British Jrournal of Ophthalmology 19 9 6; 80:5 1 9-5 2 5 Visual field loss following vitrectomy for stage 2 and 3 macular holes E Ezra, G B Arden, P Riordan-Eva, GW Aylward, Z J Gregor Abstract Aim-To describe the phenomenon of peripheral field loss following routine pars plana vitrectomy for stage 2 and 3 full thickness macular hole and to investigate the underlying mechanism. Methods-Five patients, who reported peripheral field defects after apparently uncomplicated vitrectomy, posterior cor- tical vitreous peeling, and perfluoropro- pane (C3F8) gas tamponade, were studied retrospectively with slit-lamp biomicros- copy, automated and kinetic perimetry, fundal fluorescein angiography, focal elec- troretinography (ERG), and colour con- trast sensitivity (CCS) testing. Results-All five patients, who were be- tween 50 and 73 years of age, reported an inferotemporal field defect following reso- lution of the intraocular gas bubble. In all eyes, the scotomata encroached to within 200 to 300 of fixation and to within 50 to 150 of the blind spot. In one eye, a partial alti- tudinal component was evident. All scoto- mata subsequently remained stable and three eyes developed subtle segmental nasal disc pallor and nerve fibre loss corresponding to the field defect. CCS testing revealed absent colour contrast in the scotomatous area, in the presence of a preserved focal quadrantic flash ERG, compared with normal CCS protan thresholds and focal ERGs in unaffected quadrants, indicating preserved outer retinal function in the area of the scotoma. Conclusions-These observations support the hypothesis that field defects occur as a result of retinal nerve fibre layer damage. It is proposed, on the basis of intraopera- tive observations and other evidence, that the most likely site of nerve fibre damage is at the nasal portion of the optic nerve rim or peripapillary retina, probably due to traction during cortical vitreous peel- ing. (BrJ3 Ophthalmol 1996;80:519-525) The hypothesis that tangential vitreomacular traction leads to the formation of idiopathic full thickness macular holes (FTMH),' 2 has led to the use of pars plana vitrectomy, posterior cortical vitreous peeling, and long acting intraocular gas tamponade for its treatment. Several studies have shown this to be effective in closing FTMHs and producing significant improvement in visual acuity.9 Peeling of adherent posterior cortical vitreous is considered an integral part of the procedure for stage 2 and 3 FTMHs.'-9 It is effected by engaging cortical vitreous with active aspira- tion using the vitreous cutter or a soft tipped cannula,' and stripping anteriorly. Alterna- tively, passive aspiration may be used. The manoeuvre may be associated with a significant risk of intraoperative retinal breaks due to vitreoretinal traction.4 5 9 We describe five patients who developed peripheral field loss following otherwise uncomplicated vitrectomy and posterior cortical vitreous peeling for stage 2 and 3 FTMHs and discuss the possible underlying mechanisms. Patients and methods We studied retrospectively five patients who reported the onset of a peripheral field defect following macular hole surgery. Four were female and one male, aged 50-73 (mean 63) years. Two had mild hypertension controlled with one medication. One patient (case 4) had non-insulin dependent diabetes mellitus and had been treated successfully with a macular laser grid 5 years previously in the same eye. At the time of the macular hole surgery, no significant diabetic macular oedema was present. One patient (case 2) had red-green colour deficiency. One eye was operated on for a stage 2 and four eyes for stage 3 FTMH, with preoperative visual acuities of 6/60-6/24 (mean 6/36). All five eyes had similar procedures for stage 2 and 3 FTMHs, without apparent complications. Briefly, following a three port pars plana vitrec- tomy, adherent posterior cortical vitreous was engaged, in the region of the optic disc or over the peripapillary retina, using the vitreous cut- ter with active aspiration. The layer was then stripped anteriorly beyond the equator, and the vitrectomy completed. Epiretinal membrane dissection was performed where necessary and the peripheral