LETTERS TO THE EDITOR

Visual recovery from no light perceptionin total retinal detachment with massivesubretinal haemorrhage

EDITOR,—In patients with no light perception(NLP) vision following extensive subretinalhaemorrhage, visual recovery rarely occurs. Inthis patient, however, visual recovery occurredafter total retinal detachment with massivesubretinal haemorrhage of 3 months’ dura-tion. The eye, which had NLP vision,developed obstructed angle closure glaucomathat necessitated a subretinal tap and an ante-rior chamber deepening procedure. Furtherremoval of blood from the vitreous resulted incounting fingers (CF) vision, suggesting thatsurgery may restore some vision despiterelatively long lasting massive subretinalhaemorrhage.

CASE REPORT

A 60-year-old woman with total retinaldetachment, severe ocular pain, and NLPvision was referred to us. The eye had a darkpupillary reflex, and the fundus was obscuredupon ophthalmoscopy. On slit-lamp examin-ation, a retinal detachment was observedbehind the lens and blood cells were seen per-colating slowly behind the detached retina.The detached retina pushed the lens-irisdiaphragm forward, making the anteriorchamber extremely shallow. The filtrationangle was not visible. The intraocular pressure(IOP) was 43 mm Hg. The electroretinogram(ERG) and the visual evoked (VER) and elec-trically evoked responses (EER) were non-recordable. Medical evaluation revealed atrialfibrillation, chronic myelocytic leukaemia, andhypertension. The IOP responded only tem-porarily to topical medications and oral aceta-zolamide. The patient experienced nausea andsevere ocular pain. Two days after the examin-ation, a subretinal tap was performed. Nofluid escaped after full thickness sclerotomy,indicating that there was no significant supra-choroidal fluid or a choroidal detachment.When the choroidal knuckle was pierced inthe scleral wound, copious tar-coloured fluid

drained from the wound, and the eye softened.The anterior chamber deepened, the IOP nor-malised by injection of the balanced salt solu-tion, and the ocular pain resolved postopera-tively. The patient regained dim lightperception in the inferior nasal projection 10days postoperatively. The fundus was invisiblebecause of blood in the vitreous. The ERGremained non-recordable until 7 monthspostoperatively when very small ERG re-sponses were obtained by the computer sum-mation technique. The VER and EER wererecordable 5 months postoperatively. Encour-aged by the recovery of light perception andthe electrophysiological responses, and be-cause the vitreous blood did not resolve after 7months’ observation, closed vitrectomy wasperformed. The retina was found reattached.Three months after the second surgery, thevision was CF at 4–5 feet. The visual field wasconstricted to the central 15 degrees, and thedark adaptation curve was monophasic withloss of the rod component and an elevatedcone threshold. The retina stayed reattachedbut was blotchy with pigment clumping (Fig1(A)). A dense, white subretinal sheet wasseen nasally and inferiorly near the equator(Fig 1(B)). The retinal blood vessels and theoptic nerve head appeared normal.

COMMENT

Angle closure glaucoma secondary to exten-sive choroidal detachment occurs frequently.In the present case, there was no choroidaldetachment but total retinal detachment withmassive subretinal haemorrhage. The subreti-nal tap and anterior chamber deepeningprocedure lowered the IOP and relieved pain.Chronic leukaemia with a bleeding tendency1–3

would have predisposed the patient to massivesubretinal haemorrhage upon eye rubbing. Nodisciform macular scarring was observed, butpresence of a peripheral subretinal neovascu-lar membrane could not be excluded becausesubretinal organisation in the peripheral fun-dus was found postoperatively.In animals, irreversible retinal damage from

experimental subretinal haemorrhage occursrapidly.4 Even in cases operated on within 7days of visual loss, the clots removed are moredensely fibrous and more rigidly adherent tothe surrounding tissues,5 6 making visualrecovery diYcult. The possible mechanism ofthe loss of light perception in this patient isunclear: the IOP was not suYciently high tostop intraocular circulation. The detachedretina was visible behind the clear lens. In thisrespect, it is noteworthy that the initial EERwas non-recordable, which indicated that theneural retinal network was impaired.Visual recovery was reported after subreti-

nal haemorrhage involving the macula,5 7 butthe haemorrhage was localised and brief induration. When the retina was totally de-tached with massive subretinal haemorrhageof more than 3 months’ duration, functionalrecovery was not reported when similar ocularconditions prevailed.1 2 8 9

Although the retina had deteriorated withdiVuse pigmentation, the patient regainedsome vision, possibly because the blood in thesubretinal space was not clotted, and the sub-retinal space was not packed with blood cells.Therefore, some retinal receptors escapedrapid deterioration from contact with denseblood. There might have been exudative or

transudative components in her retinal de-tachment. The patient later died from anacute leukaemic crisis; no necropsy wasperformed.

Ryo Suzuki, MD, was supported in part by JapaneseOverseas Research Fund from the Ministry ofEducation, Science and Culture, Japan.

R SUZUKIDepartment of Ophthalmology,

Yamaguchi University School of MedicineKogushi, Ube City 755, Yamaguchi, Japan

T HIROSESchepens Eye Research Institute,

100 Charles River Plaza,Boston,MA 02114,USA

Correspondence to: R Suzuki, MD, PhD.Accepted for publication 24 April 1997

1 Kozlowski IMD, Hirose T, Jalkh AE. Massivesubretinal hemorrhage with acute angle-closureglaucoma in chronic myelocytic leukemia. Am JOphthalmol 1987;103:837–8.

2 Glaser B, Smith JL. Leukemic glaucoma. Br JOphthalmol 1966;50:92–4.

3 Leveille AS, Morse PH. Platelet-induced retinalneovascularization in leukemia. Am J Ophthal-mol 1981;91:640–3.

4 Glatt H, Machemer R. Experimental subretinalhemorrhage in rabbits. Am J Ophthalmol 1982;94:762–73.

5 Bennett SR, Folk JC, Blodi CF, Klugman M.Factors prognostic of visual outcome in patientswith subretinal hemorrhage. Am J Ophthalmol1990;109:33–7.

6 Johnson MW, Olsen KR, Hernandez E. Tissueplasminogen activator thrombolysis during sur-gical evacuation of experimental subretinalhemorrhage. Ophthalmology 1992;99:515–21.

7 Vander JF, Federman JL, Greven C, SlusherMM, Gabel VP. Surgical removal of massivesubretinal hemorrhage associated with age-related macular degeneration. Ophthalmology1991;98:23–7.

