br j ophthalmol 87 postscript · 1 buratto l, ed. phacoemulsification: principles and technique....

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LETTERS

Unusual case of residual corticallens matter in anterior chamberModern cataract surgery does not allow forany residual cortical matter in the anterior orposterior chamber, not even in the capsularbag. But for a beginner, a residual cortex inthe eye is preferable to a ruptured posteriorcapsule and its associated complications.Therefore, the surgeon can stop and allow aminor complication (retained cortical mate-rial) to prevent posterior capsular rupture.

Case reportA 52 year old female patient was operated forposterior subcapsular cataract in her righteye. Her left eye had previously gone intophthisis bulbi 5 years earlier; she underwenta 360˚ buckling with vitreoretinal surgery inher left eye for traumatic total retinaldetachment 6 years earlier.

The surgery was performed by a residenteye surgeon who was in the learning stage ofphacoemulsification. During cortical aspira-tion, the matter at the 12 o’clock position wasproving difficult to handle for the surgeon.The surgeon therefore thought, in the bestinterest of the patient, that the amount ofsub-incisional cortical matter (approximately2 clock hours, extending up to the capsulor-hexis margin towards the centre) wouldabsorb over time. He did not take the riskof further manipulations and getting aposterior capsular tear.

The surgeon increased the size of thecorneal incision and implanted the all-PMMA (Single-piece, Biconvex, Mod C StepVault, from AI Optics Ltd, India) intraocularlens. (The patient could not afford any otherlens and the above lens is available free ofcost for deserving patients in our centre.) Thewound was closed with 10/0 monofilamentNylon sutures.

The first postoperative day did not revealany unusual inflammation. The eye was quieton third postoperative day (first follow up).At second follow up (10th postoperative day),the operated eye revealed a white, fluffy mass(Fig 1) in the anterior chamber. This cotton-wool ball-like mass was diagnosed to beretained sub-incisional cortical lens matter

based on normal anterior segment andfundus findings. The IOP was 28 mm Hg inher right eye. Because of the raised IOP andthe one eyed status of the patient, immediateremoval of cortical lens matter was planned.The side port was used to aspirate corticalmatter with topical 0.5% oxybuprocaine(proparacaine) eye drops, using a 23 gaugecanula. Postoperatively there was normal-isation (off oral medications) of raised IOPwithin 48 hours. All sutures were removedafter 6 weeks (Fig 2). The final best correctedvisual acuity was 6/6.

CommentThe case is reported to highlight the impor-tance of complete removal of cortical matter.The reason for difficulty in aspirating sub-incisional cortex in our case was inferiorlydecentralised capsulorhexis and cornealoedema at the incision site. Other reasonsthat can hamper the removal of such cortexcould be positive vitreous pressure, longtunnel, fluid leakage due to divarication ofincision lips, small capsulorhexis, probablemiosis and corneal folds.1 The raised IOP inour case could be due to obstruction oftrabecular meshwork by lens debris andinflammatory components in the form offoamy macrophages and lens particles2 andreduction of outflow facility of the anteriorchamber angle. Lens debris was seen as afluffy pseudohypopyon layer in the inferioranterior chamber; this can cause a mistakendiagnosis of postoperative endophthalmitis ifassociated with anterior uveitis.

The full visual recovery seen in our casecould be attributed to immediate surgicalintervention. The lens cortex retained in theeye after cataract extractions usually under-goes lyses by aqueous but may persist.3 Thetechniques that can be used to aspirate suchsub-incisional cortex could be widening ofthe incision, mobilisation of the mass withIOL, verticalisation of irrigation/aspirationtip, using 180˚ bent canula by Binkhorst,bent and angled coaxial cannulas, andbimanual (one for irrigation and one foraspiration) technique.

G Prakash, A Kumar, A Purohit, A KumarDr Rajendra Prasad Centre for Ophthalmic Sciences,All India Institute of Medical Sciences, Ansari Nagar,

New Delhi – 110029, India

Correspondence to: Dr Gunjan Prakash, 8/12,Residential Hostel, AIIMS, New Delhi – 110029,

India, [email protected]

Accepted for publication 6 February 2003

The authors do not have any proprietary or financialinterest in any product. The did not receive any public

or private support.

References

1 Buratto L, ed. Phacoemulsification: principles andtechnique. Thorofare, NJ: Slack Inc, 1998:178.

2 Epstein DL, Jedziniak JA, Grant WM. Obstructionof aqueous outflow by lens particles and byheavy-molecular-weight soluble lens proteins.Invest Ophthalmol Vis Sci 1978;17:272–7.

3 Jaffe NS, Jaffe MS, Jaffe GF. Retained lensmatter. In: Cataract surgery and its complications.6th ed. St Louis: Mosby, 1997:405.

Posterior segment complicationsof graft versus host disease afterbone marrow transplantationThe efficacy of bone marrow transplantation(BMT) for the treatment of selected diseasesof the haemopoietic system such as chronicmyeloid leukaemia (CML) is well recognised.Graft versus host disease (GVHD) is howevera common and potentially life threateningcomplication of this treatment, occurring inup to 75% of cases. It is thought to arise whenimmunocompetent donor T lymphocytesmount an immune response against hosttissues. GVHD is characterised by a triad ofenteritis, dermatitis, and hepatitis, but almostall organs may be targeted. Ocular involve-ment is frequently seen but is usually limitedto the anterior segment. Posterior segmentmanifestations are rare.

This report describes two cases of GVHDwith unusual posterior segment involvementthat highlight the diversity of presentationsin this condition.

Case 1A 45 year old white male presented withprogressive bilateral blurred vision and floa-ters 10 months post-BMT for CML. He hadno history of ocular disease. His symptomsstarted 10 days after discontinuation ofcyclosporin A as a routine protocol and wereaccompanied by alopecia, poliosis, vitiligo,and oral mucositis. A presumptive diagnosisof acute GVHD was made and cyclosporinrestarted together with prednisolone. Hisother medications were azathioprine, aciclo-vir, fluconazole, and ranitidine.

Best corrected visual acuity was 6/9 bilat-erally, with no afferent pupillary defect.There was no evidence of inflammation inanterior segments or vitreous and normalintraocular pressures. There was mild discpallor with swelling and surrounding radialchoroidal folds and several pale subretinalperifoveal lesions on the left. Systemicexamination revealed widespread patchyalopecia with poliosis, vitiligo of the arms,and mild oral mucositis. Fluorescein angio-graphy showed mild dilatation of the disccapillaries and extensive focal leakage fromthe retinal pigment epithelium, but noevidence of cystoid macular oedema. Ultra-

Figure 1 Retained cortical lens matter in theanterior chamber.

Figure 2 Eight week postoperative status ofthe same eye.

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sonography showed a thickened posteriorsclera. Optical coherence topography (OCT)showed subretinal fluid bilaterally. Cerebralmagnetic resonance imaging (MRI) andlumbar puncture revealed no abnormalities.

The clinical appearances were consistentwith posterior scleritis together with a diffuseretinal pigment epitheliopathy. A reducingregimen of high dose steroids in combinationwith acetazolamide resulted in clinicalimprovement and visual stabilisation.

Case 2A 31 year old white female underwent totalbody irradiation and BMT for ab-T cellsplenic lymphoma. One month later shedeveloped acute GVHD related erosive entero-pathy resulting in life threatening exsangui-nation. Following successful resuscitation(which precipitated admission to intensivecare for 6 weeks), she noted blurred left eyevision and described difficulty in dark adap-tation and differentiating between shades ofgrey; there was right strabismic amblyopia.The patient’s medication comprised aciclovir,cyclosporin, penicillin, propranolol, andlansoprazole.

Visual acuity was 6/18 and N14 with theright eye, and 6/12 and N5 with the left.Colour vision was normal and visual fieldswere full. There was no afferent pupillarydefect. The anterior chambers and vitreouswere quiet. The optic discs were normal. Atboth maculas (Fig 1), there were deepsubretinal cream coloured spots and retinalthickening and OCT evidence of subretinalfluid without cystoid changes. Fluoresceinangiography showed a few hyperfluorescentspots consistent with focal retinal pigmentepithelium dysfunction. Electrodiagnostictests identified diffuse rod dysfunction.

Since there was biochemical evidence ofrenal impairment, acetazolamide was con-sidered to be contraindicated to treat thesubretinal fluid. By 4 months, the bestcorrected visual acuities were 6/1222 right;6/6+2 left. Repeat electrophysiology wasunchanged, however by ten months the fullfield electroretinograms had improved tonormal limits.

CommentGVHD is presumed to be caused by donor Tlymphocytes recognising minor histocompat-ibility antigens on recipient tissues that arethen subjected to CD8-T lymphocytemediated attack. Commonly reported ocularmanifestations include pseudomembranousconjunctivitis, keratoconjunctivitis sicca, cor-neal epitheliopathy, and cataract.1 Posteriorsegment involvement is rare and includescotton wool spots2 as well as central serouschorioretinopathy.3

In both of our cases, there seems to be astriking temporal association between theonset of visual symptoms and an adverseevent in the course of the disease. In case 1,in whom the cessation of cyclosporin resultedin acute GVHD, the ocular findings wereconsistent with scleritis, a feature only oncepreviously reported.4 Postmortem studieshave demonstrated choroidal infiltrates inGVHD patients containing histiocyte-likelarge eosinophils5 and clinically these maybe represented by the pale perifoveal lesionsobserved in the left eye. Subsequently thispatient was shown to be HLA-DR4 positive, afinding common in individuals with Harada’sdisease and frequently associated withchronic GVHD.6

By contrast, the ocular findings in thesecond case were not a result of acute but aconsequence of previous life threateningGVHD during which exsanguinationoccurred. While interruption of blood flow

to the optic nerve or visual cortex can accountfor visual loss following extreme haemor-rhage, retinal ischaemia has also been docu-mented.8 The rod photoreceptor systemappears most vulnerable,7 a feature consis-

Figure 1 Images of case 2 (in each case right eye on the right). (A) Colour fundal photographs atpresentation, showing deep subretinal cream coloured spots and overlying retinal thickening. (B)Optical coherence tomography of each macula (foveae arrowed) at presentation showing evidenceof subretinal fluid without cystoid changes. (C) Fluorescein angiography (later arteriovenous phase)at presentation showing a few hyperfluorescent spots consistent with focal RPE dysfunction. (D)Colour fundal photographs 4 months later showing irregular pigmentation at the level of the retinalpigment epithelium.

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tent with the electrophysiological findings inthis case, and the patient’s difficulty withdark adaptation is in keeping with roddysfunction. Of interest was the subsequentimprovement in acuity and electrophysiolo-gical responses. Such a pattern parallelselectrophysiological studies of children afterrespiratory or circulatory arrest where initi-ally subnormal ERG responses return tonormal levels within 8 months.9 The mechan-ism that mediates this recovery is not known.

Graft versus host disease is a commoncomplication of bone marrow transplantationthat usually presents to the ophthalmologistwith anterior segment signs. However, GVHDmay also present with posterior segmentpresentations of the types described here.

