Visual Field Defects After Macular Hole Surgery

H. CULVER BOLDT, MD., PAUL M. MUNDEN, MD., JAMES C. FOLK, MD., AND MARY G. MEHAFFEY, M.D.

• PURPOSE: To describe a group of patients with dense visual field defects following macular hole surgery· • METHODS: Nine (7%) of 125 patients reviewed noted onset of dense visual field defects following uncomplicated vitrectomy with gas-fluid exchange for the treatment of macular hole. Patient records were reviewed to investigate the etiology of these defects. • RESULTS: Eight (89%) of nine eyes that had surgery for macular hole developed dense, wedge-shaped visual field defects in the temporal periph­ery. One eye had an inferonasal wedge-shaped defect extending to fixation. Seven (78%) of nine eyes had generalized or focal narrowing of the retinal arteriole extending into the area of retina corresponding to the visual field defect, and five (56%) of nine eyes developed mild to moderate segmental nasal optic disk pallor. Postoperative fluorescein angiography disclosed one eye with delayed filling of the retinal arteriole extending into the area of retina corresponding to the visual field defect. Vitrectomy specimens showed no evi­dence of nerve fiber layer or internal limiting membrane in eight (89%) of nine eyes. • CONCLUSIONS: Visual field defects can occur following vitrectomy and gas-fluid exchange for macular hole. The most common visual field defect is dense and wedge-shaped and involves the tem-

Accepted for publication March 21, 1996. From the Department of Ophthalmology, University of Iowa College

of Medicine, Iowa City, Iowa. This study was supported by an unre­stricted grant from Research to Prevent Blindness, Inc., New York, New York. Presented in part at the Annual Meeting of the Association for Research in Vision and Ophthalmology, Fort Lauderdale, Florida, April 23, 1996.

Reprint requests to H. Culver Boldt, M.D., Department of Ophthal­mology, University of Iowa Hospitals and Clinics, 200 Hawkins Drive, Iowa City, IA 52242-1091; fax: (319) 356-0363; E-mail: culver-boldt@uiowa.edu

poral visual field. Although unclear, the etiology may involve trauma to the peripapillary retinal vasculature or nerve fiber layer during elevation of the posterior hyaloid or during aspiration at the time of air-fluid exchange, followed by compression and occlusion of the retinal peripapillary vessels during gas tamponade.

S INCE KELLY AND WENDEL1 REPORTED THEIR RE-sults on the efficacy of vitrectomy and gas-fluid exchange for the treatment of macular holes,

there has been a dramatic increase in the number of vitreoretinal surgeons performing this surgery. Com­plications include cataract,2 delayed opening of the hole,3,4 retinal detachment,4,5 and retinal pigment epitheliopathy.4'8 Recently, Melberg and Thomas9

described three patients with dense, wedge-shaped, temporal visual field defects following vitrectomy and air-fluid exchange for macular hole or subfoveal cho-roidal neovascularization. The etiology of these de­fects was unclear but was postulated to be mechanical trauma during air-fluid exchange by active aspiration with an extrusion needle. We report an additional series of nine patients with visual field defects follow­ing vitrectomy and gas-fluid exchange for macular hole and describe the postoperative features associat­ed with this complication.

PATIENTS AND METHODS

BETWEEN JANUARY 1991 AND OCTOBER 1995, VITRECTO-

mies for macular hole were performed on 128 eyes of 125 patients. We identified ten patients who com­plained of peripheral visual field defects following surgery. One patient developed a postoperative retinal detachment and was excluded; the remaining nine patients had uncomplicated surgeries and follow-up.

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All patients in this study complained of their symp­toms during routine postoperative visits. Because we initially were not looking for postvitrectomy visual field defects, we did not question patients specifically for such symptoms or routinely perform postoperative perimetry following macular hole surgery.

Evaluation of these complaints included Gold-mann perimetry in all cases and 30-2 full-threshold perimetry in two patients. Patient records and photog­raphy files were reviewed for details regarding preoper­ative history and visual status, surgical technique (including method of elevating the posterior hyaloid, any difficulty in elevating the hyaloid, technique of aspirating fluid during air-fluid exchange, and type and concentration of gas used for long-term postoper­ative tamponade), perioperative intraocular pressures, and postoperative course.