8 Gass JDM. Pathogenesis of disciform detach-ment of the neuroepithelium: Senile disciformmacular degeneration. Am J Ophthalmol 1967;63:45–64.

9 Wood WJ, Smith TR. Senile disciform maculardegeneration complicated by massive hemor-rhagic retinal detachment and angle closureglaucoma. Retina 1983;3:296–303.

Bilateral angle closure glaucoma: anunusual presentation ofVogt–Koyanagi–Harada syndrome

EDITOR,—Vogt–Koyanagi–Harada (VKH)syndrome is a bilateral, diVuse, granuloma-tous uveitis associated with exudative retinaldetachment and central nervous system, audi-tory, and dermatological involvement.1 It is acommon cause of uveitis in Japan and, to alesser extent, in parts of Latin America andthe USA.We report a case of VKH syndrome with an

unusual presentation of bilateral secondaryacute angle closure glaucoma (SAACG).Because of the rarity of this presentation ofVKH syndrome (this being the first report, toour knowledge, of such a presentation outsidethe USA and Japan) we initially had diYcul-ties in diagnosing and treating it in the optimalway. We thus stress the importance ofclinicians being aware of such a VKHsyndrome presentation, especially in thoseparts of the world where the disease is rare.

CASE REPORT

A 20-year-old white woman presented in April1996 complaining of sudden onset of blurred

Figure 1 Posterior (A) and inferonasal (B)portions of the fundus after the second surgery.

British Journal of Ophthalmology 1997;81:705–709 705

vision in both of her eyes. Her past medicalhistory and her family history were unremark-able.Visual acuity was 6/24 in both eyes, improv-

ing to 6/12 with a pinhole. The corneas wereslightly oedematous, without keratic precipi-tates. The anterior chambers were shallow,with +1 cells. The pupils were normal andreacted to light. Intraocular pressures were 26mm Hg in the right eye and 29 mm Hg in theleft eye. Gonioscopy revealed closed angles inboth eyes. Owing to the corneal oedema andour reluctance to dilate the pupils at thatstage, details of the posterior poles of the eyescould not be visualised with certainty.The woman was thus diagnosed as suffering

from bilateral SAACG and was treated withtopical pilocarpine and timolol, combinedwith intravenous acetazolamide and oral glyc-erol. Since the intraocular pressures could notbe controlled with this treatment, bilaterallaser iridotomies were performed resulting inreduction of pressures to normal. This wasaccompanied by a progressive deepening ofthe anterior chambers.At this stage we dilated the pupils and

revealed +2 cells in the vitreous in both eyes.Ophthalmoscopy disclosed multiple areas ofserous retinal detachment in the posteriorpoles, combined with bilateral inferior exuda-tive retinal detachment (Fig 1). Fluoresceinangiography demonstrated multifocal leakageof dye at the level of the retinal pigmentepithelium in the early phase and late poolingof fluorescein under the areas of the detachedretina in the late phase in both eyes (Fig 2).

General physical examination, as well asneurological, dermatological, and auditoryexaminations were all normal. Lumbar punc-ture disclosed 127 lymphocytes per mm2 ofcerebrospinal fluid, with normal protein lev-els. Results of other laboratory tests, includingchest x ray, complete blood count, erythrocytesedimentation rate, serum chemistry, liverenzymes, rheumatoid arthritis titre, bloodserology, including serological syphilitic tests,and urine analysis were all within normal lim-its.Based on the presence of bilateral iridocy-

clitis, posterior uveitis with bilateral exudativeretinal detachment, and cerebrospinal fluidpleocytosis the diagnosis of VKH syndromewas made.2 The patient was treated with topi-cal steroids and cycloplegia combined with100 mg of oral prednisone daily, which wastapered down to 40 mg daily over the nextmonth. During that period the retinal detach-ments resolved and the visual acuity improvedto 6/6 in both eyes. A corneal endothelium cellcount performed after the termination of theuveitic attack was normal.

COMMENT

Glaucoma occurs in 20% to 38% of patientswith VKH syndrome.3 4 We are aware of only12 reported cases of bilateral SAACG in VKHsyndrome,4–6 of which in at least seven casesthe glaucoma was the presenting symptom.SAACG in cases of VKH syndrome is

cyclocongestive in nature, resulting fromciliary body swelling6 which may be combinedwith choroidal eVusion. Pilocarpine is con-traindicated in the management of such cases,because it increases the dilatation of the uvealblood vessels (and by that increases intraocu-lar inflammation and angle congestion) andcauses further shallowing of the anteriorchamber.7

As pointed out by Kimura et al,5 when pilo-carpine is mistakenly prescribed for suchcases, almost all patients will need an iridec-tomy or filtering operation. Since we did notdiagnose the underlying disease initially andtreated the patient with pilocarpine, we couldnot break the attack until bilateral YAG laseriridotomies were performed. This raises thesuspicion that an additional element of pupil-lary block (possibly through an increasedstickiness between the iris and the lens) wascaused by the use of pilocarpine.Corneal swelling is unusual in the presence

of healthy corneal endothelium and mildanterior uveitis.8 A corneal endothelium cellcount performed on the patient after thetermination of the uveitic attack was normal.Thus, explanations for the mild cornealoedema noted on the patient’s presentationcan only be speculative. It is not unreasonableto assume that the patient might have had along standing asymptomatic anterior uveitisand that the sudden intraocular pressure riseresulted in mild corneal oedema.In conclusion, in order to prevent unneces-

sary operations, pilocarpine should not beprescribed in SAACG due to uveitis. Sinceultrasound is almost diagnostic in VKHsyndrome3 and may provide additional infor-mation about posterior segment pathology inother predisposing diseases,9 it should be per-formed in suspected cases of SAACG beforeany medical iris manipulation is performed.

MAYA EIBSCHITZ-TSIMHONIYUVAL A GELFAND

EEDY MEZERBENJAMIN MILLER

Department of Ophthalmology, Rambam MedicalCenter and the Bruce Rappaport Faculty of Medicine,Technion-Israel Institute of Technology,Haifa, Israel

Correspondence to: Dr Y A Gelfand, Department ofOphthalmology, Rambam Medical Center, POB9602, 31096 Haifa, Israel.Accepted for publication 11 March 1997

1 Moorthy RS, Inomata H, Rao NA. Vogt-Koyanagi-Harada syndrome. Surv Ophthalmol1995;39:265–92.

2 Forster DJ, Cano MR, Green RL, Rao NA.Echographic features of the Vogt-Koyanagi-Harada syndrome. Arch Ophthalmol 1990;108:1421–6.