N G Strouthidis, P J Francis, M R Stanford,E M Graham

The Medical Eye Unit, 9th Floor, North Wing,St Thomas’s Hospital, Lambeth Palace Road, London

SE1 7EH, UK

N G Strouthidis, P J Francis, G E Holder,A C Bird

Moorfields Eye Hospital, 162 City Road, LondonEC1V 2PD, UK

Correspondence to: Dr E M Graham, The Medical EyeUnit, 9th Floor, North Wing, St Thomas’s Hospital,

Lambeth Palace Road, London SE1 7EH, UK;[email protected]


References

1 Johnson DA, Jabs DA. The ocular manifestationsof graft-versus-host disease. Int Ophthalmol Clin1997;37:119–33.

2 Coskuncan NM, Jabs DA, Dunn JP, et al. The eyein bone marrow transplantation. VI.Retinalcomplications. Arch Ophthalmol1994;112:372–9.

3 Cheng LL, Kwok AKH, Wat NMS, et al. Graftversus host disease associated conjunctivalchemosis and central serous chorioretinopathyafter bone marrow transplant. Am J Ophthalmol2002;134:293–5.

4 Kim YK, Anderlini P, Naderi AA, et al. Scleritis asthe initial clinical manifestation of graft-versus-host disease after allogeneic bone marrowtransplantation. Am J Ophthalmol2002;133:843–5.

5 Jabs DA, Hirst LW, Green WR, et al. The eye inbone marrow transplantation. II.Histopathology.Arch Ophthalmol 1983;101:585–90.

6 Holmes JA, Whittaker JA. Histocompatibilityantigen DR4 is associated with chronic graft-versus-host disease in the south Walespopulation. Br J Haematol 1989;73:424.

7 Lovasik JV, Kergoat H. Influence of transientlyaltered retinal vascular perfusion pressure onrod/cone contributions to scotopic oscillatorypotentials. Ophthalmic Physiol Opt1991;11:370–80.

8 Feher J, Antal M. Ischaemic retinal alterations incardiac arrest. Ann Ophthalmol1979;11:909–13.

9 Nickel BL, Hoyt CS. The hypoxic retinopathysyndrome. Am J Ophthalmol 1982;93:589–93.

Anterior pathway vision loss dueto subdural haematomaPatients with vision loss associated withsubdural haematomas typically present withhomonymous hemianopias secondary tocompression of the posterior cerebral arteryduring trans-tentorial herniation.1 2 In thesecases, necropsy studies have demonstratedpregeniculate involvement in addition tooccipital lobe lesions.2 We present a case

illustrating a rarely reported phenomenon ofanterior pathway vision loss associated with asubdural haematoma without any evidenceof optic disc swelling, occipital lobe disease,or radiographic signs of chiasmal or opticnerve compression.

Case reportA 51 year old man, who had previouslyundergone two craniotomies (October 1992and November 2000) for resection of anepidermoid tumour at the cerebellopontineangle, developed hydrocephalus and had a

Figure 1 Fundus photograph with right (A) and left (B) optic nerves without oedema or pallor oninitial presentation. Humphrey visual fields (C) on presentation and (D) 6 months followingcraniotomy with decompression of the subdural haematoma.

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ventriculoperitoneal shunt placed in January2001. Eleven months following placement ofthe shunt, the patient presented with ataxiaand headaches but no visual complaints. Acomputed tomograph (CT) scan showed aright subdural haematoma measuring 2.8 cmon coronal section, and 150 ml of blood weredrained via a burr hole.

One month following the drainage proce-dure, the patient presented to the hospitalwith a complaint of sudden, painless loss ofvision in his left eye occurring 24 hoursearlier. The patient had a left afferentpupillary defect with best corrected vision of20/30 in his right eye and hand movements inhis left eye. Extraocular movements were full,and the patient had normal colour vision inhis right eye. Slit lamp examination showedonly trace nuclear sclerosis cataracts bilater-ally. Fundus examination was also normal,with no evidence of optic disc oedema orpallor in either eye (Figs 1A, B).

Automated perimetry revealed a con-stricted field in the right eye and severe,global depression in the left eye (Fig 1C).

Magnetic resonance imaging (MRI) of thebrain showed that the right subdural haema-toma was still present but was decreased insize to 2.1 cm on coronal section (Fig 2A)compared to the study performed 1 monthearlier. No intraorbital abnormalities werepresent, and the optic nerves and chiasmappeared free of direct compression by thehaematoma. The blood did not appear tosurround the optic nerves (Fig 2B). Thepatient’s haematocrit and blood pressureremained within normal limits during theinitial presentation and subsequent treat-ment. The patient underwent craniotomywith further drainage of the subdural hae-matoma. After 6 months, the patient’s visionin the left eye improved to 20/200. Follow upperimetry showed less constriction on theright and improved performance on the left(Fig 1D). Funduscopic examination revealedmild optic nerve pallor in the left eye and anormal appearing right optic nerve.

CommentThis case represents a rare example ofanterior pathway vision loss due to subduralhaematoma. Most cases of vision loss withsubdural haematoma affect the posteriorvisual pathway, with mechanisms includingoccipital infarct and compression of theposterior cerebral artery during trans-tentorialherniation.1 2 Posterior lesions may presentwith anterior signs—for example, optic atro-phy was seen in three patients with occipitalinfarcts, two of whom initially presentedwith severe disc oedema.1 Necropsy studieshave shown that trans-tentorial herniationcan result in damage at the level of the optictract, chiasm, or optic nerves.2

The anterior visual pathway can be com-promised directly by gyrus herniation into thesuprasellar cistern, a mechanism associatedwith meningiomas.3 Prechiasmal vision lossdue to intracranial optic nerve infarction hasalso been reported in the setting of subduralhaematoma; in this case the mechanism waspresumably due to direct compression of thenerve against basal skull structures, althoughthis specific radiographic finding was notdescribed.4

The precise mechanism of anterior path-way vision loss due to subdural haematomain our patient, as well as in the few previousreports, remains poorly understood.1 4 MRIshowed no signs of blood in the orbits, directcompression of the optic nerves or chiasm, orgyrus herniation into the suprasellar cistern.The occipital lobes also appeared normal.Right to left midline shift due to the rightsided haematoma was present, probablyleading to vascular compromise or nervecompression that could not be visualised onMRI. Visual improvement following chiasmaldecompression of mass lesions has beenreported, and this mechanism may explainour patient’s improved visual acuity andperipheral fields following the drainage ofthe haematoma.5 Surprisingly, the subduralhaematoma in our patient was smaller at thetime of onset of visual symptoms than it hadbeen 1 month earlier.

Subdural haematomas can affect visionthrough compression or vascular compromiseat many points along the visual pathway.This case illustrates that optic neuropathy canoccur late in the setting of a subduralhaematoma, after the volume of the haema-toma has begun to decrease. Because of themany ways in which patients with subduralhaematomas can lose vision, they require

close follow up, and a sudden change invision necessitates immediate radiologicaltesting, ophthalmological examination and,possibly, urgent surgical intervention anddrainage.

D A Hollander, J M StewartDepartment of Ophthalmology, University of

California, San Francisco, CA, USA

Correspondence to: Jay M. Stewart, MD, University ofCalifornia, San Francisco, Department of

Ophthalmology, 10 Koret Way, Suite K-301, SanFrancisco, CA 94143, USA; [email protected]


References

1 Keane JR. Blindness following tentorialherniation. Ann Neurol 1980;8:186–90.

2 Lindenberg R, Walsh FB. Vascular compressionsinvolving intracranial visual pathways. Trans AmAcad Ophthalmol Otolaryngol 1964;68:677–94.

3 Klingele TG, Gado MH, Burde RM, et al.Compression of the anterior visual system by thegyrus rectus: case report. J Neurosurg1981;55:272–5.

4 Skarf B, Davis RL, Birsner HA, et al. Intracranialoptic nerve infarction from subdural hematoma:clinical and neuropathological findings. ArchNeurol 1984;41:58–60.

5 Cohen AR, Cooper PR, Kupersmith MJ, et al.Visual recovery after transsphenoidal removal ofpituitary adenomas. Neurosurg1985;17:446–52.

Surodex in paediatric cataractsurgeryPaediatric cataract surgery is associated witha high incidence of postoperative inflamma-tion.1–3 Intensive topical steroid therapy is stillrelied upon as the conventional mode ofprevention and treatment.1–4 Frequently,adjuvant systemic2–5 and/or periocular ster-oids3–5 may be required for further control,particularly if the child has a history of, or isat risk of, uveitis (for example, microphthal-mos).5–9 Non-compliance and missed applica-tion of steroid drops into the eye impedescontrol of the postoperative uveitis.

The Oculex Drug Delivery System (DDS;Oculex Pharmaceuticals, Inc, Sunnyvale, CA,USA) is a biodegradable device that allowssustained drug release after insertion into theanterior chamber (AC). Surodex is a DDSwith 60 mg of dexamethasone incorporatedinto the polymer matrix (poly(lactic-glyco-lic)-acid, PLGA) with sustained and con-trolled release of dexamethasone over 7 days,achieving higher intraocular drug levels thanwith conventional dexamethasone eyedrops.10 Randomised controlled trials foundSurodex to be as effective as 0.1% dexa-methasone eye drops in the control of post-cataract surgery inflammation.10–12 Surodex isapproved for use in cataract surgery inSingapore.

We reviewed retrospectively all paediatricpatients who underwent cataract surgerywith the insertion of one pellet of Surodexinto the AC at the conclusion of surgery.Eighteen eyes of 13 patients (nine males andfour females) were diagnosed with cataractsat a mean age of 57.4 months (range 1 day to136 months). The mean age at surgery was66.5 months (range 1 week to 139 months)and follow up period ranged from 6–18 months (mean 7.8 months). Factors pre-disposing to cataracts included hereditarycataracts (two), microphthalmos (three),

Figure 2 Magnetic resonance imaging (T1weighted coronal) of (A) right subduralhaematoma with significant right to left midlineshift but without direct compression of theprechiasmal optic nerves and (B) withoutcompression of the intraorbital optic nerves.

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severe atopic dermatitis (one) and traumaticcataract (one). The types of cataract includedtotal/mature (seven), nuclear (two), lamellar(three), subcapsular (two), posterior lentico-nus (two), and posterior polar (two).

All eyes underwent lens aspiration throughcan opener anterior capsulotomy or contin-uous curvilinear capsulorrhexis (CCC) undergeneral anaesthesia. Fourteen eyes had eitherposterior capsulotomy (with the vitrectomycutter) or a posterior CCC (surgeon’s pre-ference). Anterior vitrectomy was done in 13eyes. Eleven eyes (61.1%) were implantedwith a foldable intraocular lens (IOL)(Acrysof lens MA60BM, 10 and MA30BM,1) (pseudophakic group) (Table 1). Thisgroup was older (mean 84.81 months) thanthe aphakic group (mean age 14.31 months).Only seven eyes (63.6%) of the pseudophakicgroup underwent posterior CCC/capsulotomyand anterior vitrectomy, compared to all eyesin the aphakic group. Complications wereencountered in four eyes in the pseudophakicgroup (36.4%)—malposition of IOL, vitreousstrand in AC, posterior synechiae and raisedIOP.