Surgeries were performed by one of four vitreoreti-nal surgeons. The surgical techniques were similar to those reported by other authors.1,4'6,9 Following a core pars plana vitrectomy, the posterior hyaloid was engaged with a silicone-tipped extrusion cannula using active aspiration. Gentle elevation of the poste­rior hyaloid surface was accomplished, separating the hyaloid at least to the equator. In one eye, a lighted knife was used to assist in elevating the hyaloid. An air-fluid exchange was performed with a silicone-tipped extrusion cannula, either a backflush brush using passive aspiration or a Flynn cannulated extru­sion needle using active aspiration. This was typically performed at the nasal edge of the optic disk. After five to ten minutes, any additional fluid was aspirated. In six (67%) of nine eyes, a drop of autologous serum was then placed on the macular hole. The scleroto-mies were closed as the eye was flushed with 50 ml of a long-acting gas. A nonexpansile to slightly expansile mixture of either perfluoropropane or sulfur hexa-fluoride gas, depending on the surgeon's preference, was used. Patients were instructed to position them­selves face-down for at least 20 hours a day for one to two weeks.

Intraocular pressure was followed perioperatively using a Tono-Pen. Intraocular pressure was measured preoperatively, within six hours after surgery, at day 1 and week 1, and at least once more within the first month. If intraocular pressure was elevated enough to be of concern, topical or oral therapy was instituted

372 AMERICAN JOURNAL

and additional intraocular pressure monitoring was performed as necessary.

Preoperative and postoperative stereoscopic photo­graphs of the optic disks and maculae were obtained routinely, and postoperative fluorescein angiograms were obtained in six (67%) of nine patients. These were compared specifically to examine changes in the optic disk cup and optic nerve pallor, retinal and choroidal vascular changes, and retinal pigment epi­thelial disturbances.

The vitrectomy specimen of each case was sent to our ocular pathology laboratory. The entire contents of the vitrectomy cassette were centrifuged, and the resulting pellet was embedded in paraffin, sectioned, and stained with hematoxylin and eosin and periodic acid-Schiff to facilitate identification of basement membranes. In all nine cases, remaining tissue was available as archival paraffin blocks. In eight (89%) of nine cases, these blocks were step-sectioned, stained as described above, and examined by light microsco­py. In the case of Patient 9, archival tissue remained but was not step-sectioned for reasons explained below.

RESULTS

NINE PATIENTS WHO HAD MACULAR HOLE SURGERY IN nine eyes reported dense visual field defects, first noted following the resolution of the intraocular gas bubble. Because 125 patients had 128 vitrectomies for macular hole at our institution during this time, our incidence of symptomatic postoperative visual field defects was approximately 7%. This estimate is con­servative because there may be additional patients with peripheral visual field defects who did not report their symptoms.

The Table summarizes the characteristics for the nine patients (nine eyes). Seven left eyes and two right eyes were involved. Mean patient age was 66.5 years. Unrefracted preoperative visual acuities ranged from 20/50 +2 to 20/400. Visual field defects were initially described by the patients from one to nine months following surgery (median, two months). These defects were wedge shaped and involved the temporal visual field in eight (89%) of nine eyes (Fig. 1). Seven defects were located inferotemporally, and

OPHTHALMOLOGY SEPTEMBER 1996

TABLE

SUMMARY OF PATIENTS DEVELOPING VISUAL FIELD DEFECTS FOLLOWING MACULAR HOLE SURGERY

PATIENT AGE, SEX, NO.

1 2 3 4 5 6 7 8 9

EYE

57, F, LE. 74, F, LE. 68, F, LE. 58, M, R.E. 75, M, R.E. 72, M, L.E. 63, F, LE. 65, F, L.E. 64, F, L.E.