3 Ohno S, Char DH, Kimura SJ, O’Connor GR.Vogt-Koyanagi-Harada syndrome. Am J Oph-thalmol 1977;83:735–40.

4 Forster DJ, Rao NA,Hill RA, Nguyen QH, Baer-veldt G. Incidence and management of glau-coma in Vogt-Koyanagi-Harada syndrome.Ophthalmology 1993;100:613–8.

5 Kimura R, Sakai M, Okabe H. Transient shallowanterior chamber as initial symptom in Harada’ssyndrome. Arch Ophthalmol 1981;99:1604–6.

6 Kimura R, Kasai M, Shoji K, Kanno C. Swollenciliary processes as an initial symptom inVogt-Koyanagi-Harada syndrome. (Letter) AmJ Ophthalmol 1983;95:402–3.

7 Lewis RA.Medical therapy of glaucoma. In: Tas-man W, Jaeger EA, eds. Duane’s clinical ophthal-mology. Vol 3, Chapter 56. Philadelphia:Lippincott-Raven, 1996:5–6.

8 Van Meter WS, Holland EJ, Doughman DJ. Cor-neal edema. In: Tasman W, Jaeger EA, eds.Duane’s clinical ophthalmology. Vol 4, Chapter16A. Philadelphia: Lippincott-Raven, 1996:13–4.

9 Campo RV, Reiss GR. Glaucoma associated withretinal disorders and retinal surgery. In: TasmanW, Jaeger EA, eds. Duane’s clinical ophthalmol-ogy. Vol 3, Chapter 54E. Philadelphia:Lippincott-Raven, 1996:14.

Ultrasound biomicroscopy of angleclosure glaucoma with pseudoexfoliationsyndrome

EDITOR,—The pseudoexfoliation syndrome ischaracterised by the presence of light grey orwhite flakes on the pupillary margin and ante-rior lens capsule, the surfaces of the iris,zonules, ciliary body, hyaloid, trabecularmeshwork, and the endothelial surface of thecornea. This syndrome is generally thought tobe accompanied by open angle glaucoma.However, in some reports, the anterior cham-ber angle is narrow,1–3 and in other casesshown to be angle closure glaucoma.4 5 Therelation between the pseudoexfoliation syn-drome and angle closure glaucoma is unclear.We used the ultrasound biomicroscope todetermine the pathogenesis of angle closureglaucoma in a patient with the pseudoexfolia-tion syndrome.

CASE REPORT

An 80-year-old Japanese woman complainedof blurred vision and pain in the left eye. Angleclosure glaucoma of the left eye was diagnosedby an ophthalmologist. Pilocarpine eye dropswere prescribed, and the patient was referredto our department. On initial examination, hercorrected visual acuity was right eye 70/100and left eye 20/100, and the intraocularpressures were right eye 13 mm Hg and lefteye 37 mm Hg. Slit-lamp examination re-vealed a shallow anterior chamber in the righteye and a markedly shallow anterior chamberin the left eye. Pseudoexfoliative substancewas observed on the pupillary margin of theboth eyes; moderately dense cataract waspresent in both eyes. Gonioscopy revealed anarrow (grade 2) angle in the right and aneven narrower angle (grade 1) in the left eye. Adensely pigmented trabecular band waspresent in both eyes. Glaucomatous disc cup-

Figure 1 Fundus photography, showingmultiple areas of serous retinal detachment atthe posterior pole combined with inferiorexudative retinal detachment.

Figure 2 Fundus fluorescein angiogram (latephase), with pooling of fluorescein under thedetached retina.

706 Letters

ping was observed in both fundi by ophthal-moscopy performed without mydriasis.An ultrasound biomicroscope (50 MHz

Ultrasound BioMicroscope, Humphrey In-struments, Inc, San Leandro, CA, USA) wasused to evaluate the mechanism of the angleclosure glaucoma. Ultrasound biomicroscopydemonstrated a narrow angle at the midperipheral anterior chamber in all sections ofthe right eye, and a slit-like, narrow or closedangle in the left eye (Figs 1, 2). Thick, welldefined zonules were observed in all sectionsof both eyes, some of which were loose (Fig 1).Both lenses were spherically shaped, andanterior poles moved forward. The iris showeda marked anterior bowing that was consistentwith pupillary block. The thickness of theright lens was 5.4 mm, as measured by A-scanechography. The thickness of the left lenscould not be measured.The administration of the pilocarpine drops

was halted, and laser iridectomy was per-formed in both eyes. The anterior chambers ofboth eyes were of normal depth; the intraocu-lar pressure fell to a normal level in the left eyeafter the procedure. Ultrasound biomicro-scopic examination showed a normal, wideopen angle, except for the inferior andsuperior segments of the left eye whichshowed persistent peripheral anterior syn-echiae. The iris showed a straight configura-tion. On the following day, when ultrasoundbiomicroscopy was performed after the instil-

lation of pilocarpine, numerous loosenedzonules were seen in all sections of both eyes.Lens thickness as measured by A-scan echo-graphy was 5.9 mm in the left eye.

COMMENT

Ultrasound biomicroscopy revealed thick, welldefined zonules that appeared to be coatedwith pseudoexfoliative materials. The result-ing loosened zonules presumably caused thespherical shape of the lens and increased theaxial thickness. The anterior pole of the lensappeared to have moved forward and in-creased the intraocular pressure by creatingpupillary block.In cases with a shallow anterior chamber or

angle closure glaucoma accompanied by thepseudoexfoliation syndrome such as that pre-sented here, an immediate laser iridectomy isindicated without the use of pilocarpinedrops. The instillation of pilocarpine dropsexacerbates pupillary block so that its use iscontraindicated.When cataract surgery is per-formed in such cases, careful attention shouldbe paid to zonular dialysis.

TAKASHI GOHDOHIROSHI TAKAHASHI

HIROYUKI IIJIMASHIGEO TSUKAHARA

Department of Ophthalmology, Yamanashi MedicalUniversity, Yamanashi, Japan

Correspondence to: Shigeo Tsukahara, MD, De-partment of Ophthalmology, Yamanashi MedicalUniversity, Tamaho, Yamanashi, Japan 409-38.Accepted for publication: 10 March 1997

1 Wishhart PK, Spaeth GL, Poryzees EM. Ante-rior chamber angle in the exfoliation syndrome.Br J Ophthalmol 1985;69:103–7.