Four eyes (two in the pseudophakic andtwo in the aphakic group) did not receiveadditional postoperative topical steroids (pre-dnisolone acetate 1%). This decision wasmade for patients 4 and 12 as there wasminimal manipulation and iris traumaintraoperatively. These children were older(ages 131 and 115 months at surgery),allowing for easier follow up examination.Patient 13 had developmental delay and wasdifficult to manage. All four eyes wereassessed to be quiet by slit lamp examination2–4 weeks postoperatively. Additional ster-oids were not indicated and there was noglaucoma or endophthalmitis.

One eye (patient 17) required adjuvantperiocular dexamethasone (1 mg) for fibri-nous inflammation in the first week. The lefteye of patient 6, which had been quiescentand without treatment for 2 months, devel-oped raised IOP (30 mm Hg) at 3 monthsafter surgery. This was controlled with topicalbetaxolol. There was no glaucomatous cup-ping and visual fields could not be performedin view of the age of the child.

Patient 13 had severe atopic dermatitisrequiring systemic prednisolone. Whenvisually significant cataract developed in theleft eye, preoperative prednisolone wasincreased prophylactically and a pellet ofSurodex was inserted at the end of surgery.As there was minimal inflammation, thesystemic steroid was tapered over 2 weeks

and the steroid eye drops were stopped after3 weeks. This eye achieved a final visualacuity of 20/20.

CommentFibrinous anterior uveitis is common afterpaediatric cataract surgery, occurring invarying severities in up to 100% of cases.2 3

In our series, only two eyes (11.1%)developed inflammation that required addi-tional steroid therapy. The remaining 16 eyesachieved good control of inflammation, par-ticularly the four eyes that received Surodexwithout postoperative topical steroids. Noneexperienced rebound uveitis after 1 week,when the pellet had ceased its release ofdexamethasone. This suggests that inselected eyes, a Surodex pellet alone may beadequate to control postoperative inflamma-tion. A randomised controlled trial comparingSurodex versus conventional steroid eye droptherapy will be needed to determine theultimate efficacy of Surodex in paediatriceyes.

The efficacy of eye drops is dependent oncompliance and timely application for drugpenetration and absorption. In infants andyoung children, the systemic absorption ofthe steroid may have potentially seriouscomplications such as hyperglycaemia andimmunosuppression. Surodex significantlyreduces the total dose delivered, as the60 mg of dexamethasone in one pellet isapproximately equivalent to that in just onedrop of 0.1% dexamethasone.10 A system suchas the DDS allows for direct application of thedrug to the target site, potentially eliminatingthe problems of compliance.

The single complication encountered,which may be related to Surodex insertion,is the late onset of raised IOP (patient 6)despite the lack of marked postoperativeinflammation. The fellow eye had also under-gone cataract surgery with insertion ofSurodex without complications. Steroidresponsive glaucoma is an unlikely cause asthe drug has been shown to persist only for7 days in rabbits, although this has not beendemonstrated in human eyes.13 Gonioscopymay reveal focal peripheral anterior syne-chiae (PAS) at the site of residual pellet, butit is unlikely that this minor degree ofsynechiae may cause angle closure glaucoma,although the pellet may persist for weeks inthe angles.10 Unfortunately, gonioscopy wasnot performed in this eye. Glaucoma afterpaediatric cataract surgery is, however, acomplication that increases in frequency withlonger durations of follow up (3–22%).1 5 14

We acknowledge that there are severallimitations to these findings. Firstly, being aretrospective review, the efficacy of Surodexin preventing posterior capsular opacification,an indicator of postoperative inflammation,could not be assessed. We are also unable toestablish if Surodex alone is sufficient forpostoperative control of inflammation, thiswould require a prospective randomisedclinical controlled trial. The efficacy of controlof postoperative inflammation and safety areincomplete without the assessment of flareand endothelial cell counts but these aredifficult in children, although endothelial cellcount studies in adult eyes have shown nosignificant change.10 12 Finally, gonioscopy tovisualise the angles to look for PAS was alsonot done.

Surodex has previously been shown to besafe and effective in uncomplicated cataractsurgery in adults. This retrospective reviewprovides preliminary data to suggest thatSurodex may be an effective and safeadjunctive anti-inflammatory agent that insome paediatric eyes may eliminate the needfor other steroid administration. Furtherstudies will be required to determine theultimate safety of Surodex in paediatric eyes.

S-Y Lee, S-P Chee, V Balakrishnan,S Farzavandi, D T H Tan

Singapore National Eye Centre

S-P Chee, V Balakrishnan, D T H TanSingapore Eye Research Institute

S-P Chee, D T H TanDepartment of Ophthalmology, National University of

Singapore

Correspondence to: Soon-Phaik Chee, SingaporeNational Eye Centre, 11 Third Hospital Avenue,

Singapore 168751; [email protected]

Accepted for publication 3 March 2003

References

1 Zwann J, Mullaney PB, Awad A, et al. Pediatricintraocular lens implantation. Surgical results andcomplications in more than 300 patients.Ophthalmology 1998;105:112–19.

2 Sharma N, Pushker N, Dada T, et al.Complications of pediatric cataract surgery andintraocular lens implantation. J Cataract RefractSurg 1999;25:1585–8.

3 Malukiewicz-Wisniewska G, Kaluzny J,Lesiewska-Junk H, et al. Intraocular lensimplantation in children and youth. J PediatrOphthalmol Strabismus 1999;36:129–33.

4 Apple DJ, et al. Pediatric cataract. Surv Ophthal2000;45(Suppl):S150–68.

5 Cavallaro BE, Madigan WP, O’Hara MA, et al.Posterior chamber intraocular lens use in children.J Pediatr Ophthalmol Strabismus1998;35:254–63.

6 Yu YS, Lee JH, Chang BL. Surgical managementof congenital cataract associated with severemicrophthalmos. J Cataract Refract Surg2000;26:1219–24.

7 BenAzra D, Cohen E. Cataract surgery in childrenwith chronic uveitis. Ophthalmology2000;107:1255–60.

8 Lundvall A, Zetterstrom C. Cataract extractionand intraocular lens implantation in children withuveitis. Br J Ophthalmol 2000;84:791–3.

Table 1 Pseudophakic and aphakic groups

Pseudophakic group Aphakic group

No of eyes 11 (61.1%) 7 (38.9%)Mean age at surgery 84.8 months 14.3 monthsNo of eyes with posterior capsular opening andanterior vitrectomy 7 (63.6%) 7 (100%)No of eyes with intact posterior capsule 4 (36.4%) 0ComplicationsIntraoperative complications 0 0Postoperative complications 4 (36.4%) 1 (14.3%)1 Malposition of PCIOL 1 02 Vitreous strand in anterior chamber with peakedpupil 1 03 Posterior synechiae 1 04 Fibrinous inflammation 0 15 Raised intraocular pressure 1 0

The authors have no proprietary or financial interest inOculex Pharmaceuticals, Inc, Sunnyvale, CA, or in theproduct Surodex.

Financial support: Nil.

Presentation: Poster presentation at the XXIXthInternational Congress of Ophthalmology, Sydney,Australia. 21–25 April 2002.

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9 Paikos P, Fotopoulou M, Papathanassiou M, et al.Cataract surgery in children with uveitis. J PediatrOphthalmol Strabismus 2001;38:16–20.

10 Tan DTH, Chee SP, Lim L, et al. Randomizedclinical trial of a new dexamethasone deliverysystem (Surodex) for treatment of post-cataractsurgery inflammation. Ophthalmology1999;106:223–31.

11 Chang DF, Garcia IH, Hunkeler JD, et al. Phase IIresults of an intraocular steroid delivery system forcataract surgery. Ophthalmol1999;106:1172–7.

12 Tan DTH, Chee SP, Lim L, et al. Randomizedclinical trial of Surodex steroid drug deliverysystem for cataract surgery. Anterior versusposterior placement of two Surodex in the eye.Ophthalmology 2001;108:2172–81.

13 Kochinke F, Vajda JJ, Wong VG. Novelbioabsorbable dmg delivery system (bDDS) forthe treatment of post-surgical inflammation. InvestOphthalmol Vis Sci 1994;35(Suppl):4474.

14 Keech RV, Cibis Tongue A, Scott WE.Complications after surgery for congenital andinfantile cataracts. Am J Ophthalmol1989;108:136–41.

Pars plana ciliary epithelialproliferation in 13q deletionsyndromeThe 13q deletion syndrome is an uncommonchromosomal disorder affecting the long armof chromosome 13 which is deleted to avariable degree.1 This syndrome is phenoty-pically characterised by mental retardation,structural malformations, facial dysmorph-ism, and a predisposition to develop retino-blastoma.1 This intraocular tumour isdiagnosed in approximately 80% of caseswith this syndrome.2 Moreover, the incidenceof bilateral retinoblastoma is much higher inindividuals with this syndrome.3 4 The retino-blastoma susceptibility gene (RB-1), whichencodes for the nuclear phosphoprotein of105 kDa, is located in band 13q14.5 Theinvolvement of the q14 band on the longarm of chromosome 13 places patients withthis syndrome at significant risk for develop-ing retinoblastoma.6 In addition, childrenwith 13q deletion syndrome also show opticnerve hypoplasia and retinal dysplasia.7 Inthis case, we report additional findings ofpars plana ciliaris epithelial proliferation in13q deletion syndrome.

Case reportA 5 month old Hispanic female infant with akaryotype 46,XX, del (13) (q14.1q21.3) wasreferred to us for the evaluation of retino-blastoma. She had dysmorphic features, suchas craniosynostosis. There was no familyhistory of ocular or systemic disease. Whileunder anaesthesia, the patient’s right eye wasexamined, revealing a mass that occupied alarge area of the inferior nasal portion of theretina, and extending into the vitreous cavity(Fig 1). It obscured the optic nerve head andwas associated with retinal detachment.There were also fine vitreous seedings.Ultrasonography disclosed a retinal tumourwith intralesional calcific foci. The preopera-tive diagnosis was retinoblastoma withvitreous seedings, and she underwent enu-cleation of the globe. The left eye wasunremarkable.

Macroscopic examination revealed a grey-ish-white tumour arising from the retina thatexhibited calcific foci and was extended intothe vitreous cavity. Histological examinationof the tumour indicated a well differentiatedretinoblastoma that displayed both Flexner-Wintersteiner and Homer-Wright rosettes

(Fig 1). There was no tumour invasion ofthe uvea or the post laminar optic nerve. Inaddition, the globe showed multilayeredplaquoid non-pigmented ciliary epithelialproliferation at the pars plana ciliaris (Fig 2)and optic nerve hypoplasia. The epithelialproliferation revealed benign histologicalfeatures, unlike the malignant neoplasticproliferation of the retina. At the pars planaciliaris, the pigment epithelium showed focalproliferation.

CommentThe extent of the deletions affecting the longarm of chromosome 13 may result in variousdevelopmental anomalies that constitute 13qsyndrome.2 8 Proliferation of the pars planaciliaris non-pigmented ciliary epithelium, asnoted in the present case, and its associationwith retinoblastoma suggests that the RB-1gene, or a gene close to the RB-1 locus mayhave a role in the proliferation of the otherneuroepithelial structures of the eye, includ-ing the pars plana ciliary epithelium.