retina and entry sites carefully examined for iatrogenic breaks. This was followed by fluid-air exchange and aspiration of subretinal fluid from the cuff around the FJTMH, with a 34 gauge microcannula, and drying under air for 10 minutes. Where autolo- gous serum was used, 0.1-0.2 ml were applied to the hole for 10 minutes. Finally, the procedure was completed with an air-gas exchange. As postoperative tamponade is believed to increase surgical success,5" we pre- fer perfluoropropane (C3F8) 14-16% which provides a longer lasting gas bubble, allowing tamponade for at least 14-21 days. Postoperatively, patients were instructed to posture in the face down position for at least 2 weeks, and were examined on the first day, at 2 519 Vitreo-retinal Unit, Moorfields Eye Hospital, London E Ezra GW Aylward Z J Gregor Electrodiagnostic Department, Moorfields Eye Hospital, London G B Arden Neuro-ophthalmology Unit, Moorfields Eye Hospital, London P Riordan-Eva Correspondence to: Mr Z J Gregor, Vitreo-retinal Unit, Moorfields Eye Hospital, London EC1V 2PD. Accepted for publication 7 March 1996 on May 8, 2020 by guest. Protected by copyright. http://bjo.bmj.com/ Br J Ophthalmol: first published as 10.1136/bjo.80.6.519 on 1 June 1996. Downloaded from
Transcript
British Jrournal of Ophthalmology 1996;80:5 19-525
Visual field loss following vitrectomy for stage 2and 3 macular holes
E Ezra, G B Arden, P Riordan-Eva, GW Aylward, Z J Gregor
AbstractAim-To describe the phenomenon ofperipheral field loss following routine parsplana vitrectomy for stage 2 and 3 fullthickness macular hole and to investigatethe underlying mechanism.Methods-Five patients, who reportedperipheral field defects after apparentlyuncomplicated vitrectomy, posterior cor-tical vitreous peeling, and perfluoropro-pane (C3F8) gas tamponade, were studiedretrospectively with slit-lamp biomicros-copy, automated and kinetic perimetry,fundal fluorescein angiography, focal elec-troretinography (ERG), and colour con-trast sensitivity (CCS) testing.Results-All five patients, who were be-tween 50 and 73 years of age, reported aninferotemporal field defect following reso-lution of the intraocular gas bubble. In alleyes, the scotomata encroached to within200 to 300 offixation and to within 50 to 150ofthe blind spot. In one eye, a partial alti-tudinal component was evident. All scoto-mata subsequently remained stable andthree eyes developed subtle segmentalnasal disc pallor and nerve fibre losscorresponding to the field defect. CCStesting revealed absent colour contrast inthe scotomatous area, in the presence of apreserved focal quadrantic flash ERG,compared with normal CCS protanthresholds and focal ERGs in unaffectedquadrants, indicating preserved outerretinal function in the area ofthe scotoma.Conclusions-These observations supportthe hypothesis that field defects occur as aresult of retinal nerve fibre layer damage.It is proposed, on the basis of intraopera-tive observations and other evidence, thatthe most likely site of nerve fibre damageis at the nasal portion of the optic nerverim or peripapillary retina, probably dueto traction during cortical vitreous peel-ing.(BrJ3 Ophthalmol 1996;80:519-525)
The hypothesis that tangential vitreomaculartraction leads to the formation of idiopathicfull thickness macular holes (FTMH),' 2 hasled to the use of pars plana vitrectomy,posterior cortical vitreous peeling, and longacting intraocular gas tamponade for itstreatment. Several studies have shown this tobe effective in closing FTMHs and producingsignificant improvement in visual acuity.9Peeling of adherent posterior cortical vitreous
is considered an integral part of the procedurefor stage 2 and 3 FTMHs.'-9 It is effected byengaging cortical vitreous with active aspira-tion using the vitreous cutter or a soft tippedcannula,' and stripping anteriorly. Alterna-tively, passive aspiration may be used. Themanoeuvre may be associated with a significantrisk of intraoperative retinal breaks due tovitreoretinal traction.4 5 9 We describe fivepatients who developed peripheral field lossfollowing otherwise uncomplicated vitrectomyand posterior cortical vitreous peeling for stage2 and 3 FTMHs and discuss the possibleunderlying mechanisms.
