
69.6 years, and median age of 71 years. There were 12 male and 16 female patients. Quadrants involved were the superotemporal, 19; inferotemporal, 7; inferotemporal and inferonasal, 1; superotemporal and superonasal, 1. The follow-up period ranged from 1.0 to 8 years, with an average of 3.3 years, and a median of 2.9 years. The concomitant diseases included hypertension, 13; cardiac insufficiency, 1; diabetes mellitus, 3 (no other evidence of diabetic retinopathy in either eye); generalized arteriosclerosis, 2. Macular hemorrhages and foveal edema were present in all of the eyes before treatment. EXAMINATION AND TREATMENT
Every effort was made to ensure objectivity during the examination. An initial careful refraction by the examiner was performed to determine the best correctable vision. All patients were examined in the same standard examination areas which included a Snellen chart projected with mirrors at a distance of 20 feet. Applanation tonometry, visual fields (in most cases) using the Goldmann perimeter, ophthalmoscopic examination with the indirect ophthalmoscope and the stereoscopic biomicroscope, stereoscopic fundus color phot'ography, and fluorescein angiography were conducted prior to treatment. Two instruments were used for treatment, the xenon photocoagulator manufactured by the firm of Carl Zeiss, Oberkochen, West Germany, or the argon laser photocoagularor manufactured by Coherent Radiation, Palo Alto, California. Each pupil was widely dilated with 0.25% scopolamine and 10%o phenylephrine solution. When the xenon photocoagulator was used, valium (Diazepam) was administered slowly intravenously, until the patient demonstrated a change in mental sensorium - usually 5 to 10 mg was sufficient. Following this, 3 cc. of 2% xylocaine (Lidocaine) was unjected retrobulbarly. Treatment was then directed to the geographic areas involved. Six-degree burns of moderate intensity, sufficient to produce yellow coagulation, were placed in a nonconfluent pattern along the course of the vascular arcades to cover the entire affected area. Three-degree bums of similar intensity were placed between the involved area and the fovea. When indicated, three-degree bums were extended in a crescentric pattern to encompass the temporal aspect. Approximately 40 to 50 such applications were made in the quadrant involved (Fig. 2B).
660
Wetzig
FIGURE 2, CASE 18
A: Pretreatment fundus photograph demonstrates superior temporal branch vein occlusion with marked congestion of the veins and scattered hemorrhages and exudates throughout the superior temporal quadrant extending into the macula. B: Fundus photograph two weeks after photocoagulation demonstrates yellow xenon photocoagulation marks along the superior temporal vascular arcades. There is no hemorrhage or edema in the treated area. Retinal structures can be seen in the adjacent area. The hemorrhages in the macular region persist. c: Fundus photograph three months after treatment with xenon photocoagulation and argon laser photocoagulation shows no congestion ofthe veins and no hemorrhages or exudates. Light coagulation scars from xenon photocoagulation are seen along the superior temporal arcade. Faint argon laser photocoagulation marks can be seen temporal to the macula. D: Fundus photograph 52 months following photocoagulation shows increased pigmentation of the xenon photocoagulation marks. The macula continues to appear dry.
A similar technique was used with the argon laser photocoagulator with the exception that intravenous valium (Diazepam) and retrobulbar anesthesia were not used. In these eyes, 100 to 150 applications were made with the 100 to 200 microspot size at 3 to 5 milliwatts on the nonpulse setting. In the parafoveal region the 50 micro-spot size was used applying nonconfluent bums, avoiding the fovea, but otherwise completely covering the affected area, even extending beyond the horizontal raphe. Usually 50 to 60 bums were made with a 0.2 to 0.3 millivolt nonpulse setting.
Branch Vein Occlusion
661
FIGURE 3, CASE 5
A: Pretreatment fundus photograph demonstrates an inferior temporal and nasal branch vein occlusion with marked segmentation of the veins. The occlusion presumably is on the inferior portion of the optic disc. Hemorrhages and exudates are scattered throughout the lower half of the retina extending into the macula. B: Fundus photograph three months after photocoagulation shows no sign of venous congestion; hemorrhages and exudates have cleared and the macula appears dry. There continues to be narrowing and segmentation in the inferior temporal retinal vessels. Vision has improved to 20/30. C: Fundus photograph 41 months after treatment with photocoagulation demonstrates recurrence of diffuse scattered hemorrhages in the treated area with involvement of the macular region. The veins, however, show no marked congestion and the small flame shaped hemorrhages are scattered diffusely throughout the lower half of the retina. Vision has slowly deteriorated to 10/300.