In embryological terms, the non-pigmented ciliary epithelium is derived fromthe inner layer of the optic cup which alsogives rise to the neural retina.9 Proliferationof the pars plana ciliary epithelium in aneye that harbours retinoblastoma suggeststhat the RB-1 gene may play a part in

such epithelial proliferation. However, thisepithelial proliferation has not been pre-viously reported in eyes with retinoblastoma.Although the cause of proliferation of theciliary epithelium is not clear, this casesuggests that the non-pigmented ciliaryepithelial proliferation at the pars planaciliaris in an eye that harbours retinoblas-toma may be related to 13q deletion syn-drome. Such findings may be unique to thissyndrome, but previous reports about it havenot mentioned them. The lack of previouslyreported cases with findings of pars planaepithelial proliferation suggests that thissyndrome may have variable phenotypicexpression.

AcknowledgementsThis work was supported in part by NEI core grantEy03040 and by an unrestricted grant fromResearch to Prevent Blindness Inc, New York,USA. The clinical illustration is provided by DrLinn A Murphree.

Y UsuiDepartment of Ophthalmology, Tokyo Medical

University, Tokyo, Japan

Y Usui, N A RaoThe A Ray Irvine Ocular Pathology Laboratory, the

Doheny Eye Institute, and the Department ofOphthalmology, Keck School of Medicine of the

University of Southern California, Los Angeles, CA,USA

Correspondence to: Yoshihiko Usui, MD, Departmentof Ophthalmology, Tokyo Medical University, 6-7-1

Nishi-shinjuku, Shinjuku-ku, Tokyo 160-0023, Japan;[email protected]


References

1 Seidman DJ, Shields JA, Augsburger JJ, et al.Early diagnosis of retinoblastoma based ondysmorphic features and karyotype analysis.Ophthalmology 1987;94:663–6.

2 Ganesh A, Kenue RK, Mitra S. Retinoblastomaand the 13q deletion syndrome. J PediatrOphthalmol Strabismus 2001;38:247–50.

3 Bunin GR, Emanuel BS, Meadows AT, et al.Frequency of 13q abnormalities among 203patients with retinoblastoma. J Natl Cancer Inst1989;81:370–4.

4 Donaldson SS, Smith LM. Retinoblastoma:biology, presentation, and current management.Oncology (Huntingt) 1989;3:45–52.

5 Friend SH, Bernards R, Rogelj S, et al. A humanDNA segment with properties of the gene thatpredisposes to retinoblastoma and osteosarcoma.Nature 1986;323:643–6.

6 Kennerknecht I, Barbi G, Greher J. Diagnosis ofretinoblastoma in a presymptomatic stage afterdetection of interstitial chromosomal deletion 13q.Ophthalmic Genet 1994;15:19–24.

7 Weichselbaum RR, Zakov ZN, Albert DM, et al.New findings in the chromosome 13 long-armdeletion syndrome and retinoblastoma.Ophthalmology 1979;86:1191–201.

8 Brown S, Russo J, Chitayat D, et al. The 13q-syndrome: the molecular definition of a criticaldeletion region in band 13q32. Am J Hum Genet1995;57:859–66.

9 Beebe DC. Development of the ciliary body: abrief review. Trans Ophthalmol Soc UK1986;105:123–30.

Phacoemulsification of posteriorpolar cataracts—a surgicalchallengePosterior polar cataracts are relativelyuncommon yet they pose a significant chal-

Figure 1 The retinoblastoma shows numerousFlexner-Wintersteiner and Homer Wrightrosettes (haematoxylin and eosin; originalmagnification 6200). Inset; note a largeendophytic retinoblastoma arising from theinferior retina and obscuring the optic disc.

Figure 2 (A) Low magnification of ciliary bodyand pars plana ciliaris reveals plaquoid,thickening of non-pigmented ciliary epitheliumand double layered pigment epithelium(haematoxylin and eosin; originalmagnification 650). (B) High magnification ofthe pars plana ciliaris shows multilayeredproliferation of non-pigmented epithelium(haematoxylin and eosin; originalmagnification 6400).

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lenge to the cataract surgeon. Cataractsurgery in these cases is frequently accom-panied by a high incidence of posteriorcapsule rupture (PCR).

MorphologyPosterior polar cataracts are associated withremnants of the hyaloid system or the tunicavasculosa lentis.1 These cataracts may alsooccur without any relation to hyaloid rem-nants and appear as circular or rosette shapedopacities; they are hereditary and usuallytransmitted as a dominant trait. The gene forthis has been mapped to chromosome 16q22.2

Classification3

See Table 1 and Figure 1.

MethodsThe incidence of posterior polar cataracts inour centre is approximately 5 per 1000. Weconducted a retrospective review from 1994to 1999 and identified 31 patients (36 eyes)who had surgery for posterior polar cataracts.

ResultsFour eyes had PCR (11.1%) and the other 32had uncomplicated surgery; 34 eyes achieveda best corrected visual acuity of 6/12 or better(94.4%).

CommentOur series showed a PCR rate of 11.1% incontrast with the 26% incidence reported byOsher et al4 and 36% by Vasavada and Singh.5

No hydrodissection was attempted and onlycareful controlled hydrodelineation was per-formed. This was done using small aliquots of

balance salt solution (BSS) to loosen thenucleus while simultaneously watching thecapsular bag to ensure that the fluid wavepassed gently. In some cases, no hydroproce-dures were necessary as there was slowseparation of the nucleus by the BSS flowingfrom the phaco tip.

Vasavada and Singh described the use ofstep by step chop in situ and lateral separa-tion to minimise stress on the capsule-zonulecomplex.6 7 We preferred the use of the‘‘lambda’’ technique which involved sculpt-ing in the shape of the Greek letter (l),followed by cracking along both ‘‘arms’’ andremoval of the central piece first. Theadvantage of this is its gentleness in notstretching the capsule while removing thequadrants, especially the first one. Weemphasise that this is our preferred techni-que and other techniques would be equallyeffective in skilled hands.

We also used low vacuum, low aspiration,and low inflow parameters to ensure a morestable anterior chamber; bottle height was at50 cm, vacuum at 100 mm Hg, and aspira-tion flow rate at 20 ml per minute. Optimumpower setting was achieved when minimalmovement of the nucleus occurred whilesculpting.

The epinucleus and cortex were removedusing manual dry aspiration with Simcoecannula. This method is gentler as webelieve that the aspiration pressure is morecontrollable with our ‘‘million dollar’’ hands.There is also no ‘‘after aspiration’’ effectwhich in the automated unit can continue forseveral milliseconds even after the foot hasbeen taken off the pedal. The disadvantage ofmanual aspiration is the increased surgicaltime.

The status of the posterior capsule (PC)dictated the action of the surgeon. If the PCwas absent or torn but with no vitreous loss,a dispersive viscoelastic was injected over thedefect to tamponade and push the vitreousface backwards. A dispersive rather than acohesive viscoelastic is preferable as it is moreadapted to maintaining a space and stabilis-ing the anterior vitreous face. If there wasPCR with vitreous loss, a two port anteriorvitrectomy was performed. Intraocular lensimplantation in these cases would depend onthe extent of the PCR and the integrity of theremaining PC.

Surgical management of posterior polarcataracts poses a special challenge to thecataract surgeon. It is important that thesurgeon and the patient understand thetechnical difficulties associated and are awareof potential complications. It may be prudentto address these cases at the end of anoperating list or to shorten the list inanticipation of prolonged surgical time. Thesurgeon should use a technique that he or sheis most familiar and comfortable with. Withemphasis on gentleness, together withpatience and a well practised technique, theincidence of PCR can be minimised inphacoemulsification for posterior polar catar-acts.

M W Lee, Y C LeeLee Eye Centre, 44–46 Persiaran Greenhill, Ipoh,

Perak, 30450, Malaysia

Correspondence to: Dr Mun W Lee, Lee Eye Centre,56 Heyscroft Road, Withington, Manchester M20

4XF, UK; [email protected]


References

1 Luntz MH. Clinical types of cataracts. Duane’sOphthalmology 1996;CD ROM.

2 Maumenee III. Classification of hereditarycataracts in children by linkage analysis.Ophthalmology 1979;86:1554–8.

3 Anon. Consultation section: Cataract surgicalproblem. J Cataract Refract Surg1997;23:819–24.

4 Osher RH, Yu BC, Koch DD. Posterior polarcataracts: a predisposition to intraoperativeposterior capsular rupture. J Cataract RefractSurg 1990;16:157–62.

5 Vasavada A, Singh R. Phacoemulsification ineyes with posterior polar cataract. J CataractRefract Surg 1999;25:238–45.

6 Vasavada A, Singh R. Step-by-step chop in-situand separation of very dense cataracts. J CataractRefract Surg 1998;24:156–9.

7 Vasavada A, Singh R. Surgical techniques fordifficult cataracts. Curr Opin Ophthalmol1999;10:46–52.

Molluscum contagiosum in animmune reconstituted AIDSpatientIn spite of lower viral loads and increasing Tcell counts, AIDS patients receiving highlyactive antiretroviral therapy (HAART) are notalways successful in mounting an immuneresponse to some opportunistic pathogens. Infact, CMV retinitis, which was known tooccur in HIV patients with CD4 counts below506106/l, has been described in immunereconstituted patients with CD4 counts above2006106/l.1 It is therefore important to makeobservations about the clinical spectrum ofinfectious disease in immune reconstitutedAIDS patients. Here we report an isolated

Table 1 Classification of posterior polar cataracts

Type 1 Opacity associated with posterior subcapsular cataract.Type 2 Opacity with ringed appearance like an onion.Type 3 Opacity with dense white spots at the edge often associated with thin or absent posterior

capsule.Type 4 Combination of the above 3 types with nuclear sclerosis.

Figure 1 (A) One spot polar cataract. (B) Onion polar cataract. (C) Polar cataract with hole inposterior capsule. (D) Polar cataract with nuclear sclerosis.

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lesion of molluscum contagiosum in animmune reconstituted AIDS patient.

Case reportA 46 year old Hispanic female presented witha history of burning, tearing, and itching ofher left eye for 1 month. Three years earliershe had been diagnosed with AIDS during ahospital admission for Pneumocystis cariniipneumonia (PCP). At that time her CD4count had been 276106/l and her viral load905 000. After 3 months of HAART withcombivir, norvir, and fortovase her viral loaddropped to 15 000 and her CD4 count rose to1846106/l. Her viral load became undetect-able 6 months after initiation of therapy andhas remained so for 2K years. Her recentCD4 count was 4356106/l.

Best corrected visual acuity was 20/25 ineach eye. A 2 mm smooth, dome-shaped,translucent papule with central umbilicationwas present inferior to the medial aspect ofthe left lower lid margin (Fig 1). The lesionwas excised and histopathology revealedinvasive acanthosis with lobules of epithelialhyperplasia invaginating into the dermis.Intranuclear and intracytoplasmic inclusionbodies typical of molluscum contagiosumwere noted (Fig 2). The lesion did not recurafter biopsy.