Patients and methodsWe studied retrospectively five patients whoreported the onset of a peripheral field defectfollowing macular hole surgery. Four werefemale and one male, aged 50-73 (mean 63)years. Two had mild hypertension controlledwith one medication. One patient (case 4) hadnon-insulin dependent diabetes mellitus andhad been treated successfully with a macularlaser grid 5 years previously in the same eye. Atthe time of the macular hole surgery, nosignificant diabetic macular oedema waspresent. One patient (case 2) had red-greencolour deficiency.One eye was operated on for a stage 2 and
four eyes for stage 3 FTMH, with preoperativevisual acuities of 6/60-6/24 (mean 6/36). Allfive eyes had similar procedures for stage 2 and3 FTMHs, without apparent complications.Briefly, following a three port pars plana vitrec-tomy, adherent posterior cortical vitreous wasengaged, in the region of the optic disc or overthe peripapillary retina, using the vitreous cut-ter with active aspiration. The layer was thenstripped anteriorly beyond the equator, and thevitrectomy completed. Epiretinal membranedissection was performed where necessary andthe peripheral retina and entry sites carefullyexamined for iatrogenic breaks. This wasfollowed by fluid-air exchange and aspirationof subretinal fluid from the cuff around theFJTMH, with a 34 gauge microcannula, anddrying under air for 10 minutes.Where autolo-gous serum was used, 0.1-0.2 ml were appliedto the hole for 10 minutes. Finally, theprocedure was completed with an air-gasexchange. As postoperative tamponade isbelieved to increase surgical success,5" we pre-fer perfluoropropane (C3F8) 14-16% whichprovides a longer lasting gas bubble, allowingtamponade for at least 14-21 days.
Postoperatively, patients were instructed toposture in the face down position for at least 2weeks, and were examined on the first day, at 2
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Vitreo-retinal Unit,Moorfields EyeHospital, LondonE EzraGW AylwardZ J Gregor
ElectrodiagnosticDepartment,Moorfields EyeHospital, LondonG B Arden
weeks, 6 weeks, and at 3 monthly intervalsthereafter. Chloramphenicol eyedrops 0.5%four times daily, dexamethasone 0.1% fourtimes daily, and atropine 1% twice daily wereused for all operated eyes.
All five patients reported a peripheral fielddefect after the gas bubble had completelyresolved. A full ocular and neuro-ophthalmicassessment was performed between 8 and 16weeks after surgery, and all field defects wereconfirmed with Humphrey and Goldmannperimetry. As this was an unexpected finding,preoperative fields were not available for com-parison. In all eyes, we attempted to determinethe postoperative configuration of the hole,identify any retinal or retinal vascular pathol-ogy, assess retinal nerve fibre layer (RNFL)integrity and optic disc characteristics, and torecord macular, peripheral retinal, and opticnerve function.
Clinical examination included a full slit-lamp and funduscopic examination followedby neuro-ophthalmic assessment. Best cor-rected visual acuity, Ishihara colour scores,pupillary reflexes (graded as trace, mild, mod-erate, severe), automated Humphrey perimetry(30-2 and 60-2), and Goldmann kineticperimetry were determined. Full fundal exami-nation was performed with direct and indirectophthalmoscopy, 78 D fundal lens, threemirror Goldmann contact lens, and macularcontact lens with full mydriasis. Optic discdrusen were excluded in all patients byultrasound and blue pre-fluorescein photogra-phy. All patients had fundal photography,including red-free images, and fundal fluores-cein angiography between 8 and 16 weekspostoperatively, after which photography wasrepeated at 3 month intervals. Electrodiagnos-tic testing was performed between 12 and 24weeks postoperatively in all patients.
ELECTRODIAGNOSTIC AND PSYCHOPHYSICAL
EVALUATIONWe performed focal electroretinography(ERG) to evaluate outer retinal function in thescotomatous area, compared with the unaf-fected quadrants in the same eye and corre-sponding quadrants in the fellow eye. Corticalvisual evoked potentials (VEP) were alsoobtained.