PREOPER-ATIVE VA»

20/200 20/140 - 1 20/200 20/100 20/40 - 1 20/70 - 2 20/140 - 1 20/70 20/50 +2

PREOPERATIVE POSTERIOR VITREOUS

DETACHMENT

--------+

POSTOPER­ATIVE VA«

20/50 - 2 20/400 20/60 +1 20/50 - 2 20/140 20/60 +1 20/100 +1 20/50 +1 20/20

TIME FROM SURGERY TO VF» DEFECT

(MOS)

4 1 9 2 3 2 1.5 2 4.5

LOCATION OF VFt

DEFECT

IT* wedge V wedge IT wedge IT wedge IN1 wedge IT wedge IT wedge IT wedge IT wedge

FOLLOW-UP (MOS)

32 5

13 9 7

12 43 7 6

OPTIC DISK PALLOR

+ -+ + --+ -+

ARTERIOLAR NARROWING

+ (P) - ( S " )

+ ffl + (gr + (g) + (f) + (g) + (f)

—

*VA indicates visual acuity with correction. *νΤ-" Indicates visual field. *IT indicates inferotemporai. *T indicates temporal 'IN indicates inferonasal. f indicates focal narrowing. *s indicates sheathed only. **g indicates generalized narrowing.

one defect was temporal. An absolute scotoma usually extended to within 30 to 40 degrees of fixation, but a relative scotoma extended to the blind spot. This was confirmed in our two patients with 30-2 visual fields. In one eye, the defect was inferonasal and extended to fixation. There were no homonymous visual field defects in the fellow eye. No eye had received prior ocular surgeries except in the case of Patient 5, who underwent vitrectomy and membranectomy for an impending macular hole; nevertheless, the hole pro­gressed to full thickness six weeks later and the eye underwent vitrectomy, membranectomy, and gas-fluid exchange. The visual field defect was not noted by the patient until after the second surgery.

Perioperative nursing and anesthesia records were reviewed, and none of the patients had a significant hypotensive or hypertensive episode during hospitali-zation. None of the patients had a history of glauco­ma, and there were no abnormalities by preoperative examination or photography in the optic disks to suggest glaucoma. Three of nine patients had a history of hypertension, and none of the patients had a history of atherosclerotic disease. By comparison, of

the 115 patients who had macular hole surgery but did not report visual field defects, 57 (49.6%) had hypertension. On preoperative examination, eight (89%) of nine eyes with macular holes had either complete attachment of the posterior hyaloid or limited vitreofoveal separation of the hyaloid. Patient 9 had a posterior vitreous detachment with a Weiss ring documented before vitrectomy. Postoperatively, all patients had brief elevations above baseline of intraocular pressure. The maximum intraocular près-

élévations recorded within the first month sure ranged from 20 mm Hg to 45 mm Hg (mean, 28.4 mm Hg). By comparison, of the 115 patients who had macular hole surgery but did not report visual field defects, the maximum postoperative intraocular pres­sure elevations ranged from 16 mm Hg to 46 mm Hg (mean, 26.4 mm Hg). This difference was not statisti­cally significant (P = .39). All intraocular pressure elevations were transient and responded to medical intervention. No patient had a total gas fill, and no patient needed removal of intraocular gas or fluid to control intraocular pressure.

In eight (89%) of nine eyes, air-fluid exchange was

V O L . 1 2 2 , No . 3 VISUAL FIELD DEFECTS AFTER MACULAR HOLE SURGERY 3 7 3

Fig. 1 (Boldt and associates). Goldmann perimetry of the postoperative visual field defects following macular hole surgery. The visual field numbers correspond to the patient numbers in the Table.

performed using a silicone-tipped passive aspiration instrument (backflush brush). In one eye, active aspiration was employed using a silicone-tipped extru­sion needle (Flynn cannulated extrusion needle). Autologous serum was used as a surgical adjunct in six (67%) of nine eyes.

Postoperative follow-up ranged from five months to 43 months (mean, 14.9 months). At the most recent examination, the macular holes were anatomically closed in seven (78%) of nine patients. Postoperative visual acuity with current spectacle correction ranged from 20/20 to 20/400.

In seven of nine eyes, the retinal branch arteriole entering the area of retina corresponding to the visual field defect appeared mildly to moderately narrowed.