CommentImmunocompetent patients with molluscumcontagiosum involving the eyelid typicallysuffer from an isolated lesion that is selflimited. Larger, more numerous and wide-spread molluscum contagiosum lesions havebeen documented in patients with AIDS,individuals immunosuppressed from usingprednisone and methotrexate, or patientswith lymphoreticular malignant neoplasms

or sarcoidosis.2–5 In HIV infected individualsthe disease runs a more protracted coursewith persistent lesions and there appears tobe an inverse relation of the CD4 count andthe number of molluscum contagiosumlesions.6

The present case shows that the patient’sreconstituted immune system from HAARTcan limit molluscum contagiosum infectionto a single lesion at the eyelid, clinically andhistologically identical to molluscum conta-giosum lesions found in immunocompetenthosts. Such limited expression of molluscumcontagiosum could be from a competent Tcell response as noted in individuals withnormal immune function or those withreconstituted immune response fromHAART.5 7 Thus, clinically the presence of asolitary molluscum contagiosum lesion in anHIV infected individual suggests appropriateresponse to HAART.

T AlbiniDepartment of Ophthalmology, Los Angeles County

Hospital, USA

N RaoDepartment of Pathology A, Ray Irvine Pathology

Laboratory, Doheny Eye Institiute, USA

Correspondence to: N Rao, Doheny Eye Institute,DVRC #211, 1450 San Pablo Street, Los Angeles, CA

90033, USA; [email protected]


References

1 Johnson SC, Benson CA, Johnson DW, et al.Recurrences of cytomegalovirus retinitis in ahuman immunodeficiency virus infected patient,despite potent antiretroviral therapy and apparentimmune reconstitution. Clin Infect Dis2001;32:815.

2 Dugal P, Rao N. Ocular infections in the acquiredimmunodeficiency syndrome. Int Ophthamol Clin1993;33:103–27.

3 Smith KJ, Skelton H, Yeager J. Molluscumcontagiosum: ultrastructural evidence for itspresence in skin adjacent to clinical lesions inpatients infected with human immunodeficinecyvirus type I. Arch Dermatol 1992;128:223.

4 Lombardo, PC. Molluscum contagiosum and theacquired immunodeficiency syndrome. ArchDermatol 1985;121:834.

5 Cattelan AM, Sasset L, Corti L, et al. A completeremission of recalcitrant molluscum contagiosumin an AIDS patient following highly activeretroviral therapy. J Infect 1999;38:58.

6 Schwartz JJ, Myskowski PL. Molluscumcontagiosum in patients with humanimmunodeficiency virus infection: a review oftwenty-seven patients. J Am Acad Dermatol1992;27:583.

7 Charteris DG, Bonshek RE, Tullo AB. Ophthalmicmolluscum contagiosum: clinical andimmunopathological features. Br J Ophthalmol1995;79:476.

Malignant melanoma of theconjunctiva metastasising to theparotid glandConjunctival melanoma is rare, accountingfor just 2% of ocular malignancies.1 Wepresent an unusual case of conjunctivalmelanoma with subsequent metastasis tothe parotid gland. A diagnosis was madeafter fine needle aspiration cytology of theparotid gland was performed in light of theprevious history.

Case reportA 79 year old white man presented to the eyeclinic in September 1999. He had been noted3 years previously to have a small inclusioncyst of the bulbar conjunctiva in his right eye,which he complained had increased in sizeand was becoming red and sore. Examinationshowed an inflamed pedunculated lesion1 cm in diameter arising from the nasallimbal conjunctiva (Fig 1). The lesion wasgranulomatous and amelanotic. There wasadjacent corneal opacity. Ocular examinationwas otherwise unremarkable.

The appearance of the lesion was felt to beunusual with a presumptive diagnosis ofconjunctival malignancy. Excision biopsywith conjunctival autografting was per-formed.

Histology revealed a primary nodularmalignant melanoma, at least 7 mm thick,composed of epithelioid sparsely pigmentedmelanocytes positive for S100 and vimentinimmunostains. Excision was deemed incom-plete.

The patient was referred for adjuvanttreatment with cryotherapy. To date, therehas been no sign of local recurrence.

In June 2001, the patient was referred byhis general practitioner to the oral surgeryservice at the same hospital with a 6 monthhistory of pain on the right side of his neck.He had also noticed some right facial swell-ing. Clinical examination disclosed a diffuse,firm mass over the lower pole of his rightparotid gland, measuring 4 cm in diameter.There were no overlying skin changes.

Magnetic resonance imaging (MRI) of thehead and neck showed a well defined lesionwithin the right parotid gland involving thedeep lobe and the deeper portion of the

Figure 1 Note solitary umbilicated lesioninvolving lower eyelid margin.

Figure 2 Histologically, the molluscumcontagiosum shows intracellular eosinophilicinclusion bodies (haematoxylin and eosin6120).

Figure 1 Pedunculated lesion arising from thenasal limbal conjunctiva, right eye.

Figure 2 FNA cytology of the parotidswelling. Highly pleomorphic malignantepithelioid melanocytes with scatteredlymphocytes in the background. Scalebar = 25 mm.

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superficial lobe. A few small lymph nodeswere visible at several sites bilaterally butnone appeared enlarged. Computed tomogra-phy (CT) of the chest, abdomen and pelvisrevealed single nodules measuring 3–5 mmat both lung bases, which may represent lungmetastases.

An orthopantomogram was normal, andfine needle aspiration (FNA) cytology wasperformed. This showed scattered lympho-cytes and highly pleomorphic non-lymphoidmalignant cells, some containing flecks ofpigment (Fig 2). While these appearancesalone would not allow definitive diagnosis ofmelanoma, in the clinical context they weresufficient to conclude that the parotid swell-ing was likely to be metastatic melanoma.This was confirmed on subsequent parotidexcision biopsy, which revealed extensiveinvolvement of the parotid nodes and parotidparenchyma, extending into the externaljugular vein.

CommentMalignant melanoma is a relatively raretumour in the parotid gland, with mosttumours representing metastasis from cuta-neous head and neck primaries.2 Very occa-sionally, as in this case, the primary tumouris non-cutaneous in origin.

Conjunctival melanoma metastasising tothe parotid has been noted in previousseries,3 but remains rare. This case is unusualwith respect to the initial size and appear-ance of the tumour, the previous history ofa conjunctival cyst, and that definitivediagnosis of a metastatic lesion from aconjunctival primary was made by FNA.This method has been helpful in the diag-nosis of other types of tumour in theparotid,4 and indeed in parotid melanomasof different origin.5 In this case, the patient’sprevious ophthalmic history had beenunknown to the maxillofacial surgeon mana-ging the case, and the diagnosis only becameclear during reporting of the cytology, whenthe FNA findings could be compared withprevious histology. This illustrates the impor-tance of exhaustive history taking and thevalue of a cohesive local histopathologyservice.

F CuthbertsonDepartment of Ophthalmology, St James’s University

Hospital, Beckett Street, Leeds LS9 7TF, UK

J Luck, S RoseRoyal United Hospital, Combe Park, Bath BA1 3NG,

UK

Correspondence to: Dr Fiona Cuthbertson,Department of Ophthalmology, St James’s University

Hospital, Beckett Street, Leeds LS9 7TF, UK;[email protected]


References

1 McCartney AC. Pathology of ocular melanomas.Br Med Bull 1995;51:678–93.

2 Prayson RA, Sebek BA. Parotid gland malignantmelanomas. Arch Pathol Lab Med2000;124:1780–4.

3 Esmaeli B, Wang X, Youssef A, et al. Patterns ofregional and distant metastasis in patients withconjunctival melanoma. Ophthalmology2001;108:2101–5.

4 Nasuti JF, Yu GH, Gupta PK. Fine needleaspiration of cystic parotid gland lesions: aninstitutional review of 46 cases with histologiccorrelation. Cancer 2000;90:111–16.

5 Chieng DC, Cangiarella JF, Waisman J, et al. Fineneedle aspiration cytology of desmoplasticmalignant melanoma metastatic to the parotidgland: case report and review of the literature.Diagn Cytopathol 2000;22:97–100.

Bilateral Aspergillusendophthalmitis in a patient withchronic lymphocytic leukaemiaAspergillus species are ubiquitous saprophyticmoulds, commonly growing in soil, storedhay, and decaying vegetation. Even thoughexposure to Aspergillus is universal, infectionin humans is uncommon.1 Aspergillus infec-tion of ophthalmic interest usually causeskeratitis or orbital cellulitis; Aspergillusendophthalmitis is a relatively rare conditionthat has a devastating course, with blindnessas its usual outcome.2 The clinical diagnosis isdifficult and the treatment is disappointing.In most cases, ocular involvement resultsfrom spread of aspergillosis infection fromothers organs and typically occurs in injectingdrug users and in patients with immunedeficiency of various causes. The leucopeniaappears to be a predisposing condition for theoccurrence of aspergillosis.3

We report an unusual case of bilateralendogenous Aspergillus endophthalmitis in apatient with chronic lymphocytic leukaemiain the absence of any detectable focus ofaspergillosis infection elsewhere in the bodyand that showed a good response to specificsystemic therapy.

Case reportA 51 year old white man with a previousdiagnosis of chronic lymphocytic leukaemiaand use of an immunosuppressive agent wasreferred to ophthalmological examinationbecause of a red eye, pain, and blurred vision

in his right eye. The clinical picture worsenedand diagnosis of endophthalmitis was made.Intravitreous amphotericin B injection wasperformed and did not control the case.Culture of vitreous fluid was positive forCandida. This eye was eviscerated because ofincreasing pain, progressive infection, andpoor response to treatment. Posterior histo-pathological study was conclusive forAspergillus endophthalmitis in the right eye(Fig 1B and 2). At the same time, fundusexamination of the left eye showed twosubretinal exudatives lesion located at nasaland inferior retina with retinal oedemaassociated with superficial haemorrhages(Fig 1A). The vitreous was clean and thecentral macula remained intact. Visual acuitywas 6/6 in this eye.

Vitreous biopsy or culture may yieldnegative results in some cases of earlyintraocular Aspergillus endophthalmitis.3 Wedid not take a vitreous biopsy of the left eye,since we already had the diagnosis in theright eye and the visual acuity was 6/6. Thiseye was treated with intravenous amphoter-icin B and oral itraconazole with a goodresult. The patient remained stable withresolution of the lesions and no focus ofsystemic aspergillosis was found.

CommentFungal endophthalmitis is uncommon. Inmost of the cases Candida is the causalorganism.4 5 Few cases of Aspergillusendophthalmitis in a patient with chroniclymphocytic leukaemia have been described,4

and according to the literature endogenousAspergillus endophthalmitis represents a man-ifestation of disseminated aspergillosis,usually a fatal infection.6 7 This case isunusual because it is bilateral and no focusof systemic aspergillosis was found.

The cases of intraocular inflammationsecondary to Aspergillus are more common inthe central macula and have a poor prog-nosis.1 In our case the localisation of thechorioretinitis in the left eye was out of theposterior area and the patient’s visual acuityremained 6/6.

The major antifungal agent used in asper-gillosis is amphotericin B. Without hostimmune competence, treatment is rarelyeffective. Penetration of intravenous ampho-tericin B into the vitreous cavity of thenormal or inflamed eye is poor.8 9 The azolecompounds have been used to reduce thesignificant toxicity and enhance the efficacy

Figure 1 (A) Fundus photography showing ayellowish subretinal lesion surrounded by fluidand haemorrhages, nasal to the disc, in the lefteye. (B) PAS stain showing the presence ofAspergillus in the cornea of the evisceratedright eye.

Figure 2 Lesion nasal to the disc aftertreatment.