Focal ERGWe used an ERG and visual stimulator whichconsists of a 5 cm bowl, concave side pointingto the patient's eye, which is back illuminatedby a number of light emitting diodes (LEDs).The light from the diodes is diffused, and whenthe bowl is placed as near as possible to the eye,it forms a ganzfeld. The diodes are containedin a 5 cm plastic tube mounted on apantographic arm, and could thus easily bedirected to the eye from any point in visualspace. In this investigation, the bowl was with-drawn to 28 cm from the cornea, so as to illu-minate a 100 segment of the visual field. Thetube containing the bowl was mounted onto alarge sheet of white plastic on which fixationspots were placed appropriately. The fixationspots and the plastic surround were illumi-
nated with red light to minimise stray light. Bymoving the fixation spot in front of the patient,and angling the stimulator appropriately, thedesired regions of retina could be illuminated.
Focal ERG responses were recorded fromthe fovea and from the scotomatous area. Thelatter were then compared with focal ERGsfrom unaffected quadrants in the affected eyeand from quadrants in the fellow eye.
Focal foveal responses were recorded withthe subject fixating on the centre of the stimu-lus, using an inbuilt luminous fixation pointbuilt into the bowl. Individual quadrants werestimulated by the subject fixating on a point19.4 cm from the centre of the bowl, so as tostimulate a segment of visual field 310 to 380from fixation (that is, within the scotoma inaffected quadrants). For example, to stimulatethe inferotemporal quadrant of the rightfield-that is, the superonasal retina-the sub-ject fixates on a point 19.4 cm superonasally tothe centre of the stimulus.
In order to demonstrate that the responseswere indeed focal, rather than attributable tostimulation of other areas by scattered light, weused an orange stimulus of 3 ms, 460 Td-s610 nm superimposed on a 32 Td-s 665 nmbackground. This produces large cone re-sponses foveally, but very small responses inthe retinal periphery to be tested, where thedensity of cones is much less, thus proving thatscatter from the periphery to the fovea wasnegligible. For the focal ERG studies describedhere, a combination of orange (3 ms 460 Td-s610 nm) and blue (3 ms 57 Td-s 460 nm) lighton a 32 Td 665 nm background was used sothat the predominantly rod driven ERGs fromthe retinal periphery and the cone drivenERGs at the fovea could be elicited by the samestimulus.
Since the ERG amplitude has a considerableintersubject variation, focal peripheral ERGswere also expressed as a fraction of the ampli-tude of the foveal response, decreasing the dis-persion of results.
Visual evoked cortical responses (VER)The cortical evoked response to the sameflashes was recorded. The large nI-p 1 complexrecorded after foveal stimulation was absentwhen the periphery was stimulated in all quad-rants of affected and normal fellow eyes. Thusthe stimulus conditions made it possible torecord focal VER responses only when thefovea was stimulated. Standard full VERresponses were also recorded in affected andfellow eyes.
Colour contrast sensitivity (CCS)Colour contrast thresholds were measuredwith the computer graphics system describedby Arden et al,10 which has been used for con-trast threshold testing in glaucoma," using amodification of the 'ring' technique describedby TakYu and Arden." The original programhas been modified so that the thresholds ineach of 4 quadrants can be estimated simulta-neously. The patients were placed 22 cm fromthe screen, so that the colour contrast thresh-olds were determined 30-35' from fixation-
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Visualfield lossfolowing vitrecwmy for stage 2 and 3 macular holes
A B
F
Figure 1 Postoperative Goldmann perimetry, with III4e and I4e targets, shows inferotemporal or temporal scotomas in alleyes (A-E). Humphrey automated perimetry (30-2) in case 1 shows a similar defect (F). Case 4 (D) had morewidespread constriction and case 5 (E) had a partial altitudinal component.