2 Layden WE, ShaVer RN. Exfoliation syndrome.Am J Ophthalmol 1974;78:835–41.

3 Ritch R. Exfoliation syndrome and occludableangles. Trans Am Ophthalmol Soc 1994;92:845–944.

4 Herbst RW. Angle closure glaucoma in a patientwith pseudoexfoliation of the lens capsule. AnnOphthalmol 1976;8:853–6.

5 Skuta GL, Parrish II RK,Hodapp E, Forster RK,Rockwood EJ. Zonular dialysis during extracap-sular cataract extraction in pseudoexfoliationsyndrome. Arch Ophthalmol 1987;105:632–4.

The cotton bud as a missile causingpenetrating eye injury

EDITOR,—Airguns have been responsible for asubstantial number of eye injuries over thepast 70–80 years. In published series airgunshave accounted for up to 7% of severe eyeinjuries.1 Sevel and Atkins reported a finalvisual acuity of 6/60 or less in 77% of patientsfollowing an airgun pellet injury to the eye.2 Arecent study demonstrated that injuriescaused by the discharge of airguns were thecommonest cause of enucleation secondary totrauma in the paediatric and adolescentpopulation.3 We report an unusual case ofsevere eye injury resulting from an apparentlyharmless household item used inappropriatelyas air weapon ammunition.

CASE REPORT

A 15-year-old boy broke a plastic cotton budand fired it from a 0.22 air rifle. The cottonbud hit his older brother from a range of 5–7metres. The cotton bud penetrated the eyelid,sclera, and pars plana in the superonasalquadrant of the right eye. As an impulsiveaction the patient removed the cotton budfrom his eye immediately. On examination inthe accident and emergency department hehad a scleral wound with ciliary body exposedand no perception of light in the aVected eye

(Fig 1). The cornea was oedematous and noview of the fundus was possible. At primaryrepair apposition of the scleral wound was notpossible and therefore closure was achievedusing an autologous half thickness scleral flap.The patient had no perception of light at 1

day, 1 week, and 1 month following the opera-tion. The eye became hypotonous and phthisi-cal and remained uncomfortable. Five monthsafter the injury the eye was enucleated. Histo-logical examination of the eye (Fig 2) demon-strated a superonasal penetrating woundresulting in massive subretinal haemorrhageand subsequent organisation causing a totalfibrotic funnel retinal detachment. There wereoccasional areas of chronic inflammationwithin the eye but no evidence of sympatheticophthalmitis.

COMMENT

Eye injuries from the discharge of airguns tendto be accidental rather than malicious.4 Theinjury described in this report can be regardedas the result of poor gun safety rather than adeliberate attempt to injure.In a series of 105 eye injuries caused by dis-

charge of airguns5 only one penetrating injuryavoided enucleation and in this case finalvision was reduced to hand movements only.More recently in a series of 60 ocular airguninjuries 11 out of 16 penetrating injuriesrequired enucleation and none of the eyesretained visual acuity better than countingfingers.6 In all of these cases the injury resultedfrom lead pellets, or ball bearings, or darts.Weknow of only one other case of eye injuryresulting from unconventional airgun ammu-

Figure 1 Clinical photograph of right eye onpresentation with penetrating injury in superiorsclera.

Figure 2 Enucleated eye with total fibroticfunnel retinal detachment (asterisk), massivesubretinal haemorrhage (arrowheads), and siteof penetrating injury (arrow) (haematoxylinand eosin, × 1.5).

Figure 1 Ultrasound biomicroscopic image ofthe anterior segment of the inferior section in theright eye. Zonule is loose and the lens has aspherical shape. The iris shows a marked anteriorbowing with the presence of pupillary block. Theangle is narrow at the mid peripheral anteriorchamber.

Figure 2 Ultrasound biomicroscopic image ofthe anterior segment of the inferior section in theleft eye. Zonules are thick and well defined, andthe lens has a spherical shape. The angle is closedwith pupillary block.

Letters 707

nition, a contusional injury caused by a pieceof pear fired from an air weapon.6

Most air rifles available in the UK havemuzzle velocities of between 600 and 800 feetper second (185 m/s to 250 m/s). It has beendemonstrated that an airgun pellet onlyrequires a velocity of 236 feet per second (72m/s) to penetrate the globe.7 In our case a mis-sile weighing less than 0.13 g was responsiblefor a devastating injury. We contend that airweapons belong on the shooting range ratherthan in the back garden.

We wish to thank Mr T Rimmer for allowing us toreport the details of his patient and Dr Ian Cree forcarrying out the pathological examination.

GREGOR L CAMPBELL-HEWSONCONOR V EGLESTONSUSAN M ROBINSON

Accident and Emergency Department,Addenbrooke’s Hospital, Cambridge CB2 2QQ

Correspondence to: Gregor L Campbell-Hewson.Accepted for publication 26 March 1997

1 LaRoche R,McIntyre L, Schertzer RM. The epi-demiology of severe eye injuries in childhood.Ophthalmology 1988;95:1603–7.

2 Sevel D, Atkins A. Pellet gun injuries of the eye.S Afr Med J 1978;54:566.

3 Marshall DH, Brownstein S, Addison DJ,MacKenzie SG, Jordan DR, Clarke WN. Airguns: the main cause of enucleation secondaryto trauma in children and young adults in thegreater Ottawa area in 1974–1993. Can JOphthalmol 1995;30:187–92.

4 Schein OD, Enger C, Tielsch JM. The contextand consequences of ocular injuries from airguns. Am J Ophthalmol 1994;117:501–6.

5 Bowen DI, Magauran DM. Ocular injuriescaused by air gun pellets: an analysis of 105cases. BMJ 1973;1:333–7.

6 Moore AT, McCartney AC, Cooling RJ. Ocularinjuries associated with the use of airguns. Eye1987;1:422–9.

7 De Lori F, PomerantzeV O, Cox MS. Perforationof the globe under high speed impact; itsrelation to contusion injuries. Invest Ophthalmol1969;8:290–301.

Ankyloblepharon filiforme adnatum

EDITOR,—Ankyloblepharon filiforme adnatumis a rare benign congenital anomaly firstdescribed by Von Hasner in 1881.1 Fusion ofthe eyelid margins is a normal stage in humandevelopment but an abnormal occurrence atbirth.1 The developing eyelid margins remainfused until the fifth gestational month, butmay not be completely separated until theseventh month.2 Ankyloblepharon is charac-terised by full thickness fusion of the lid mar-gins.Ankyloblepharon filiforme adnatum com-

prises single or multiple fine bands of extensiletissue connecting the lid margins at the greyline and it reduces the palpebral fissure byinterfering with the movements of lids.The abnormality has been reported as an

isolated finding, in association with otheranomalies or as a part of a well definedsyndrome.