Twenty-two patients were treated with xenon arc only; four patients were treated with only argon photocoagulation, and two patients were treated with both xenon and argon photocoagulation. If there was no evidence of clearing in the foveal region in three to four months, further treatment was considered. Immediately following treatment, the patients did not experience any discomfort and they were not aware of any change in the visual acuity unless the parafoveal treatment technique was used. These patients were aware of round scotomas which they described as "black spots"
662
Wetzig which eventually turned gray after a few weeks, at which time the patient was no longer aware of them. Follow-up examination consisted of determining the best visual acuity utilizing identical techniques to those used for the initial examination. The visual acuity used in this study to evaluate the efficacy of treatment is that level of vision after the vision was stabilized at two consecutive visits and at least a thirty day interval. Applanation tension was taken on each return visit. The patient was first seen two weeks following treatment at which time color fundus photography and fluorescein angiography were repeated. The patient was seen again at three months and at six months following treatment, each time the color fundus photography was repeated. Thereafter, the patient was seen at six month intervals. Visual acuity usually was found to be stabilized after nine to twelve months. Thereafter, fluorescein angiography and color fundus photography were repeated on a yearly basis. In some patients visual fields were also repeated. Two weeks following treatment, there was usually a marked clearing of the edema and hemorrhage in the treated areas to such an extent that the previously obscurred retinal vessels could be seen. The coagulation marks subsequently began to show signs of pigmentation. The untreated foveal region appeared to clear more slowly (Fig. 2B). Fluorescein angiography four weeks posttreatment showed restoration of circulation in the previously occluded vessels. There was no evidence of perivenous leakage and a reduction in the diffuse leakage was noted (Fig. 1B). In most eyes, the macular edema and hemorrhage cleared after six months (Fig. 2c). Visual acuity gradually improved after three months. In some eyes, cystoid edema did not resolve and the vision remained static or worsened. There appeared to be occlusion of branches other than those in the treated areas, with subsequent deterioration of vision (Fig. 3c). Visual field patterns were variable. In the pretreatment visual field, the density of scotoma varied with the density of the obstruction, hemorrhage, and exudates. The post-treatment fields were also extremely variable. The only consistent finding was dense scotoma at the treatment site. When the treatment applications were placed in a nonconfluent pattern, the patient was not aware of the scotoma. Fluorescein angiography did not demonstrate new vessel formations in any of the treated areas and none of the eyes had hemorrhage into the vitreous cavity.
Branch Vein Occlusion
663
TABLE II. CHANGE IN VISUAL STATUS OF EYES INCLUDED IN THIS STUDY COMPLETION OF TREATMENT BY PHOTOCOAGULATION
Change in Visual Status after Treatment Improved Static Worse Total
Number of Eyes Per Cent 12 43% 11 39% 5 18% 28 100%0
TABLE III. FINAL VISUAL ACUITY OF EYES TREATED WITH PHOTOCOAGULATION AND OF UNTREATED EYES
Untreated Eyes Michels and Gutman and Gass Series* Zegarra Series** Average follow-up (yrs.) 3.3 3.6 2.07 20/40 or better 11 ( 39%) 24 ( 60 %) 23 ( 53%) 20/50 through 20/100 4 ( 14%) 12 ( 28%) 7 ( 17.5%) 20/200 or worse 13 ( 46%) 8 ( 19%) 9 ( 22.5%) Total 28 (100%) 43 (100%o) 40 (100 %) 20/50 or better 13 ( 46%) 26 ( 60%) 26 ( 65 %) 20/25 or better 6 ( 21%) 13 ( 30%) 17 ( 42.5%) * Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:;166, 1974.31 ** Gutman F A, Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974.33
Treated Eyes (This Study)
TABLE IV. INITIAL VISUAL ACUITY OF EYES TREATED WITH PHOTOCOAGULATION AND OF UNTREATED EYES
20/40 or better 20/50 through 20/100 20/200 or worse
Unknown** Total
Untreated Series Treated Series Michels and Gutman and (This Study) Gass Series* Zegarra Series*** 6 (21 %) 17 (40%) 17 (42.5%) 7 (25 %) 13 (309%) 11 (27.5%) 15 (54 %) 12 (28%) 12 (30 %) 28