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of intravenous amphotericin B; oral flucona-zole is the drug of choice because it hasexcellent penetration in central nerve systemand vitreous.1 Itraconazole may be used.Intravitreous amphotericin B and vitrectomyhave given the best results in the treatmentof these cases.2 Our patient received intrave-nous amphotericin B and oral itraconazoleand this therapy was sufficient to control theinfection.

This case shows that Aspergillusendophthalmitis should be considered in allpatients with immune deficiency even in theabsence of systemic aspergillosis. Treatmentwith intravenous amphotericin B may be ableto control these cases and should beattempted more often.

D de O Machado, R Goncalves, E M Fernandes,W R Campos, F Orefice

Department of Ophthalmology, Federal University ofMinas Gerais, Brazil

A L L CuriDepartment of Ophthalmology, Federal Fluminense

University Niteroi, Brazil

Correspondence to: Andre L L Curi, R Francisco Dutra163/701, Icaraı, Niteroi, RJ, Brazil Cep 24220150;

[email protected]


References

1 Weishaar PD, Flynn HW Jr, Murray TG, et al.Endogenous aspergillus endophthalmitis: clinicalfeatures and treatment outcomes. Ophthalmology1998;105:57–65.

2 Sihota R, Agorwal HC, Grover AK, et al.Aspergillus endophthalmitis. Br J Ophthalmol1987;71:611–13.

3 Rao NA, Hidayat AA. Endogenous mycoticendophthalmitis: variation in clinical andhistopathologic changes in candidiasis comparedwith aspergillosis. Am J Ophthalmol2001;132:244–51.

4 Kalina PH, Campbell J. Aspergillus terreusendophthalmitis in a patient with chroniclymphocytic leukemia. Arch Ophthalmol1991;109:102–3.

5 Hara KS, Reju JH, Lie TS, et al. Disseminatedaspergillus terreus infection inimmunocompromised hosts. Mayo Clin Proc1989;64:770–5.

6 Graham DA, Kinyoun JL, George DP.Endogenous aspergillus endophthalmitis afterlung transplantation. Am J Ophthalmol1995;119:107–9.

7 Hunt KE, Glasgow BJ. Aspergillusendophthalmitis: an unrecognized endemicdisease in orthotopic liver transplantation.Ophthalmology 1996;103:757–67.

8 Green WR, Bennett JE, Goos RD. Ocularpenetration of amphotericin B. Arch Ophthalmol1965;73:769–75.

9 Fisher JF, Taylor AT, Clark J, et al. Penetration ofamphotericin B into the human eye. J Infect Dis1983;147:164.

Late bleb needlingSurgical manipulation of the trabeculectomybleb has become a recognised postoperativeprocedure to increase the success of glaucomasurgery. The first needling revision of aglaucoma drainage bleb was described in19411 and there are several reports of thesuccessful restoration of failing blebs withinthe first 3 years following trabeculectomy.2–6

We report the results of five cases of latebleb needling with 5-fluorouracil (5-FU)where trabeculectomy had been performedbetween 8 and 30 years earlier.

Case reportsThe demographic details of all cases aresummarised in Table 1.

Glaucoma surgery had taken place between8 and 31 years before bleb needling and in nocase had antimitotics been used at theoriginal surgery. Before bleb needling theaverage intraocular pressure (IOP) among thepatients was 29.4 mm Hg (range 19–58).Each patient showed glaucomatous dete-rioration despite being on maximum toler-ated medical therapy, taking on average threeocular hypotensive agents, and in two casesoral acetazolamide. In all cases an opensclerotomy was confirmed by gonioscopy.

All procedures were performed in theoutpatient clinic, by either a consultant orassociate specialist, using a slit lamp. The eyewas anaesthetised with amethocaine eyedrops 1%, and phenylephrine eye drops2.5% were used for vasoconstriction. Afterseveral drops of chloramphenicol the con-junctiva was entered several millimetres fromthe flap site with a 27 gauge needle mountedon an insulin syringe. In one case aqueousflow was established after perforating scartissue around an encysted bleb, whereas inthe others it was necessary to dissect beneaththe scleral flap and enter the anteriorchamber. After creating a bleb and confirm-ing a reduction in IOP by applanationtonometry, 5 mg 5-FU (25 mg/ml) wereinjected into the subconjunctival spacearound the bleb. After needling, all hypoten-sive therapies were stopped and replaced byintensive topical steroids and chlorampheni-col. The steroid was titrated, and repeatinjections of 5-FU with or without needlingwere given, according to the IOP andappearance of the bleb.

After 12 months’ follow up from the lastneedling (Table 2), average IOP was reducedto 14 mm Hg (range 9–17). There was nochange in the patients9 visual acuity. Twocases developed a mild corneal epitheliopathythat healed within 8 weeks. There were noother complications from the needling proce-dure.

CommentAlthough trabeculectomy is the preferredglaucoma drainage procedure, only 67% ofpatients may achieve an adequate targetpressure after 1 year.5

In recent years glaucoma surgery hasdeveloped with the use of antimitotics andintense postoperative surveillance with blebmanipulation. Reports show that bleb need-ling used in combination with subconjuncti-val 5-FU injections can rectify a failing blebin the early postoperative phase but there arefew reports confirming its effect in the latepostoperative period.2 3 Some studies haveindicated that the success of bleb needling isunrelated to the time lapsed from the originalsurgery2 3 though in these studies the max-imum interim period was less than 4.5 years.

The patients presented in this study hadhad their original glaucoma surgery at least 8years previously and bleb needling wascarried out before listing the patient for arepeat trabeculectomy with mitomycin C. Theonly adverse effect noted was a temporarycorneal epitheliopathy, probably related totoxicity of the 5-FU. Other reported adverseevents after bleb needling include hyphaema,bleb leak, shallow anterior chamber, choroi-dals effusion and endophthalmitis, but thereare no reports of long term hypotony as hasbeen described following mitomycin C trabe-culectomy.

These case reports indicate that bleb need-ling may be successful in achieving a longlasting IOP reduction even several years afterthe original surgery. The procedure does notrequire dextrous skills beyond that of atrained general ophthalmologist. It appearsat least as safe as trabeculectomy and avoidsa formal operation. If it does fail the surgicalfield is still intact for a ‘‘redo’’ trabeculect-omy.

C T Ung, H Von Lany, K G ClaridgeTaunton and Somerset NHS Trust, Musgrove Park,

Taunton TA1 5DA, UK

Table 1 Demographic details of patients

Caseno Drainage procedure

Delay to needling(years)

No ofneedlings

No of 5-FUinjections

1 72 M Bilateral Scheie’s 31 2 42 88 F Left ECCE+trabeculectomy 10 4 53 80 F Right trabeculectomy 12 1 44 35 M Right trabeculectomy 8 1 25 71 M Bilateral trabeculectomy 13 1 2

ECCE = extracapsular cataract surgery.

Table 2 Results of pre-bleb and post-bleb needling with a 12 month follow upperiod

Caseno Age (years) Sex

IOP (mm Hg) No of medications

Pre Post Pre

1 72 M 19 9 3+ acetazolamide 02 88 F 25 14 3 13 80 F 20 17 3 14 35 M 58 12 2+ acetazolamide 05 71 M 25 16 2 0

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Correspondence to: Ms Katherine Claridge, Tauntonand Somerset NHS Trust, Musgrove Park, Taunton

TA1 5DA, UK; [email protected]

References

1 Ferrer H. Conjunctival dialysis in the treatment ofglaucoma recurrent after sclerotomy. Am JOphthalmol 1941;24:788–90.

2 Ewing RH, Stamper RL. Needling revision withand without 5-fluorouracil for the treatment oftailed filtering blebs. Am J Ophthalmol1990;110:254–9.

3 Shin DH, Juzych MS, Khatana AK, et al. Needlingrevision of failed filtering blebs with adjunctive 5-fluorouracil. Ophthalmic Surg 1993;24:242–8.

4 Gillies WE, Brooks AMV. Restoring the function ofthe failed bleb. Aus and NZ J Ophthalmol1991;19:49–51.

5 Edmunds B, Thompson JR, Salmon JF. TheNational Survey of Trabeculectomy. II.Variationsin operative technique and outcome. Eye2001;15:441–8.

6 Mardelli PG, Lederer CM Jr, Murray PL, et al.Slitlamp needle revision of failed filtering blebsusing mitomycin C. Ophthalmology1996;103:1946–9.

The success rates for endonasaldacryocystorhinostomyTsirbas and Wormald are to be congratulatedon their landmark paper in lacrimal surgerydescribing endonasal dacryocystorhinostomy(DCR) with mucosal flaps,1 which is alsoknown as powered endonasal DCR.2 3 Theirresults are seemingly impressive, with anato-mical success rate of 95% and functionalsuccess rate of 89%, closely approachingthose of external (transcutaneous) DCR. Ihave three comments that I hope will helpreaders who are less familiar with endonasallacrimal surgery, put this paper into perspec-tive.

Firstly, the mucosal flaps have a greaterrole peroperatively than postoperatively. Thelarge nasal mucosal flap reflected mediallyover the middle turbinate protects thatstructure peroperatively from inadvertentdamage during mechanical/powered instru-mentation. After the bony opening has beenmade (osteotomy) this flap is trimmed in thedescribed C shape, which prevents it fromflapping over the common canalicular open-ing and occluding it; it has only a negligiblepostoperative role covering raw bony edges inpart. The creation of a useful lacrimal sacmucosal flap is entirely dependent on the sizeof the sac, being large when there is amucocele and small when the sac is smalland shrunken. In external DCR the fashionedmucosal flaps are well apposed and sutured,and are assumed to have a major role inreducing scarring from secondary intentionhealing. In comparison, the mucosal ‘‘flaps’’described in this paper probably have only aminor role in the postoperative period.

Secondly, the disadvantage of this techni-que is undoubtedly the reported 46% rate ofconcomitant septoplasty, in order to create anadequate nasal space for safe instrumenta-tion. Concomitant septoplasty is only occa-sionally needed in endoscopic endonasalsurgical dacryocystorhinostomy (EES-DCR),probably in less than 5% of cases operated,yet the results of that faster and less invasivesurgery are approximately 85%. Septoplasty is

hardly ever required in external DCR, usuallyonly in occasional trauma cases where thenasal space is exceedingly narrow. Theauthors have recognised that maintainingan unimpeded common canalicular openingfree from fine bone fragments, mucosal tags,or flaps enables free tear drainage into thenose and is a key factor for a high successrates in DCR surgery. In order to achieve thisthey consistently make a very large rhinost-omy (20 mm615 mm) by removing both thethin lacrimal and the thicker maxilla bone.The drawback of doing this endonasally isthat there are risks of mucosal damage andsubsequent synechiae from the bone punches(rongeurs) used to remove maxilla boneanterior to the sac, and the diamond burrused to remove the thick maxilla bonesuperior. Hence, there is the need for thehigh septoplasty rate to create an adequatelylarge size nasal space.