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Age / sex 50/F 69/M 61/F 62/F 73/MMedical history Nil Mild hypertension Nil NIDDM Mild hypertensionSide Right Left Right Right LeftRefraction Plano Plano + 1.00 left eye Plano -3.00 left eyeHole stage 2 3 3 3 3Preop VA 6/36 6/24 6/24 6/60 6/60Postop hole Open Closed Open Closed ClosedPostop VA 6/60 6/12 6/18 6/9 6/12Field loss Inferotemporal Temporal wedge Inferotemporal Inferotemporal Inferotemporal
that is, in the regions where the ERGs wererecorded. Colour vision was tested along stan-dard protan colour confusion axes. In thesepatients we assumed that the colours wereisoluminant, and did not make individual cor-rections as was done in the original descriptionof the tests.
ResultsThe patient data are summarised in Table 1.All five patients had uneventful macular holesurgery and neither papillary nor peripapillaryhaemorrhages were noted intraoperatively inany of the eyes. No hypotensive episodes wererecorded during general anaesthesia in any ofthe patients.
In the early postoperative period, intraocularpressure (IOP) remained normal throughout,except in case 2, where an IOP of 35 mm Hgwas noted on the first postoperative day,returning to normal after a single oral dose ofacetazolamide 500 mg. The hole was closed inthree eyes and remained open in two eyes.Although good gas fills were present in all eyesduring the first 2 to 3 postoperative weeks, par-tially obscuring fundal examination, a suffi-ciently detailed view was present in all eyes andno signs suggestive of optic disc or retinal vas-cular pathology were evident during thisperiod.
* Quadrant not tested.The values are also expressed as ratios of the foveal response and the two right hand columnscompare the scotomatous quadrant and the unaffected quadrants (mean) of the same eye.
VISUAL FUNCTION AND PERIPHERAL FIELDSAll patients noted an absolute inferotemporalscotoma between 4 and 8 weeks postopera-tively, as the gas diminished. In the eyes withclosed holes, best corrected visual acuities of6/9-6/12 were recorded and in those with openholes, acuities of 6/60 and 6/18. Ishihara scoresvaried from 5/13 to 12/13 and colour desatura-tion varied from mild to moderate and did notrelate to whether the hole had been closed.Three eyes exhibited a mild relative afferentpupillary defect.
Similar, absolute field defects were recordedin all five cases, with the inferotemporal quad-rant universally affected (Fig 1), encroachingto within 20-30° of fixation and to within 5-15°of the blind spot, which remained normal.Goldmann perimetry provided accurate map-ping of scotomata, particularly in the area ofthe blind spot. In case 5, a partial altitudinalcomponent was present, and in another eye(case 4), more widespread constriction wasevident. All defects remained stable through-out the follow up (6-12 (mean 7.8 months))during which time at least three field examina-tions were performed. Nuclear lens opacifica-tion was noted in cases 2 (mild) and 4 (moder-ate).
OPTIC DISC AND RETINAL NERVE FIBRE LAYERFINDINGSFour eyes had anatomically normal discs withcup to disc ratios of between 0.2 and 0.5. Oneeye had a small crowded disc without a physi-ological cup (case 1). Of the five eyes, threedeveloped subtle nasal disc pallor and RNFLloss, anatomically consistent with the patternof field loss.
OTHER FUNDUS FENDINGSIn case 4, background diabetic retinopathyremained unchanged postoperatively, withoutevidence of fresh maculopathy. In case 5, mildhypertensive vascular changes had been notedbefore surgery and remained unchanged post-
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Visualfield loss following vitrectomy for stage 2 and 3 macular holes
ACombined orange (3 ms 460 Td-s 610 nm) and blue (3 ms 57 Td-s 460 nm)stimulus on 32 Td 630 nm background
Foveal(stimulus 100 circle on fovea)
1: cone b=50-0 ms, 7-129 pV2: rod b=84-4, 16-162 pV
Supernasal field=inferotemporal retina(stimulus 100 circle centred 34-50 fromfixation, at 1350)
1: cone b=46-0 ms, 4-297 pV2: rod b=948, 11-865 pV
Orange (3 ms 460 Td-s 610 nm) stimulus on 32 Td 665 nm background
Foveal(stimulus 100 circle on fovea)
1: cone a-b=50-8 ms, 5-859 pV
Supernasal field=inferotemporal retina(stimulus 100 circle centred 31-50 fromfixation, at 1350)
1: cone a-b=52-4 ms, 1-66 pV
Figure 2(A) Demonstration of thefocal ERG response (case 3).A combination of orangeand blue light (top) produces both a foveal and peripheral response. Orange light alone(bottom) produces only a foveal response andfails to generate an ERG in the periphery ofthe unaffected quadrant, as the rod response to this wavelength is poor. This phenomenonalso demonstrates that contamination of the focal ERG, due to light scatter, is notsignificant.
operatively. Otherwise, fundal examination andfluorescein angiography did not reveal any
other retinal pathology.