1 43
40
20/50 or better 8 (28.5%) 19 (44%) 20 (50 %) 2 (57 %) 20/25 or better 3 (57%) 9 (22.5%) * Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:166, 1974.31 ** Michels R G, and Gass, J D M: Personal Communication.32 * Gutman F A, and Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974.33
Wetzig
664
TABLE V. CHANGE IN VISUAL STATUS OF EYES AFTER TREATMENT BY PHOTOCOAGULATION (THIS STUDY) AND UNTREATED EYES WITH INITIAL VISUAL ACUITY OF 20/200 OR LESS
Untreated Series Gutman and Michels and Treated Eyes Change in Zegarra Series** Gass Series* This Study Visual Status 6 ( 50%o) 8 ( 67%) 6 ( 40%) Improved 6 ( 50%) 4 ( 33%) 9 ( 60%) Unimproved or Worse 12 (100%o) 12 (100%) 15 (100%) Total * Michels R G, Gass J D M: Natural course of retinal branch vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:166, 1974.31 ** Gutman F A, Zegarra H: The natural course of temporal retinal branch occlusion. Trans Am Acad Ophthalmol Otolaryngol 78:178, 1974.33 TABLE VI. CHANGE IN VISUAL STATUS AFTER TREATMENT WITH PHOTOCOAGULATION IN RESPECT TO QUADRANT INVOLVED
Quadrant Involved Superior Inferior Total
Improved 9 3 12
Static 9 2 11
Worse 2 3 5
RESULTS
The results of treatment are evaluated on the basis of visual improvement (Table I and II). A visual improvement is defined as an increase of two lines or more on the Snellen chart. Static is a change of less than two lines, and worsening is a decrease of two lines or more. In a total of 28 eyes, 12 (43%) were improved, 11 (39%) were static, and 5 (18%) were worse. The cause of worsening in three eyes was progression of cystoid edema and in one eye progression of the occlusive disease in vessels in other untreated areas of the retina. Those eyes that remained unchanged demonstrated cystoid edema or atrophy in the region of the macula. The final visual status achieved is shown in Table III. The relationship of change in visual status in regard to quadrant involved is shown in Table VI. Five patients (71%) in the age group under 65 showed improvement in visual acuity after photocoagulation. Seven patients (33%) in the age group of 65 or over demonstrated visual acuity improvement.
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0665
SELECTED REPRESENTATIVE CASE HISTORIES CASE 11
A 64-year-old white woman was referred for evaluation of branch vein occlusion. She had noted blurring of vision in the left eye for two months. She was known to have had essential hypertension of "several years"
duration. Ophthalmoscopic examination: best corrected vision, right eye 20/20, left eye 3/300. Applanation pressure, right eye 14, left eye 17. The right eye was normal. Ophthalmoscopic examination of the left eye revealed flame hemorrhages scattered throughout the superior temporal quadrant with hemorrhages extending into the fovea and beneath it. There was marked constriction at the first arterio-venous crossing, the presumed site of the occlusion. Yellow exudates were noted below the macula (Fig. lc). Fluorescein angiography demonstrated obstruction distal to the first arteriovenous crossing with delayed emptying of dye, perivenous leakage, and diffuse leakage into the adjacent structures (Fig. IA). Xenon photocoagulation with 6° aperture was applied along the course of the superior temporal vessels and marks were made immediately above the macula. These marks are best demonstrated in the late follow-up pictures as they are not readily demonstrable in the presence of hemorrhages and exudates (Fig. 1D). Repeat fluorescein angiography four weeks after treatment (Fig. 1B) showed apparent resolution of the obstruction as demonstrated by the absence of delayed leakage from the superior temporal vein, reduction in caliber of vessels, and the absence of perivenous leakage and diffuse leakage. The vision was 20/40+ 17 months after treatment. The macula appeared to be flat, dry, and uninvolved. Light coagulation scars could be seen immediately above the macula. Above the visualized scars no marks could be seen because of the preretinal gliosis (Fig. 1D). CASE 18