CASE REPORT

A 7lb 5oz (3317 g), white female baby wasborn at 40 weeks’ gestation to a 26-year-oldthird gravida. The pregnancy was normal andthe mother denied having taken any drugs orbeing exposed to x rays. The previous two sib-lings, aged 4 and 2 years, both males, werehealthy. There was no family history ofcongenital anomalies or consanguinity.The baby was noted to have fused left

eyelids at birth; apart from this she wasperfectly healthy. A detailed paediatric assess-ment failed to reveal any other congenitalabnormalities.

A more detailed ophthalmic examinationshowed that there was a single adhesionbetween the eyelids margins of the left eye(Fig 1). The lids could be easily parted toreveal an underlying normal eye. Ocularmotility, anterior segment, and fundus werenormal. This adhesion was extensible and wasdivided by a No 15 blade. There was minimalbleeding. At her follow up appointment 4months later no abnormality was noted.

COMMENT

This was the third case of isolated anky-loblepharon filiforme adnatum seen at ourhospital in the past 15 years. The other twobabies, a boy and a girl, were also completelynormal apart from the ankyloblepharon fili-forme adnatum. The annual birth rate is4500, giving an incidence of 4.4 per 100 000births.Ankyloblepharon filiforme is usually a

solitary malformation of sporadic occurrenceor a part of one of three Mendelian disorders.3

In most familial cases it occurs togetherwith cleft lip and palate, as an autosomaldominant condition in otherwise healthy rela-tives (MIM 106250).4 In some patients itappears as a part of Hay–Wells syndrome,4

also known as ankyloblepharon-ectodermaldysplasia-clefting syndrome (MIM 106260)or as a part of the popliteal pterygiumsyndrome (MIM 263650), characterised byintercrural webbing of the lower limbs.4

CHANDS (curly hair-ankyloblepharon-naildysplasia) also has it as a part of its phenotype(MIM 214350). Other reported associationsinclude hydrocephalus, meningocele and im-perforate anus,5 bilateral syndactyly, cardiacproblems such as patent ductus arteriosus andventricular septal defects, ectodermalsyndromes,5 and Edwards syndrome.6 Thehistology of these connecting strands has beenshown to consist of vascularised central coresurrounded by stratified squamousepithelium.7

The aetiology of this abnormality is un-known and a number of theories have beenproposed. The currently accepted theory isthat this condition is due to an interplay oftemporary epithelial arrest and rapid mesen-chymal proliferation, allowing union of lids atabnormal positions.8

The innocuous appearance of ankylo-blepharon filiforme adnatum belies its clinicalimportance. Although it may appear as a soli-tary anomaly in an otherwise healthy infant, itis frequently associated with a wide range ofsystemic malformations. The eye itself has notbeen reported to be abnormal except in arecent case report where ankyloblepharon fili-

forme adnatum was seen to be associated withinfantile glaucoma and iridogoniodysgenesis.8

The bands frequently resolve spontaneouslyafter a few months or may be released by asimple operative procedure.4

The major practical importance of thisanomaly is that when it occurs, it should alertthe physician to the possible presence of othercongenital problems.

SUNILA JAINANTHONY J ATKINSON

BRYAN HOPKISSONEye Department, Northampton General Hospital,

Cliftonville, Northampton NN1 5BD

Correspondence to: Sunila Jain, Eye Department,Leicester Royal Infirmary, Infirmary Square, Leices-ter LE1 5WW.Accepted for publication 28 April 1997

1 Duke-Elder S. System of ophthalmology. Vol III.London: Kimpton, 1964:869–71.

2 Weiss AH, Riscile G, KousseV BG. Ankylo-blepharon filiforme adnatum. Am J Med Genet1992;42:369–73.

3 McKusick VA.Mendelian inheritance of man. 9thed. Baltimore: Johns Hopkins Press 1990:71,240, 1434.

4 Hay RJ, Wells RS. The syndrome of ankylo-blepharon, ectodermal defects and cleft lip andpalate: an autosomal dominant condition. Br JDermatol 1976;94:277–89.

5 Kayarian EL, Goldstein P. Ankyloblepharon fili-forme adnatum with hydrocephalus, menin-gocele and imperforate anus. Am J Ophthalmol1977;84:355–7.

6 Clark DI, Patterson A. Ankyloblepharon fili-forme adnatum in trisomy 18 (Edwards syn-drome). Br J Ophthalmol 1985;69:471–3.

7 Judge H, Mott W, Gabriels J. Ankyloblepharonfiliforme adnatum. Arch Ophthalmol 1929;2:702–8.

8 Scott MH, Richard JM, Farris BK. Ankylo-blepharon filiforme adnatum associated withinfantile glaucoma and iridogoniodysgenesis. JPediatr Ophthalmol Strabismus 1994;31:93–5.

Discoid corneal oedema and highintraocular pressure following PRK

EDITOR,—We present an unusual cornealoedema which was observed following scleralindentation during a buckling procedure in apatient who had undergone successful pho-torefractive keratectomy (PRK), and in a sec-ond patient who presented with steroidinduced high intraocular pressure followingPRK.

CASE REPORTS

Patient 1A 33-year-old man underwent bilateral PRKby the Visx 20/20 excimer laser, with a 6 mmablation zone. The refraction before theprocedure was −6.00/−2.00 × 177° in theright eye and −5.00/−1.75 × 180° in the left.The corrected visual acuity was 20/20. Fivemonths after PRK the patient’s uncorrectedvision was 6/9 in both eyes. With correction ofplano/−0.75 × 175° in the right eye and −0.50in the left, his vision was 20/20 in each eye.The steroid drops were stopped a month pre-viously.Six months after PRK, he noticed a shadow

on the nasal field of his right eye and deterio-ration of vision. On admission the visual acu-ity in the right eye was 6/60 and the IOP 15mmHg. The cornea showed no pathology andthere was no noticeable haze. The anteriorchamber was deep and clear. Funduscopyrevealed detachment of the temporal and infe-rior retina with two peripheral horseshoe tearsat 9 and 6 o’clock. Examination of the left eyewas unremarkable apart from a +1 paracentralarcuate corneal subepithelial haze.During buckling procedure, at the stage of

scleral indentation and localisation of the

Figure 1 Ankyloblepharon filiforme adnatumshowing an extensile band of tissue connectingeyelid margins.