FOCAL ERG AND CCS THRESHOLDSFocal foveal ERGs andVERs were preserved inall affected eyes. Focal ERGs of 4.00-9.77 jiV(mean 7.38, SD 2.30, SE 1.03) were recordedin the inferotemporal scotomatous quadrants,and 3.36-9.61 jV (mean 6.74, SD 2.46, SE1.10) in the unaffected inferonasal quadrants(Fig 2, Table 2) of each affected eye. Thewaveforms ofthe ERGs were, therefore, similarin scotomatous and non-scotomatous quad-rants. The ratios of focal ERG amplitude fromaffected scotomatous quadrants/fovea andfrom unaffected quadrants/fovea were compa-
rable in all eyes. Furthermore, focal ERGsfrom affected quadrants were comparable withquadrantic responses from fellow control eyes.
CCS testing was carried out in three of fiveaffected eyes (one case had a congenital colourvision defect and one had diabetes, which isknown to affect colour vision). In these eyes,colour contrast was abolished in the scotoma-tous areas. Colour contrast was, however,recordable at the edges of scotomatous areasand revealed elevated contrast threshold, par-ticularly for protan, compared with points onthe same isoptre in unaffected quadrants andin fellow eyes.
DiscussionWe have described five patients who developedperipheral field loss following routine macularhole surgery, a phenomenon which has beenpreviously described in only one eye followingsurgery for a stage 3 FTMH.13 All eyesdeveloped an absolute peripheral scotoma,affecting the inferotemporal quadrant, notcontiguous with the blind spot, which re-mained stable. The consistent pattern of fieldloss implies a common aetiology and site.The observations presented in this study
confirm that field defects were caused byretinal nerve fibre loss rather than outer retinaldamage. The preservation of the focal ERG inthe affected quadrant, with an absent colourcontrast threshold to protan, rules out outerretinal pathology. Photoreceptor toxicity, dueto intraocular gas or autologous serum, andouter retinal or choroidal ischaemia are there-fore unlikely to play a role. Retinal vascularocclusion would also appear unlikely in view ofthe lack of clinical signs postoperatively, andthe lack of ERG b-wave abnormality.'4 15 Pres-ervation of focal foveal VER and full VERresponses, which are dominated by the papillo-macular region suggests that the RNFL waslargely intact in this area. The possibility of amechanical effect, from the gas bubble, on theRNFL also appears rather remote, as similardefects have been described after vitrectomyand posterior cortical peeling for excision ofsubfoveal choroidal neovascular membranes,13where gas tamponade was not used.The precise location of nerve fibre damage
cannot be determined on the basis of the elec-trophysiological tests available for this study, inthat the VEE measures overall retinocorticalfunction, while the ERG reflects outer retinalfunction. Although the pattern ERG (PERG)may be used to assess inner retinal function,responses can only be analysed if the stimulusis focused on the fovea and it is therefore oflimited use in detecting focal inner retinalabnormalities.However, considerable circumstantial evi-
dence indicates that the site of nerve fibredamage is at the optic disc or peripapillaryRNFL rather than at the peripheral RNFL,and is probably due to traction during corticalitreous peeling. Firstly, field defects have not,
thus far, been described in eyes undergoingsurgery for stage 4 holes, where the vitreouscortex is already detached. Secondly, intraop-erative observations during this manoeuvresuggest that vitreopapillary traction occurs inmost cases, and that the firmest vitreous adhe-sions occur at the optic disc and peripapillary
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Figure 2(B) Focal ERGs in case 3 (right eye) using a combination oforange and bluelight. Quadrantic andfoveal responses are shown according to the area of retina stimulatedwith respect to the perimetry chart. Thefocal ERGfrom the inferotemporal quadrant(bottom right), within the scotoma, is preserved.