Thirdly, their follow up times are incon-sistent and need to be standardised in orderfor readers to understand the results andcompare them with those of other endonasalDCR techniques. The success rates formechanical endonasal DCR reported byTsirbas and Wormald1 appear to be very good(95% anatomical and 89% functional suc-cess), but their follow up period varied fromonly 2 months to 28 months (mean 9.7).Some of the patients who had only a shortfollow up time may subsequently fail. Apaper published in the American Journal ofOphthalmology by the same authors using thesame technique,3 where they had a minimalfollow up of 9 months, had a lower anato-mical success rate (91%).

It is important to define success and whatthis really means, and for lacrimal surgeonsto agree consistent outcome criteria. Perhapslacrimal surgeons should agree the followingcriteria for DCR surgical success, irrespectiveof whether it is by an external or endonasalroute?

N Assess the outcome a minimum of 6months after surgery, being at least 3months after removal of tubes. Or is 1 yearafter surgery better?

N Assess subjective success based on thepatient’s symptoms.

N Assess objective success (anatomical suc-cess) based on (i) patency on syringingand (ii) presence of a functioning rhinost-omy. The latter is evaluated using thefunctional endoscopic dye test, which ispositive when 2% fluorescein instilled inthe conjunctival fornix is seen emergingfrom the rhinostomy a few seconds later.4 5

Despite these minor quibbles, the authorsare to be congratulated on advancing endo-nasal lacrimal surgery.

J M OlverWestern Eye Hospital, Marylebone Road, London

NW1 5YE, UK;[email protected]

References

1 Tsirbas A, Wormald PJ. Mechanical endonasaldacryocystorhinostomy with mucosal flaps.Br J Ophthalmol 2003;87:43–7.

2 Wormald PJ. Powered endonasaldacryocystorhinostomy. Laryngoscope2002;112:69–72.

3 Tsirbas A, Wormald PJ. Endonasaldacryocystorhinostomy with mucosal flaps.Am J Ophthalmol 2003;135:76–83.

4 Moore WM, Bentley CR, Olver JM. Functional andanatomic results after two types of endoscopicendonasal dacryocystorhinostomy: surgical andholmium laser. Ophthalmology2002;109:1575–82.

5 Minasian M, Olver JM. The value of nasalendoscopy after dacryocystorhinostomy. Orbit1999;18:167–76.

Trypan blue stains the epiretinalmembrane but not the internallimiting membraneWe read with great interest the paper by Liet al about staining of the internal limitingmembrane (ILM) and epiretinal membrane(ERM) with trypan blue (TB).1 We would liketo comment on one aspect of this paper,when the authors claimed that a goodstaining of both the ILM and the ERM wasachieved with TB. We disagree that ILM isstained by TB, and propose that TB onlystains the ERM, not the ILM.

The authors affirm ‘‘ILM staining’’ with TBas they observed histologically the presenceof ILM in four eyes with macular holes atstage III and IV. In one of those eyes,immunohistochemistry was performed, andan epiretinal membrane was observed. In theother three cases, immunohistochemistryexamination was not performed because ofinsufficient tissue. Most of the stage III andIV macular holes are known to be associatedwith an epiretinal membrane,2 and probablyan ERM would be seen in addition to the ILMin those three cases if immunohistochemistryfor glial elements were performed. Therefore,we believe that TB stained the ERM asso-ciated with the macular holes, but not theILM. In their study, staining with TB of sevenpatients with idiopathic epiretinal membranewas successfully performed. ERM of prolif-erative vitreoretinopathy is also reported tobe well stained by TB.3 We speculate that TBhas binding affinity to some of the glial cellelements of the highly cellular ERMs, eitherthose associated with macular holes or not.

Indocyanine green (ICG) is another newdye for intraocular staining that has gainedwide acceptance among retina surgeons inthe past few years.4 In contrast with thecellular affinity of TB, ICG stains the acellularILM, because of the fast binding of ICG tocollagen proteins of the ILM. ERM tends tobe stained negatively by ICG, well becausethe hydrophilic ICG does not penetrate cellmembranes easily.5

TB staining seems to be a good alternativeto ICG staining in the surgical managementof macular diseases. Further studies arewarranted on the intraocular kinetics of thatdye.

E B Rodrigues, C H Meyer, J C Schmidt, P KrollDepartment of Ophthalmology, Philipps-University

Marburg, Germany

Correspondence to: E B Rodrigues, MD; Departmentof Ophthalmology, Philipps-University Marburg,

Germany; [email protected]

Accepted for publication 4 April 2003

References

1 Li K, Wong D, Hiscott P, et al. Trypan bluestaining of internal limiting membrane and

Accepted of publication 11 February 2003

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epiretinal membrane during vitrectomy: visualresults and histopathological findings.Br J Ophthalmol 2003;87:216–19.

2 Tornambe P, Augustin AJ. Macular holes. Reviewof the current status of knowledge of pathogenesisand treatment methods. Ophthalmologe2002;99:601–8.

3 Feron EJ, Veckeneer M, Parys-VanGinderdeuren R, et al. Trypan blue staining ofepiretinal membranes in proliferativevitreoretinopathy. Arch Ophthalmol2002;120:141–4.

4 Schmidt JC, Meyer CH, Rodrigues EB, et al.Staining of internal limiting membrane invitreomacular surgery: a simplified technique.Retina 2003 (in press).

5 Forster RE, Petersen MR, Da Mata AP, et al.Negative indocyanine green staining of epiretinalmembranes. Retina 2002;22:106–7.

Thermochemotherapy inhereditary retinoblastomaSchueler and associates describe their experi-ence with thermochemotherapy (TCT) inbilateral retinoblastoma.1 The reported resultsof transpupillary thermotherapy used incombination with chemotherapy areencouraging, with 86–96% tumour control.2 3

In the current series, however, local recur-rence occurred in 38%.

The dosage of carboplatin used in thecurrent series was 10 mg/kg body weight,which is lower than the standard dosage of18.6 mg/kg body weight.4 Lower dose ofcarboplatin, the key drug in the chemother-apy regimen for retinoblastoma, could haveinfluenced the higher recurrence rate.

The authors mention that they treatedsubmacular tumours with TCT. However, inour experience, tumours located in themacular area are better treated initially withchemotherapy for 3–6 cycles in order toachieve maximum possible reduction intumour size before considering thermother-apy. Chemotherapy reduced maculartumours tend to shrink away from the foveatowards one of the major arcades or the opticnerve, thus exposing the foveal region.Residual tumours beyond 3–6 cycles ofchemotherapy could be treated with thermo-therapy. A smaller scar thus produced mayoptimise residual central vision.

The high mean total duration of thermo-therapy in the current series is probablybecause of a smaller spot size of 0.4 mm.The diode laser (Iris Medical Inc, MountainView, CA, USA) with an operating micro-scope adapter allows for a spot size of 0.8, 1.2,and 2.0 mm.3 The relatively newer large spotindirect ophthalmoscope delivery system pro-vides a 1.2 mm spot size.3 A larger spot sizewill indeed reduce the duration of thermo-therapy and allow for a more uniform cover-age. Corneal, iris, and lens complications areminimised with better convergent beamoptical systems currently available.

We believe that with higher dose ofcarboplatin, staggered thermotherapy forsubmacular tumours, use of better opticalsystems for delivery and a larger spot size forthermotherapy, and judicious selection ofcases, the tumour regression and visionsalvage with TCT could be further optimised.

R Murthy, S G Honavar, M Naik, V A P ReddyOcular Oncology Service, LV Prasad Eye Institute,

Hyderabad, India

Correspondence to: Santosh G Honavar, MD, OcularOncology Service, LV Prasad Eye Institute, LV Prasad

Marg, Banjara Hills, Hyderabad 500 034, India;[email protected]

Accepted for publication 21 April 2003

References

1 Schueler AO, Jurklies C, Heimann H, et al.Thermochemotherapy in hereditaryretinoblastoma. Br J Ophthalmol 2003;87:90–5.

2 Lumbraso L, Doz F, Urbeita M, et al.Chemothermotherapy in the management ofretinoblastoma. Ophthalmology2002;109:1130–6.

3 Shields CL, Santos CM, Diniz W, et al.Thermotherapy for retinoblastoma. ArchOphthalmol 1999;117:885–93.

4 Shields CL, Honavar SG, Shields JA, et al. Factorspredictive of recurrence of retinal tumors, vitreousseeds, and subretinal seeds followingchemoreduction for retinoblastoma. ArchOphthalmol 2002;120:460–4.

Causes of severe visualimpairment and blindness inchildren in EthiopiaWe read with great interest the article byKello et al.1 The authors have to be congra-tulated for the hard hitting and well writtenarticle. A current concern for people involvedin paediatric eye care is the emergence ofwhat is probably the third epidemic ofretinopathy of prematurity (ROP) in devel-oping countries.2 3 It is therefore significantthat no case of ROP was found in thepopulation screened in this study. Severalfactors could account for this.

N The very low or nil prevalence of ROP incountries such as Ethiopia, where thestudy was carried out, is most probablybecause of lack of intensive care facilitiesfor premature infants and their lowsurvival rates.

N The variation in the incidence of ROPbetween ethnic groups could also accountfor this, with the available evidencesuggesting that African-American infantsare less prone to severe outcome ROP thanwhite infants.4 5

N However, it is also important to note thatthe article mentions that children withmental retardation were not examinedowing to the admission criteria of theblind schools that preclude their admis-sion. This too could have accounted for thegross underestimation of the prevalence ofROP as suggested by Jacobson et al.6 Inaddition, these children with mental han-dicap could be suffering from cerebralpalsy and would have been at high riskfor ROP because of the higher incidence ofretinal vascular anomalies associated withboth cerebral ischaemia and prematurity.7

N A large number of infants had phthisisbulbi (51 cases). In children with bilateralphthisis bulbi, there is a possibility that anunknown proportion developed the condi-tion secondary to end stage ROP.

In conclusion, if improvement in perinatalcare occurs in Ethiopia, the overall numbersof children with ROP would increase as isseen in other developing countries like Indiawith infant mortality rates (IMRs) between10–60 per 1000 live births.3 Lack of ophthal-mologists experienced in the management ofROP could be effectively circumvented byintroduction of digital retina camera technol-

ogy to improve access to subspecialty care8 forcases requiring treatment. As a lower costoption, screening infants under 1200 g alonemight be more cost effective9 and could bethe first step, with modification of thescreening guidelines made later, consequentto research undertaken within the countryitself.

V Vedantham, P K RatnagiriAravind Eye Hospital and Postgraduate Institute ofOphthalmology, Madurai, Tamil Nadu 625 020,

India

Correspondence to: V Vedantham, Department ofRetina-Vitreous, Aravind Eye Hospital and

Postgraduate Institute of Ophthalmology, 1 AnnaNagar, Madurai, Tamil Nadu 625 020, India;

[email protected]

References

1 Kello AB, Gilbert C. Causes of severe visualimpairment and blindness in children in schoolsfor the blind in Ethiopia. Br J Ophthalmol2003;87:526–30.

2 Wheatley CM, Dickinson JL, Mackey DA, et al.Retinopathy of prematurity: recent advances inour understanding. Arch Dis Child Fetal NeonatalEd 2002;87:F78–82.

3 Gilbert C, Rahi J, Eckstein M, et al. Retinopathy ofprematurity in middle-income countries. Lancet1997;350:12–14.

4 Schaffer DB, Palmer EA, Plotsky DF, et al.Prognostic factors in the natural course ofretinopathy of prematurity. Ophthalmology1993;100:230–7.