708 Letters

tears, while elevating the IOP close to arterialpressure, the central cornea became very hazy,to the point where it was almost impossible tovisualise the retina. The corneal oedemaoccupied the whole 6 mm zone of PRK abla-tion and involved the epithelium and subepi-thelial layers. An attempt to scrape theoedematous epithelium over the central cor-nea was diYcult and we realised that there wasoedema deeper to the epithelium. Thereforethe procedure was stopped after severalstrikes. Subsequently, the eye was kept soft byrepeated paracentesis of the anterior chamber.The localisation of the retinal tears wascontinued and cryopexy performed throughthe hazy cornea with great diYculty. Twentyfive minutes later, while placing the scleralsutures of the sponge, the cornea becameclearer and the retinal tears were clearlyobserved. The location of the tears was doublechecked and found to be correct. During therest of the surgery, the PRK zone continued tobe oedematous, while the rest of the corneawas clear.The following day, the cornea was found to

be perfectly normal, except for small punctateepithelial erosions. The retina was well at-tached. Endothelial specular microscopy per-formed 1 week after the surgery revealed anormal and equal cell count of 2500 cells/mm2

in both eyes.

Patient 2A 56-year-old man underwent PRK in his lefteye for moderate myopia in July 1993. Hisbest corrected visual acuity of that eye beforePRK was 6/6(−) with correction of −5.75/−0.50 × 180°. The IOP was 18 mm Hg bilat-erally; the anterior and posterior segmentswere unremarkable.The patient was treated with dexametha-

sone (0.1%) drops six times a day followingPRK, and after 6 weeks of local steroid treat-

ment he presented with a complaint of leftvisual blur. On admission, his best correctedvisual acuity was 6/60 in this eye. The IOP wasfound to be 18 mm Hg in the right eye and 52mm Hg in the left eye. A central discoid 6 mmzone of epithelial and subepithelial oedemawas observed. The anterior chamber was deepand there was no evidence of papillary block.The IOP was reduced within 2 hours to 20mm Hg by local application of Iopidine(0.5%), Tiloptic (0.5%), and pilocarpine(2%) drops and intravenous injection of500 mg acetazolamide. The discoid cornealoedema completely regressed within 4 hours.He was subsequently treated by Tiloptic(0.5%) drops twice daily and FML drops fourtimes daily which were tapered oV within 3months. Final refraction, 2 years later, re-vealed visual acuity of 20/20(−) with −0.50spherical correction. The cornea was found tobe completely normal with no evidence ofhaze. Specular microscopy 2 years after PRKrevealed a normal and equal cell count of2300 cells/mm2 in both eyes.

COMMENT

Histopathological studies have characterisedthe changes occurring during healing of rabbitand monkey corneas following PRK. In thesemodels, a subepithelial haze develops at 3weeks after ablation and is caused by a subepi-thelial accumulation of active keratocytes,vacuoles containing glycosaminoglycans, andnewly synthesised type III collagen fibres, withgreater interfibre spacing than normal.1 2 Thissubepithelial newly formed extracellularmatrix2 persisting for several months, mayfacilitate the accumulation of subepithelialfluids when IOP is significantly increased,enhancing the diVusion of water into the cor-neal stroma from the anterior chamberthrough the endothelial barrier. The newlyformed hyperplastic epithelium is probably

more permeable to water than its neighbour-ing peripheral epithelium3 and may becomeoedematous during this period. The absenceof Bowman’s layer may also contribute to thesubepithelial and intraepithelial fluid accumu-lation. Infrequently there is a need to removean oedematous epithelium during bucklingprocedure, for better visualisation of theretina. In our two patients, it seems that boththe epithelium itself and the subepithelialtissue became oedematous. The only commonpathogenic mechanism among these twopatients is the high IOP, which compromisedthe homeostasis of the PRK treated cornea.The relative rapidity of development andregression of the superficial corneal oedemamay be explained mainly by the hydrostaticeVect of a significantly increased IOP. It seemsthat with the future increase in PRK proce-dures in myopic patients, we will be facing anew intraoperative complication which hasnot yet been reported in the English literature.

GIORA TREISTERORLY HAREL

Herzlia Medical Center, Herzlia, Israel

ISRAEL KREMEREin Tal Eye Center, Tel-Aviv, Israel

Correspondence to: Israel Kremer, MD, Ein Tal EyeCenter, 17 Brandeis Street, Tel-Aviv, Israel.Accepted for publication 28 April 1997

1 SundarRaj N, Geiss MJ III, Fantes F, Hanna K,Anderson SC, Thompson KP, et al. Healing ofexcimer laser ablated money corneas: an immu-nohistological evaluation. Arch Ophthalmol1990;208:1604–10.

2 Lohamnn C, Gartry DS, Kerr Muir MG,Timberlake GT, Fitzke FW, Marshall J. ‘Haze’in photorefractive keratectomy: origins and con-sequences. A review. Lasers Light Ophthalmol1991;4:15–34.

3 Malley DS, Steinert RF, Puliafito CA, Dobi ET.Immunofluorescence study of corneal woundhealing after excimer laser anterior keratectomyin the monkey eye. Arch Ophthalmol 1990;108:1316–22.

Letters 709

CORRESPONDENCE

Coeliac disease and Behçet’s disease

EDITOR,—A large number of diseases havebeen reported to be associated with coeliacdisease, many with a probable immunologicalpathogenesis.1 Behçet’s disease and coeliacdisease share the feature of recurrent oralulceration and indeed this may be the onlypresenting feature of coeliac disease.2 A recentreport suggested that there may be an associ-ation between these two diseases and thatscreening for evidence of coeliac disease byantibody screening might be useful in Behçet’sdisease to detect otherwise aymptomaticindividuals.3 That study tested only 11 indi-viduals but found one with positive antibodytests for coeliac disease, the diagnosis beingconfirmed by jejunal biopsy.We have tested the sera of 52 patients

attending the supraregional Behçet’s diseaseclinic at Leeds. All patients fulfilled thediagnostic criteria of the Behçet’s DiseaseInternational Study Group.4 We used fourcoeliac antibody tests (IgG and IgA anti-gliadin antibodies (AGA), IgG anti-reticulinantibodies (ARA), and IgG anti-endomysialantibodies (EMA)). The EMA was negative inall cases, as was the IgA AGA and IgG ARA.Four patients were weakly positive for IgGAGA.The combination of IgA AGA and IgG

EMA has been suggested as the most sensitiveand specific combination of serologicalscreening tests for coeliac disease5 and thesefindings do not support the previously re-ported association.