region (Gregor, Ezra, and Aylward, unpub-lished data). This is invariably the mostdifficult area of posterior vitreous cortex toseparate, irrespective ofwhere the cortex is ini-tially engaged and detached, and is accompa-nied by papillary and peripapillary RNFLelevation and superficial haemorrhages, justbefore separation occurs, particularly at thenasal papillary rim. Although most haemor-rhages appear to be benign, (Gregor, Ezra, andAylward, unpublished data) they do indicatethat some vascular disruption in the RNFL, asa result of tractional forces, does occur. In con-trast, peripheral cortical vitreous peeling ap-pears to be far easier, requiring far less aspira-tion, and although accompanied by mildrippling of the retina, is rarely associated withhaemorrhages.
Histopathological studies have also shownthat the most adherent areas of posterior corti-cal vitreous are at the optic disc.'6 Clinicalobservations on the progression of uncompli-cated spontaneous posterior vitreous detach-ment (PVD) have confirmed this to be the lastarea to separate.'7 In addition, vitreopapillarytraction has been observed in eyes whichdevelop optic disc haemorrhagesl'20 and pe-ripheral field loss in association with spontane-ous PVD.'8 other retinal pathology.1/2
All five eyes in our study demonstrated tem-poral field loss which may reflect the fact thatvitreopapillary adhesions are firmer at the nasalaspect of the disc and that greater forces arerequired to separate them. This would cer-tainly be in keeping with intraoperative obser-vations, where the nasal aspect is the last toseparate and is the most frequent site of super-ficial haemorrhage (Gregor, Ezra, and Ayl-ward, unpublished data). Observations duringspontaneous PVD have also confirmed thatnasal papillary adhesions are the last toseparate"7 and that the nasal rim is predisposedto haemorrhagesl'20 which may be associatedwith temporal field loss.'8 The generalised fieldconstriction in case 4, in view of the absence ofan afferent pupillary defect suggests that it mayhave been secondary to nucleoscierosis ratherthan diffuse nerve fibre loss.
Finally, anatomical studies have shown thataxons in the RNFL, originating from moreperipheral ganglion cells, pass to the peripheraloptic nerve and the axons from more centralganglion cells enter at the central portion of thenerve head.2' 22 The preservation of the blindspot in all eyes in this study suggests that theoptic disc rim rather than the central portion isaffected and would correlate with the observa-tions already cited. The partial altitudinalcomponent in case 5 also indicates that fibreloss may have occurred predominantly at thenasal rim, possibly due to microvasculardisruption in this area.Although papillary and peripapillary traction
clearly occurs during cortical vitreous peeling,its mechanical effects remain unclear. Whethernerve fibre loss occurs as a result of shearingforces or microvascular damage, or both, is amatter for speculation. Furthermore, the pres-ence of cardiovascular risk factors in threepatients may indicate a predisposition to nervefibre loss in cases with an already compromisedpapillary and peripapillary circulation, whereinsults to the nerve fibre layer are less well tol-erated. The visual field loss documented inthese patients has implications for any vitreo-retinal procedure involving posterior vitreouscortex stripping. Careful surgical technique,using the minimum amount of force to effectvitreous separation, is clearly important. Pas-sive aspiration may reduce tractional forces butmay not provide sufficient force to completethe manoeuvre in all cases. The true incidenceof this complication following macular holesurgery remains unclear, as subclinical fielddefects may occur and remain undetected insome patients. In this respect, prospectivestudies comparing preoperative and postopera-tive fields, in all subjects undergoing surgeryfor stage 2 and 3 holes, appear warranted.
The work was supported by the Guide Dogs for the Blind Asso-ciation and the Moorfields Special Trustees (Stringer Bequest).The authors would also like thank Mr Michael Sanders forhis contribution to the discussion.
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