The arteriolar narrowing was not present on preoper­ative photos and these findings were confirmed inde­pendently by three observers (H.C.B., P.M.M., J.C.F.). In four (44%) of nine eyes, the arteriole on and adjacent to the nasal portion of the optic disk was irregularly narrowed, with focal areas of sheath­ing. Three (33%) of nine eyes had moderate general­ized narrowing of the involved arterioles. One eye had arteriolar sheathing without definite vascular narrow­ing. On fluorescein angiography, the retinal artery filling time was normal except in the case of Patient 4, in which filling of the involved arteriole was delayed. Comparing preoperative and postoperative photo­graphs and angiograms, we found no retinal arteriolar changes outside the area corresponding to the visual

374 AMERICAN JOURNAL OF OPHTHALMOLOGY SEPTEMBER 1996

field defects. The focal arteriolar narrowing seen on the color photographs was confirmed angiographical-ly. In one eye, a small blot-shaped intraretinal hemor­rhage was noted ten weeks postoperatively in the superonasal midperiphery, within the area corre­sponding to the visual field defect. Comparison with preoperative photographs showed that five (56%) of nine eyes had developed focal segmental optic disk pallor in the area of the disk corresponding to the visual field defect. Two (22%) of nine eyes had focal areas of coarse retinal pigment epithelial changes within the area of the fundus corresponding to the visual field defect. However, these areas were too small and located too far nasally from the optic nerve to account for the entire visual field defect. Some loss of nerve fiber layer was frequently apparent, correspond­ing to the wedge-shaped visual field defects, but these defects could not be well documented by red-free photography.

Initial histopathologic examination of the nine original vitrectomy specimens disclosed no evidence of internal limiting membrane, nerve fiber layer, or deeper retinal elements in eight (89%) of nine eyes. Preoperative examination of Patient 9 disclosed a macular hole with a mild epiretinal membrane and a total posterior vitreous detachment. The epiretinal membrane was peeled from the macula but did not extend to the disk. Fragments of internal limiting membrane within this specimen were felt to arise from peeling of the epiretinal membrane. One speci­men had several cells from the nonpigmented ciliary epithelium. Step-sectioning of the archival blocks, excluding those from Patient 9, disclosed no inter­nal limiting membrane, nerve fiber layer, or retinal elements.

CASE REPORTS

• CASE 3: A 68-year-old woman in 1994 had an eight-month history of metamorphopsia and de­creased vision in her left eye. She was healthy, with no history of hypertension or atherosclerosis. Visual acuity with correction was R.E.: 20/20 —1 and L.E.: 20/200. The right fundus was normal; the left eye had a 500^m-diameter macular hole with an overlying pseudo-operculum and a cuff of subretinal fluid (stage

3 macular hole, according to the Gass classifica­tion10). Visual fields were full to confrontation. One week later, a pars plana vitrectomy was performed, elevating the posterior hyaloid with a silicone-tipped extrusion cannula. The hyaloid was stripped to the equator and removed with the vitrectomy instrument. An air-fluid exchange was performed with a backflush brush. Autologous serum was placed on the hole after reaspirating residual fluid. A gas-gas exchange of 18% perfluoropropane was performed, and the eye was closed. There were no intraoperative or perioperative complications. The intraocular pressure ranged from 24 mm Hg to 25 mm Hg for the first week, then remained below 19 mm Hg for the remainder of the follow-up period.

Nine months after surgery, the patient described a shadow in her temporal visual field that had been present for several months. Visual acuity with correc­tion was R.E.: 20/20 - 1 and L.E.: 20/150, pinhole 20/100. On Goldmann perimetry of the left eye, a dense visual inferotemporal field defect extended within 30 degrees of fixation (Fig. 1). Goldmann perimetry in the right eye was normal. There was nasal pallor of the optic disk with irregular narrowing of the superonasal branch retinal arteriole (Fig. 2). No pigmentary changes were noted in the peripheral fundus, and the macular hole was closed. Four months later, following cataract extraction with pos­terior chamber lens implantation, visual acuity with correction was L.E.: 20/60 +1 . Goldmann perimetry confirmed the persistent inferotemporal defect, which was unchanged. On examination, the fundus of the left eye was stable except for one intraretinal hemor­rhage at the 10:30 meridian in the midperiphery.