Work in the authors’ laboratories is supported by theUK Medical Research Council, Northern and York-shire Health Authority and The Wellcome Trust.

M A ALDERSLEYDepartment of Medicine,

St James’s University Hospital, Leeds

T E JAMESDepartment of Ophthalmology,

St James’s University Hospital, Leeds

A F MARKHAMMolecular Medicine Unit,

St James’s University Hospital, Leeds

P D HOWDLEDepartment of Medicine,

St James’s University Hospital, Leeds

1 Corazza GR, Gasbarrini G. Coeliac disease inadults. Baillière’s clinical gastroenterology1995;9:329–50.

2 Ferguson R, Basu MK, Asquith P, Cooke WT.Jejunal mucosal abnormalities in patients withrecurrent aphthous ulceration. BMJ 1976;1:11–3.

3 Triolo G, Triolo G, Accardo-Palumbo A. Be-hçet’s disease and coeliac disease. Lancet 1995;346:1495.

4 International Study Group for Behçet’s disease.Criteria for diagnosis of Behçet’s disease. Lancet1990;335:1078–80.

5 Corrao G, Corazza GR, Andreani ML, TorchioP, Valentini RA, Galatola G, et al. Serologicalscreening of coeliac disease: choosing theoptimal procedure according to various preva-lence values. Gut 1994;35:771–5.

BOOK REVIEW

Sports Ophthalmology. By Bruce Zagel-baum. Pp 280. £67.50. Oxford: BlackwellScientific, 1996.I found this excellent text both interesting andenjoyable. It provides a systematic and clearapproach to ophthalmology in relation tosport with some fascinating anecdotes to illus-trate the points being addressed.The book is divided into four main areas.

Firstly, there is an introduction to sports oph-thalmology with a broad overview of the sub-ject. Secondly, several sports are examined indetail—looking at how they are played, howinjuries occur, and how they can be prevented.The sports discussed indicate that this text isclearly aimed at a North American audienceas it concentrates on baseball, basketball, (ice)hockey, and (American) football, althoughother important sports such as the racquetsports and boxing are included.The third part of the book looks at the

details of ocular injuries which can occur dur-ing sport. This is divided into a chapter on theanatomy of the eye and orbit, followed by abreakdown of anterior segment and posteriorsegment injuries. This is a very clear and themajority of injuries should be well understoodby medical and non-medical readers alike.Finally, there are a couple of short chapters

on medical legal aspects of sports ophthalmol-ogy and visual training.The book is well illustrated, mainly in black

and white or line diagrams, but there is also anexcellent array of colour photographs of inju-ries. The emphasis of this book is very stronglyon injuries of the eye associated with sport andmethods of protecting and preventing the eyefrom suVering these injuries; although there isno specific chapter regarding a general ap-proach to prevention. There is very little in theway of optimum methods of correcting visionor the various visual requirements for eachdiVerent sport. These areas are possibly ofmore concern to the sports optometrist. Thebook however is aimed at ‘ophthalmologists,optometrists, team doctors, trainees, andprimary care physicians’. In view of theemphasis on injury, this perhaps casts the neta little too wide and indeed at almost £70.00this may perhaps put it out of reach of anyoneother than those with a very strong interest inthis field.

C MCEWAN

NOTICES

Traditional healers

The latest issue of the Journal of CommunityEye Health (no 21) focuses on the role oftraditional healers in the prevention of blind-ness in the developing world. Editorial by PaulCourtright and Susan Lewallen, and articleson traditional healers in Zimbabwe, Nepal,and northern Nigeria. For further informationplease contact Ann Naughton, ICEH, Insti-tute of Ophthalmology, 11–43 Bath Street,

London EC1V 9EL. Tel: 0171 608 6910.Annual subscription: £25. Free to eye healthworkers in developing countries.

Tübingen Practical Angiography Course

The Tübingen Practical Angiography Course(International Faculty) will take place on 6September 1997 at the Auditorium, Univer-sity Dental Clinic, Osianderstrasse 2–8, Tü-bingen, Germany. Further details; F Gelisken,MD, Congress Secretariat Dept III, Univer-sity Eye Clinic, Schleichstrasse 12, 72076Tübingen, Germany. (Tel: +49 (0) 70712987448; fax: +49 (0) 7071 293746; email:ingrid.kreissig@uni-tuebingen.de)

5th International Symposium on OcularCirculation and Neovascularisation

The 5th International Symposium on OcularCirculation and Neovascularisation will be heldon 15–19 September 1997 in Kyoto, Japan.Further details: Professor Dr MasanobuUyama, Secretary General of the OrganisingCommittee, Department of Ophthalmology,Kansai Medical University, Moriguchi, Osaka570, Japan. (fax: 81-6-997-3475.)

2nd International Symposium on ARMD

The 2nd International Symposium on ARMDwill be held at Glasgow University, Scotlandunder the auspices of the Royal College ofOphthalmologists on 16–18 September 1997.Further details: Dr G E Marshall, EyeDepartment, Western Infirmary, 38 ChurchStreet, Glasgow G11 6NT, UK. (Tel: 0141211 2094; fax: 0141 339 7485; email:gem1b@clinmed.gla.ac.uk)

XXXIst National OphthalmologyCongress

The XXXIst National Ophthalmology Con-gress will be held on 16–20 September 1997in the Istanbul Convention and ExhibitionCentre, Istanbul, Turkey. Further details;Murat Karacorlu, MD, Congress ScientificSecretariat, Valikonagi Cad, Sezai Selek SokNo 8/5, Nisantasi, Istanbul 80200, Turkey.(Fax: +90 (212) 233 2425; email:mkaracorlu@iris.com.tr)

6th International PaediatricOphthalmology Meeting

The 6th International Paediatric Ophthalmol-ogy Meeting will be held on 24–25 September1997 in Dublin, Ireland. Topics include grandround, neuro-ophthalmology, strabismus,childhood tumours. Further details: Ms Kath-leen Kelly, Suite 5, Mater Private Hospital,Eccles Street, Dublin 7, Ireland. (Tel: +3531838 4444, ext 1759; fax: +3531 838 6314.)