A 68-year-old white man was first seen because of a "blood clot" in the left eye. The patient was aware of blurred vision in the left eye of about 21 day's duration. He had been on treatment for essential hypertension for one and one-half years. Ophthalmoscopic examination: vision, right eye, 20/25. Left eye, best corrected vision, 20/400. Applanation pressure, right eye 14, left eye 17. The right eye was normal. In the left eye there were scattered hemorrhages and edema involving the entire superior temporal quadrant of the retina. There was marked congestion of the veins and scattered hemorrhages extended into the fovea (Fig. 2A). Xenon photocoagulation was applied along the course of the superior temporal vessels in a nonconfluent pattern with a 60 aperture (Fig. 2B). These marks are obscurred somewhat by the
666
Wetzig
associated hemorrhage and edema. Four weeks following treatment, there appeared to be marked clearing of the hemorrhages and edema in the treated area. The vessels are more visible. The hemorrhage in the macular region persisted after three months and argon laser photocoagulation was applied to the perimacular region. Following treatment, there was a gradual resorption of the hemorrhages and the macula appeared flat and dry (Fig. 2c and 2D). The best corrected vision 68 months after treatment was 20/200. CASE 5
A 70-year-old white woman was seen because of blurred vision and visual distortion of four day's duration. Ophthalmoscopic examination: best corrected vision, right eye 20/40, left eye 20/40-. Examination showed occlusion of the inferior temporal and inferior nasal veins in the right eye with hemorrhages and exudates (Fig. 3A). Xenon photocoagulation was applied to the inferior nasal and inferior temporal vascular arcades. Three months after treatment there was absorption of hemorrhages with light coagulation scars in the treated areas (Fig. 3B). Vision improved to 20/30. Forty-one months after treatment the patient complained of increased blurred vision in the right eye. The corrected vision in the right eye was 20/60 with additional hemorrhages in the inferior half of the retina (Fig. 3c). Eighty-four months following treatment, vision deteriorated to 10/300. DISCUSSION
The fact that 43% of eyes with branch vein occlusion had an improved visual acuity appears impressive and seems to support the basic concept of protecting the macula from secondary involvement. However, one must compare these results with the natural course of the disease. Unfortunately, only limited data appear in the literature at the present time. The only studies in the literature to date on the natural course of the disease are those of Michels and Gass31'32 and Gutman and Zegarra3 (Table 3). This paper has made an attempt to compare the results of the treatment by photocoagulation as compared with the observations of Michels and Gass and of Gutman and Zegarra (Tables 3,4 and 5). The initial visual acuity in the Michels and Gass series, and the Gutman and Zegarra series is given in Table 4 and is compared with the initial visual acuity of cases in this study before photocoagulation. It is to be expected that in this study there are relatively few patients in the group with better visual acuity, since those with near normal vision were excluded and those with worse visual acuity were specifically con-
Branch Vein Occlusion
0667
sidered for this study. The follow-up of the treated patients and the nontreated patients demonstrated some improvement in visual acuity in both groups. In analyzing the final results of patients with visual acuity of 20/200 or less (Table 5), it is obvious that treatment was to no avail, as compared to the natural course of the disease. Although the basic concept of a protective barrier and reduction in overall circulation protecting the fovea from secondary involvement following branch vein occlusion may be rational, it appears not to have influenced the course of the final result as compared to the untreated cases. We must conclude from this data that the use of photocoagulation in the proposed manner is not of obvious major benefit. The findings are inconclusive since this is a retrospective study. Patients were not treated in the same stage of the disease nor in an identical manner. If there were massive hemorrhages and exudates in the perifoveal region and underlying structures, caution was taken to avoid coming too close to the fovea. Only when the obstruction was partial and the landmarks could be seen clearly, could photocoagulation