• CASE 7: A 62-year-old woman in 1991 had a one-day history of metamorphopsia in the left eye. Her medical history was significant for hypertension treated with hydrochlorothiazide and for hypertriglyc-eridemia. Visual acuity with correction was R.E.: 20/20 and L.E.: 20/70 —1. There were minimal hard drusen in both maculae, with a 150^m-diameter macular hole with a small cuff of subretinal fluid and an attached posterior hyaloid in the left eye (stage 2 macular hole, according to the Gass classification10). During the next 5 Vi months, visual acuity in the left eye decreased to 20/140 —1. She then decided to undergo vitrectomy. The hyaloid was elevated using a

VOL.122, No. 3 VISUAL FIELD DEFECTS AFTER MACULAR HOLE SURGERY 3 7 5

Fig. 2 (Boldt and associates). Patient 3. Left, Preoperative disk photograph of the left eye, showing a healthy neuroretinal rim, essentially normal peripapillary retinal vessels, and a stage 3 macular hole (the circular white objects in the overlying temporal macula are artifacts). Right, Postoperative photograph of the same eye showing segmentai disk pallor superonasally with focal narrowing and sheathing of the superonasal arteriole (arrow).

silicone-tipped cannulated extrusion needle, and a backflush brush was used to perform the air-fluid exchange. A gas-gas exchange using 20% sulfur hexafluoride was then performed. There were no intraoperative or perioperative complications. The intraocular pressure was 26 mm Hg several hours after surgery and 19 mm Hg or less on all subsequent visits during the follow-up period.

One week following surgery, the macular hole appeared to be open, and visual acuity was L.E.: 20/100. Ten weeks after surgery, the patient described a peripheral black area in the field of vision of the left eye; visual acuity was 20/140 and the macular hole was still open. The optic disk had mild focal pallor superonasally, and there was generalized narrowing with mild focal sheathing of the superonasal branch retinal arteriole (Fig. 3, top and bottom left). Gold-mann perimetry of the left eye disclosed a temporal and inferotemporal dense visual field defect extending within 35 degrees of fixation, and a central scotoma (Fig. 1). Visual field in the right eye was normal. Fluorescein angiography disclosed generalized nar­rowing of the superonasal branch retinal arteriole with delayed filling of the superonasal branch venule; the remainder of the retinal circulation and the

choroidal circulation filled normally. Repeated visual fields over three years demonstrated the visual field defect to be permanent and static. Subsequent exami­nations disclosed pigment clumping in the supero­nasal midperiphery (Fig. 3, bottom right). A cataract extraction with posterior chamber implant was per­formed as nuclear sclerosis progressed. On last exami­nation, three and one-half years following surgery, visual acuity was L.E.: 20/100 + 1 , the macular hole was open, and the peripheral pigmentary changes in the left eye were stable.

DISCUSSION

DURING THE PAST FIVE YEARS, VITREORETINAL TECH-niques using vitrectomy and air-fluid exchange have been applied toward treating macular diseases, such as macular hole and subfoveal choroidal neovasculariza-tion. These eyes generally have intact peripheral visual fields before surgery. It may be more likely for patients with such eyes to detect and report postoper­ative visual field defects than it is for patients under­going surgery for more diffuse disease processes, such as extensive retinal detachments or proliferative dia-

376 AMERICAN JOURNAL OF OPHTHALMOLOGY SEPTEMBER 1996

Fig. 3 (Boldt and associates). Patient 7. Top, Preoperative disk photograph of the left eye, showing a healthy neuroretinal rim and normal peripapillary retinal arterioles (this photograph was taken before the development of the macular hole). Bottom left, Postoperative photograph, showing segmentai disk pallor superonasally with generalized narrowing and mild sheathing of the superonasal retinal arteriole (arrow). Bottom right, Postoperative fundus photograph of the superonasal midperiphery of the same eye, just posterior to the equator, showing coarse pigmentary clumping, retinal pigment epithelial atrophy, and retinal arteriolar narrowing.