British and Eire Association ofVitreoretinal Surgeons (BEAVRS)

A meeting of the British and Eire Associationof Vitreoretinal Surgeons (BEAVRS) will beheld in Birmingham on 16–17 October 1997.Further details: Mr Graham R Kirkby,consultant ophthalmic surgeon, The Birming-ham and Midland Eye Centre, City Hospital,

British Journal of Ophthalmology 1997;81:710–711710

NHS Trust, Birmingham B18 7QU. (Tel:0121-554 3801; fax: 0121-507 6791.)

Diabetic Retinopathy and VireoretinalSurgery Advanced Topics

A meeting under the auspices of the OYce ofContinuing Medical Education will be heldon 17–18 October 1997 at the Thomas BTurner Building, Johns Hopkins MedicalInstitutions, Baltimore, Maryland, USA. Fur-ther details: OYce of Continuing Medicaleducation, Johns Hopkins Medical Institu-tions, Turner 20, 720 Rutland Avenue,Baltimore, MD 21205-2195, USA. (Tel:(410) 955-2959; fax: (410) 955-0807; email:cmenet@som.adm.jhu.edu)

International Centennial Meeting onPseudoxanthoma Elasticum

PXE International, Inc, along with the Na-tional Institute of Arthritis, Musculoskeletaland Skin Diseases (NIH), is sponsoring anInternational Centennial Meeting on Pseu-doxanthoma Elasticum (PXE) on 6–7 No-vember 1997 in Bethesda, MD, USA. Themeeting will focus on genetic, extracellularmatrix, and clinical issues. Further details:Sharon Terry, MA, President PXE Inter-national, Inc, 23 Mountain Street, Sharon,MA 02067, USA. (Tel and fax: 617 784 3817;email: pxe@tiac.net)

10th Annual Wilmer Institute’s CurrentConcepts in Ophthalmology

The 10th Annual Wilmer Institute’s CurrentConcepts in Ophthalmology will be held on11–13 December 1997 at the Johns HopkinsMedical Institutions, Baltimore, Maryland.Further details: Program Coordinator, JohnsHopkins Medical Institutions, OYce of Con-tinuing Medical education, Turner 20/720Rutland Avenue, Baltimore, MD 21205,USA. (Tel: 410 955-2959: fax: 410 955-0807;email: cmenet@som.adm.jhu.edu; homepage:http://ww2.med.jhu.edu.cme)

20th Annual Wilmer Institute’s CurrentConcepts in Ophthalmology

The 20th Annual Wilmer Institute’s CurrentConcepts in Ophthalmology will be held on5–10 February 1998 at the Hyatt RegencyCerromar Beach Hotel, Dorado, Puerto Rico.Further details: Program Coordinator, Johns

Hopkins Medical Institutions, OYce of Con-tinuing Medical education, Turner 20/720Rutland Avenue, Baltimore, MD 21205,USA. (Tel: 410 955-2959: fax: 410 955-0807;email: cmenet@som.adm.jhu.edu;homepage:http://ww2.med.jhu.edu.cme)

15th Annual Wilmer Institute’s CurrentConcepts in Ophthalmology

The 15th Annual Wilmer Institute’s CurrentConcepts in Ophthalmology will be held on15–20 March 1998 at Manor Vail Lodge, Vail,Colorado. Further details: Program Coordi-nator, Johns Hopkins Medical Institutions,OYce of Continuing Medical education,Turner 20/720 Rutland Avenue, Baltimore,MD 21205, USA. (Tel: 410 955-2959: fax:410 955-0807; email: cmenet@som.adm.jhu.edu;homepage:http://ww2.med.jhu.edu.cme)

XXVIIIth International Congress ofOphthalmology

The XXVIIIth International Congress of Oph-thalmology will be held in Amsterdam on21–26 June 1998. Further details: EurocongresConference Management, Jan van Goyenkade11, 1075 HP Amsterdam, the Netherlands.(Tel: +31-20-6793411; fax: +31-20-6737306;internet http://www.solution.nl/ico-98/)

First Combined InternationalSymposium on Ocular Immunology andInflammation

The First Combined International Sympo-sium on Ocular Immunology and Inflamma-tion eill be held in Amsterdam on 27 June–1

July 1998. The meeting is sponsored by theInternational Ocular Immunology and In-flammation Society, the International UveitisStudy Group, and the Immunology andImmunopathology of the Eye organisation.Further details: Professor Aize Kijlstra, TheNetherlands Ophthalmic Research Institute,PO Box 12141, 1100 AC Amsterdam, Neth-erlands (email: a.kijlstra@amc.uva.nl)

2nd International Conference on OcularInfections

The 2nd International Conference on OcularInfections will be held on 22–26 August 1998in Munich, Germany. Further details: Profes-sor J Frucht-Pery, 2nd International Confer-ence on Ocular Infections, PO Box 50006, TelAviv, 61500, Israel. (Tel: 972 3 5140000; fax:972 3 5175674 or 5140077; email: ocular@kenes.com)

Correction

Errors occurred in the abstract and Table 1 ofthe paper by Riise et al that appeared in theMay issue of the BJO (1997;81:378–385).The first sentence in the Methods section of

the abstract should read as follows:‘The phenotypes of aVected siblings in 11

Scandinavian families with two or more mem-bers who had at least three of the features: reti-nal dystrophy, polydactyly, obesity, hypogeni-talism, and mental retardation, werecompared.’The correct version of Table 1 appears

below. We apologise for these errors.

Table 1 Features of the patients in the families described by various groups

Authors Laurence–Moon Bardet BiedlSolis-CohenWeiss Alström

No of patients in the family 4 2 2 4 3

No of patients with features:Retinal dystrophy 4 2 2 4 3Obesity 2 2 2 4 3Hypogenitalism 4 2 2 3 1Polydactyly — 2 2 2 0Brachydactyly — 2 2 3 0Short stature 3 — — 2 0Mental retardation 4 — 2 4 0Diabetes mellitus — — — 1 3Nerve deafness — — — — 3Renal disease — — — 1 2Paraplegia 3 — 0 — —

— = not described; 0 = not found.

Correspondence, Book review,Notices, Correction 711

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1 Kaye SB, Shimeld C, Grinfield E, Maitland NJ,Hill TJ, Easty DL. Non-traumatic acquisition ofherpes simplex virus infection through the eye.Br J Ophthalmol 1992; 76: 412-8.

2 Jakobiec FA, Font RL. Orbit. In: Spencer WB, ed.Ophthalmic pathology: an atlas and textbook. 3rded. Philadelphia: Saunders, 1986: 2461-76.

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British Journal of Ophthalmology 1997;81:712712