marks be placed more accurately in an attempt to barricade the fovea from the advancement of blood and edema in the adjacent area. Also, the numbers are admittedly small, making statistical evaluation difficult. Also, stricter criteria must be imposed to ensure proper evaluation of the natural course of the disease. In an attempt to find if the age of the patient plays a role in visual recovery, the results of the patients below the age of 65 and above the age of 65 are compared. Of the five patients under the age of 65, 71% had improvement, whereas of the seven patients over the age of 65, 33% had visual improvement. This would indicate that the younger age group had a better prognosis for visual improvement after treatment by photocoagulation. In analyzing the possible importance of the location of the branch vein occlusion, the difference between superior and inferior involvement is not significantly different (Table 6). CONCLUSION
This study of tIe potential protective value of photocoagulation in the treatment of acute branch vein occlusion did not demonstrate significant differences between the natural course of the disease and treatment. The shortcomings of a retrospective study in uncontrolled conditions are obvious. The basic concept of the use of
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Wetzig
photocoagulation in attempting to spare macular function remains intriguing and deserves further evaluation. This study also demonstrates the difficulty of evaluating the efficacy of a treatment modality in individual clinical practice. More conclusive evaluation can be obtained only when a prospective study on a large number of patients with a more similar pretreatment status, treated under controlled conditions and evaluated by unbiased observers is made as was done in the cooperative study of photocoagulation in the treatment of diabetic retinopathy.34
1.
2. 3. 4.
5. 6. 7. 8. 9.
10. 11. 12. 13. 14.
15. 16. 17.
REFERENCES Leber T: Die Kronkheiten der Netzhaut und der Sehnerven. Hbd Ges Ophthalmol Graefe-Saemisch, 1877. Seitz R: The Retinal Vessels. St Louis, C V Mosby 1964, p 750. Duff I F, Falls H F, Linman J: Anticoagulant therapy in occlusive vascular disease of the retina. Arch Ophthalmol 46:601, 1951. Wise G N, Dollery C T, Henkind P: The Retinal Circulation. New York, Harper & Row, 1971, p 352. Meyer-Schwickerath G: Light-coagulation. St Louis, C V Mosby, 1960. Shimizu K, Tobari J: Treatment of retinal vein obstruction by photocoagulation. Jpn J Clin Ophthalmol 25:1529, 1971. Krill A, Archer D, Newell F: Photocoagulation in complications secondary to branch vein occlusion. Arch Ophthalmol 85:48, 1971. Wetzig P, Thatcher D B: The treatment of acute and longstanding venous occlusion by photocoagulation. Modern Problems in Ophthalmology. Vol. 10. Basel, Karger, 1972. Blankenship G, Okun E: Retinal tributary vein occlusion. Arch Ophthalmol 89:363, 1973. Campbell J, Wise G N: Photocoagulation therapy of branch vein obstruction. Am J Ophthalmol 75:28, 1973. Suga K, Nagata M: Treatment of retinal venous branch occlusion by photocoagulation. Technique and effect of photocoagulation. Jpn J Clin Ophthalmol 27:1021, 1973. Archer D B, Ernest J T, Newell F W: Classification of branch retinal vein obstruction. Trans Am Acad Ophthalmol Otolaryngol 78:148, 1974. Gitter K, Rosen E S: Angiographic analysis of patterns treated by photocoagulation for venous occlusive disease, In Schimizu K (ed): Fluorescein Angiography. Tokyo, Igaku Shoin Ltd, 1974 p 422. Asayama T, Fukuchi S: Experimental studies in the effectual mechanism of photocoagulation for retinal venous occlusion. 1. Histopathological changes in experimental retinal venous occlusion. Acta Soc OphthalmolJpn 77:1567, 1973. Bonnet M: Advantages - disadvantages of the use of photocoagulation in the treatment of the macular sequelae of retinal venous thrombosis. Bull Soc Ophtalmol Fr 73:719, 1973. Mosquera J M: Results of photocoagulation in the treatment of retinal venous branch occlusions. Arch Optalmol B Aires 49:171, 1974. Suga K, Nagata M: Treatment of retinal branch venous occlusion by photocoagulation. 2. Three types of fluorescein angiographic features and new mechanisms of photocoagulation. Jpn Clin Ophthalmol 27:1403, 1973.
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