betic retinopathy. However, vitrectomy alone for mac­ular disease does not seem to be associated with visual field defects. For example, peripheral visual field defects do not appear to be associated with vitrectomy for macular pucker. The additional steps performed

routinely during macular hole surgery, as opposed to vitrectomy for macular pucker, include mechanical separation of the posterior hyaloid and gas-fluid exchange. It is likely that one or both of these steps play a major role in the development of peripheral

V O L 122, No . 3 VISUAL FIELD DEFECTS AFTER MACULAR H O L E SURGERY 377

visual field defects following vitrectomy for macular hole. Although nine (7%) of our 125 patients report­ed visual field defects following vitrectomy for macular hole, the actual incidence of peripheral visual field defects may be even higher. We did not question each patient about postoperative visual field defects, nor did we obtain postoperative visual fields on all 125 patients. A prospective study would be necessary to examine the true incidence of these defects better.

The Appendix lists several possible etiologies for the peripheral visual field loss following vitrectomy. In the majority of patients with idiopathic macular hole, there is either no posterior vitreous detachment or only a limited vitreofoveal separation of the cortical vitreous. Mechanical separation of the cortical vitre­ous from the retina is felt to be crucial in the surgical repair of a macular hole. The cortical vitreous is frequently tightly adherent at the disk.11 During elevation and separation of the peripapillary cortical vitreous, traction on the peripapillary retina is com­mon. We typically separated the posterior hyaloid, using active aspiration with a soft-tipped extrusion cannula, starting nasal, inferior, or superior to the disk. In none of our patients did the surgeon note what appeared to be tearing of the retina or nerve fiber layer. However, separation of the posterior hya­loid in a monkey model has been shown to produce enough retinal traction to avulse internal limiting membrane, nerve fiber layer, and even deeper retinal elements (Russell SR, M.D., Hageman GS, Ph.D., oral communication, August 1995). Notably, there was no intraoperative indication during the monkey vitrectomies that retinal damage was occurring, but the damage was clearly evident by histopathologic examination. We noted no evidence of internal limiting membrane, nerve fiber layer, or deeper retinal elements on histopathologic examination of our pa­tients' eyes, except for the eye of Patient 9. A posterior vitreous separation was already present in this eye, so there was no need to detach the posterior hyaloid. Fragments of internal limiting membrane were found in this specimen, probably as a result of peeling the parafoveal epiretinal membrane. Our histopathologic findings nevertheless do not eliminate a role for mechanical shearing of the nerve fiber layer in these peripheral visual field defects. Internal limiting mem­brane or nerve fiber layer could be sheared or dam­aged during elevation, but remain attached to the

378 AMERICAN JOURNAL OF

retina and not be collected in the vitrectomy speci­men. If a large enough volume of nerve fibers is damaged, segmental optic disk pallor might occur.

Indeed, there is indirect evidence that the hyaloid is tightly adherent to the nasal peripapillary retina. Nasal peripapillary hemorrhages as a result of vitreo-papillary traction from partial posterior vitreous de­tachment have been described.12 However, such shearing forces would seem more likely to affect the superficial nerve fibers. The topographic orientation of the peripapillary nerve fiber layer is such that nerve fibers from peripheral retinal elements are located deeper in the nerve fiber layer than are nerve fibers from more posteriorly positioned retinal elements.13,14

Therefore, shearing damage to the superficial nerve fiber layer near the disk would be expected to cause visual field defects adjacent to the optic nerve and to spare the peripheral visual field. This is just the opposite of the typical visual field defect seen in our series. In addition, Patient 9 had a posterior vitreous detachment preoperatively, and no membrane was peeled from the peripapillary retina or optic nerve. Obviously, a different etiology must be considered for the visual field defect in this patient.

If the peripheral visual field defects in our patients arose from mechanical trauma to the nerve fiber layer, one might see some secondary narrowing of the retinal vessels in the involved section of retina. Decreased retinal vessel diameters have been reported in eyes with nerve fiber layer loss secondary to glaucoma,1516 anterior ischemie optic neuropathy,16

and descending optic atrophy.17 In many of these eyes, the narrowing was focal and involved the peripapil­lary arterioles.16,18 This narrowing possibly arises from decreased need for a vascular supply in the corre­sponding superficial retina. We detected generalized arteriolar narrowing in three eyes, focal arteriolar narrowing in four eyes, and focal arteriolar sheathing in one additional eye. Although these arteriolar changes may be secondary to nerve fiber layer loss, it is also possible that mechanical shearing forces trans­mitted to retinal arterioles during separation of the hyaloid might result in focal inflammation and tran­sient occlusion of the vessels. Because the majority of the surgical attempts to separate the cortical vitreous from the retina are performed nasal to the nerve, the nasal vessels may be more likely to sustain damage from such a mechanism. If the arteriolar occlusion

OPHTHALMOLOGY SEPTEMBER 1996

damages a large enough volume of nerve fibers, segmental optic disk pallor might occur. Systemic factors such as hypertension or atherosclerotic disease may predispose retinal arterioles to damage, but we found no evidence of this in our retrospective study.

Another opportunity for mechanical trauma in macular hole surgery occurs during air-fluid exchange. Aspiration of fluid was often performed just nasal to the optic nerve in our patients. Melberg and Thomas9

postulated that active aspiration just nasal to the nerve may have caused the temporal wedge-shaped visual field defects in their three patients. In our series, however, active aspiration of fluid was per­formed in only one (11%) of nine patients. In the other eight patients, fluid was aspirated passively using a soft-tipped silicone brush vented to atmospheric pressure. It seems less likely that this instrument would damage the nerve fiber layer or retinal arteri­oles, but we cannot exclude this possibility.

A potentially important additional source of trau­ma is the gas bubble used to tamponade the retina postoperatively. Postoperative compression of the peripapillary nerve fiber layer or retinal vessels that have been acutely damaged during mechanical sepa­ration of the posterior hyaloid may play a role in the development of peripheral visual field defects. There is recent experimental data indicating that prolonged contact of the gas bubble with the retina might also exert a toxic effect on the retina.19

Infarcts of the choroid associated with visual field defects were reported in the early days of vitrectomy and phacoemulsification20'22 and were attributed to severe sustained intraoperative increases in intraocu­lar pressure. Acute outer retinal whitening can be seen, associated with central and paracentral visual field defects. Over several weeks, the central visual field recovers partially, and retinal whitening is re­placed by mottled changes in the retinal pigment epithelium. Retinal vessel caliber and a normal optic disk tend to be preserved. This retinal whitening has been quite dramatic and most prominent in the macula, and we doubt that such prominent changes would be overlooked in the postoperative period, even with the gas bubble partially obscuring visualization of fundus details. This whitening has also been most prominent in the macula. Pigmentary changes have occasionally been reported with posterior ciliary ar­tery occlusions,23,24 and extramacular involvement can

be wedge-shaped. Indeed, two (22%) of nine patients in our series had pigmentary changes in the area of the visual field defect, located toward the center of the visual field defect, and were certainly much smaller in area than the defect. Our current techniques for vitrectomy allow for better pressure control, and none of our patients had elevation of the intraocular pressure intraoperatively. Although peripheral visual field defects were reported following vitrectomy for subfoveal choroidal neovascularization,9 during which intraocular pressure is typically elevated transiently during membrane removal to control bleeding, even transient elevation of intraocular pressure is not necessary during macular hole surgery. In addition, Hutton, Fuller, and Snyder25 recently described sever­al patients with peripheral visual field defects follow­ing vitrectomy for macular hole who had intact photoreceptor function in the involved area of retina, as determined by focal electroretinography. This should not occur if the visual field defects arose from occlusion of the choroidal circulation.

Retinal or ciliary artery occlusion might occur perioperatively from nontraumatic etiologies, such as systemic hypotension or elevated intraocular pressure. We could not document any significant systemic hypotensive episodes in our patients, and the postop­erative intraocular pressure increases were generally not very high and were relatively brief. In addition, we cannot explain why the vast majority of these defects would predominantly involve the nasal portion of the fundus.

Anterior ischemie optic neuropathy can occur perioperatively. No disk swelling was noted in any of our patients, but the disk edema seen in anterior ischemie optic neuropathy might be difficult to visu­alize through the gas bubble. In addition, altitudinal field defects are typical of anterior ischemie optic neuropathy, whereas temporal wedge-shaped defects are rather uncommon.26

Glaucomatous visual field loss, which could occur from elevated postoperative pressures, is also unlikely. The recorded intraocular pressure elevations in eight (89%) of nine patients were brief and less than 34 mm Hg. These intraocular pressure elevations were not statistically different from those seen in the 115 eyes in this study, which had vitrectomy for macular hole but no reported visual field defect. We noted no increase in cupping or focal notching of the neuroret-

VOL. 122, NO. 3 VISUAL FIELD DEFECTS AFTER MACULAR HOLE SURGERY 379

inai rim in any of our patients. A temporal wedge-shaped visual field defect is uncommon with glauco-matous optic atrophy.

Light toxicity has been described as a cause of postoperative scotomas following vitrectomy .6,2? Hold-ing the endoilluminator close to the retina for pro­longed periods of time can cause photochemical damage to the photoreceptors and retinal pigment epithelium. This can result in pigmentary changes at the level of the retinal pigment epithelium. We take great care to keep the illumination low and the light pipe away from the retina. Although we noted retinal pigment epithelial changes in the area of the visual field defect in two (22%) of nine patients, the area and location of the pigmentary changes were too small to account for the size of the defects. The field loss in all our patients extended to the periphery, typical for vascular or nerve fiber-related pathology, as opposed to the discrete scotomas expected from focal areas of damage to photoreceptors and retinal pig­ment epithelium.

We feel that the most likely cause for inferonasal visual field defect extending to fixation in the eye of Patient 5 (our only eye with a nasal visual field defect) is a branch retinal artery occlusion. The visual field defect corresponds with the superotemporal branch retinal arteriolar distribution, and this arteriole has generalized narrowing on fundus photography and fluorescein angiography. It is uncertain whether the visual field loss in the other eight patients developed from the same mechanism as that for Patient 5.

In summary, peripheral visual field defects can occur following vitrectomy for macular hole with a disturbingly high incidence. The cause of these defects has yet to be determined, but damage to the peripapillary retinal arterioles, nerve fiber layer, or both, seems the most likely etiology. Damage may be exacerbated by compression of acutely injured tissues by the gas tamponades and by face-down positioning. The most prevalent postoperative finding we detected was focal or generalized narrowing of the arteriole entering the area of retina corresponding to the visual field defect. Arteriolar narrowing may represent resid­ual changes from a perioperative vascular occlusion or may be secondary to the loss of nerve fiber layer. Although we could not document the presence of nerve fiber layer in the vitrectomy specimens from surgery, we still feel that damage to the inner retina

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APPENDIX

Possible mechanisms for peripheral visual field defects after macular hole surgery

1. Mechanical trauma during separation of the posterior hyaloid

Damage to retinal arterioles Damage to nerve fiber layer or retina

2. Mechanical compression because of gas tamponade

3. Toxicity because of gas tamponade 4. Mechanical trauma during air-fluid exchange

Damage to retinal arterioles Damage to nerve fiber layer or retina

5. Posterior ciliary artery occlusion Choroidal infarct Anterior ischemie optic neuropathy

6. Glaucomatous damage from elevated intraocular pressure

7. Light toxicity

during elevation of the posterior hyaloid may play a role in the pathogenesis of some of these visual field defects. If this is so, then the incidence of such visual field defects might be reduced by using investigational agents capable of inducing posterior vitreous detach­ment pharmacologically.28 Indeed, there may be sev­eral different mechanisms involved in creating these visual field defects. Until further studies can be performed, therefore, patients undergoing vitrectomy for macular hole should be warned of the possibility of postoperative peripheral visual field defects.

REFERENCES

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