5 Saunders RA, Donahue ML, Christmann LM, et al.Racial variation in retinopathy of prematurity.Arch Ophthalmol 1997;115:604–8.

6 Jacobson L, Fernell E, Broberger U, et al. Childrenwith blindness due to retinopathy of prematurity:a population-based study. Perinatal data,neurological and ophthalmological outcome. DevMed Child Neurol 1998;40:155–9.

7 Pennefather PM, Tin W. Ocular abnormalitiesassociated with cerebral palsy after preterm birth.Eye 2000;14:78–81.

8 Schwartz DS, Harrison SA, Ferrone PJ, et al.Telemedical evaluation and management ofretinopathy of prematurity using a fiberopticdigital fundus camera. Ophthalmology2000;107:25–8.

9 Lee SK, Normand C, McMillan D, et al. Evidencefor changing guidelines for routine screening forretinopathy of prematurity. Arch Pediatr AdolescMed 2001;155:387–95.

CORRECTIONS

An error occurred in the author listings fortwo letters in the September issue. In theletter by Lee et al (Br J Ophthalmol2003;87:1184–5) the order should be D KLee, E B Suhler, W Augustin, R R Buggage.

In the letter by Buggage et al (Br JOphthalmol 2003:87:1190–1) the order shouldbe R R Buggage, D G Callanan, D F Shen, C-CChen. The journal apologises for the error.

In the article by Williamson et al in theSeptember issue (Br J Ophthalmol2003;87:1126–9), the author list containedan error. The correct spelling is N Strouthidis.The journal apologises for the error.

In the article by Courtright et al in theSeptember issue (Br J Ophthalmol2003;87:1079–82), the author list containedan error. The correct spelling is AHoechsmann. The journal apologises for theerror.

Accepted of publication 5 May 2003

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NOTICES

Elimination of avoidable blindnessThe latest issue of Community Eye Health (No46) discusses the resolution of the WorldHealth assembly on the elimination of avoid-able blindness. For further informationplease contact: Journal of Community EyeHealth, International Resource Centre,International Centre for Eye Health,Department of Infectious and TropicalDiseases, London School of Hygiene andTropical Medicine, Keppel Street, LondonWC1E 7HT, UK (tel: +44 (0)20 7612 7964;email: [email protected]; website:www.jceh.co.uk). Annual subscription (4issues) UK £28/US$45. Free to developingcountry applicants.

Second sightSecond Sight, a UK based charity whose aimsare to eliminate the backlog of cataract blindin India by the year 2020 and to establishstrong links between Indian and Britishophthalmologists, is regularly sending volun-teer surgeons to India. Details can be foundat the charity’s website (www.secondsight.org.uk) or by contacting Dr Lucy Mathen([email protected]).

SPecific Eye ConditionS (SPECS)SPecific Eye ConditionS (SPECS) is a not forprofit organisation which acts as an umbrellaorganisation for support groups of any con-ditions or syndrome with an integral eyedisorder. SPECS represents over 50 differentorganisations related to eye disorders rangingfrom conditions that are relatively commonto very rare syndromes. The website acts as aportal giving direct access to support groups’own websites. The SPECS web page is avaluable resource for professionals and mayalso be of interest to people with a visualimpairment or who are blind. For furtherdetails about SPECS, contact: Kay Parkinson,SPECS Development Officer (tel: +44 (0)1803524238; email: [email protected];website: www.eyeconditions.org.uk).

The British Retinitis PigmentosaSocietyThe British Retinitis Pigmentosa Society(BRPS) was formed in 1975 to bring togetherpeople with retinitis pigmentosa and theirfamilies. The principle aims of BRPS are toraise funds to support the programme ofmedical research into an eventual cure forthis hereditary disease, and through theBRPS welfare service, help members andtheir families cope with the everyday con-cerns caused by retinitis pigmentosa. Part ofthe welfare service is the telephone help line(+44 (0)1280 860 363) for any queriesrelating to retinitis pigmentosa, especiallyfor those recently diagnosed with retinitispigmentosa (tel: +44 (0)1280 821 334; email:[email protected]; website: www.brps.demon.co.uk).

Surgical Eye ExpeditionsInternationalVolunteer ophthalmologists in active surgicalpractice are needed to participate in shortterm, sight restoring eye surgery clinicsaround the world. Contact: Harry S Brown,Surgical Eye Expeditions International, 27East De La Guerra, C-2, Santa Barbara, CA

93101-9858, USA (tel: +805 963 3303; fax:+805 965 3564; email: [email protected] [email protected]; website: www.seeintl.org).

Rise in organ transplant numbersAccording to UK Transplant, the UK has seenthe highest number of organ transplants insix years. Last year (1 April 2002 to 31 March2003), 2777 patients had their lives saved ordramatically improved through the generos-ity of 1064 donors. This equated to a 6%increase compared to the previous 12 months(1 April 2001 to 31 March 2002). Further-more, during 2002–3, the highest number ofpeople benefited from a cornea transplant forfive years (1997-98) and 240 more people hadtheir sight restored than the previous year.For further information see UK Transplant’swebsite (www.uktransplant.org.uk).

Elimination of avoidable blindnessThe 56th World Health Assembly (WHA)considered the report on the elimination ofavoidable blindness (doc A56/26) and urgedMember States to: (1) Commit themselves tosupporting the Global Initiative for theElimination of Avoidable Blindness by settingup a national Vision 2020 plan by 2005; (2)Establish a national coordinating committeefor Vision 2020, or a national blindnessprevention committee to help implementthe plan; (3) Implement the plan by 2007;(4) Include effective monitoring and evalua-tion of the plan with the aim of showing areduction in the magnitude of avoidableblindness by 2010; (5) To support themobilisation of resources for eliminatingavoidable blindness. The WHA also urgedthe Director-General to maintain andstrengthen WHO’s collaboration withMember States and the partners of theGlobal Initiative for the Elimination ofAvoidable Blindness as well as aid in thecoordination and support of national cap-ability.

Glaucoma Society 24th AnnualMeeting and DinnerThe Glaucoma Society 24th Annual Meetingand Dinner will take place on 20 November2003, from 8:30 am to 5:00 pm at The RoyalCollege of Physicians, London, UK. Furtherdetails: Ms Janet Flowers (email: [email protected]).

Detachment course withinternational faculty on: retinal andvitreous surgery with casepresentations preceding the annualmeeting of Iranian Society ofOphthalmologyThe detachment course with internationalfaculty on: Retinal and Vitreous Surgery withCase Presentations preceding the AnnualMeeting of Iranian Society ofOphthalmology will be held on 29-30November 2003 and 1-4 December 2003respectively, at the Razi Conference Center,Hemmat Hyw, Tehran, Iran. Further details:Scientific programme: Prof Ingrid Kreissig,University of Tuebingen, Schleichstr. 12,Breuningerbau, 72076 Tuebingen, Germany(tel: +49 7071 295209; email:[email protected]). Local orga-nisation: Dr Arman Masheyekhi, Dr SiamakMoradian, Dept of Ophthalmology,Labbanfinejad Medical Center, Pasdaran

Ave, Boostan 9, Tehran, 16666, Iran (fax:+98 21 254 9039; email: [email protected]).

5th International Symposium onOcular Pharmacology andTherapeutics (ISOPT)The 5th International Symposium on OcularPharmacology and Therapeutics (ISOPT) willtake place 11-14 March 2004, in Monte Carlo,Monaco. Please visit our website for details ofthe scientific programme, registration, andaccommodation. To receive a copy of the Callfor Abstracts and registration brochure,please submit your full mailing detailsto http://www.kenes.com/isopt/interest.htm.Further details: ISOPT Secretariat (website:www.kenes.com/isopt).

XVth Meeting of the InternationalNeuro-Ophthalmology SocietyThe XVth Meeting of the InternationalNeuro-Ophthalmology Society will take place18-22 July 2004, in Geneva, Switzerland.Further details: Prof. A Safran, UniversityHospital Geneva, c/o SYMPORG SA, Geneva(fax: +4122 839 8484; email: [email protected]; website: www.symporg.ch).

4th International Congress onAutoimmunityThe 4th International Congress onAutoimmunity will take place 3–7November 2004 in Budapest, Hungary. Thedeadline for the receipt of abstracts is 20 June2004. Further details: Kenes InternationalGlobal Congress Organisers and AssociationManagement Services, 17 Rue du Cendrier,PO Box 1726, CH-1211 Geneva 1, Switzerland(tel: +41 22 908 0488; fax: +41 22 732 2850;email: [email protected]; website: www.kenes.com/autoim2004).

Wake up call as dream timedeadline loomsScientists have less than a month left to applyfor a new Dream Time award from NESTA,the organisation that invests in UK creativityand innovation. Dream Time supports excep-tional achievers (with at least 10 yearsexperience in their field) who want time toexperiment or follow a passion, but whointend to continue with their career and putwhat they have discovered to good use. Up to12 exceptional individuals from the fields ofscience, technology and the arts will eachreceive up to £40,000 to pursue their goalsand push at the boundaries of knowledge andpractice. NESTA is looking for people whocan demonstrate evidence of exceptionalachievement. This would include a significantbody of work collated over at least a decade intheir field, the ability to work in new waysand a commitment to the proposed area ofexploration. Dream Time is a development ofNESTA’s existing Fellowship Programme,which has helped talented and creativeindividuals to innovate and explore newideas emerging through periods of personaldevelopment. As with all its awards, NESTAis looking for people who demonstrateexcellence, promise, creativity, innovationand commitment. Funding can be used on afull- or part-time basis, in tandem withprofessional careers or temporarily away fromthe constraints of employment. Offeredawards can be for any period of time up to

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one year. Dream Time Fellows will be askedto provide 10% in kind support for their planand will be required to plan ways ofdisseminating their findings with their pro-fessional community. To apply, visit NESTA’swebsite: www.nesta.org.uk/dreamtime.

14th Meeting of the EASD EyeComplication study groupThe 14th Meeting of the EASD EyeComplication (EASDEC) study group willtake place on the 21–23 May 2004. There willbe key lecture notes on the following topics:

Peter Gaede (Denmark)–Results of the Steno2 study, Hans Peter Hammes (Germany)–Animal models of diabetic retinopathy,Massimo Porta (Italy)–Screening with theLondon protocols: 12 years after, and AnselmKampik (Germany)–Surgical options in dia-betic retinopathy. There will also be casepresentations and oral and poster presenta-tions. The EASDEC board comprises FBandello (President), PJ Guillausseau (VicePresident), C-D Agardh (Past President), PMassin (Secretary), M Porta (Treasurer). TheScientific and Organizing Committeeincludes: F Bandello, PJ Guillausseau, P

Massin, C-D Agardh, M Porta, A Kampik, MUlbig, and G Lang. There are three travelgrants available, at 1000 Euro each, for youngscientists (less than 35 years at the time ofthe meeting). Application for the grantshould be made together with the submissionof the abstract. For further information,contact: Department of Ophthalmology,Ingrid Mannl, Ludwig-Maximilians-University, Mathildenstr. 8, 80336 Munich,Germany (tel: +49–89–5160–3800; fax: +4989 5160 4778; e-mail: [email protected]. The deadline for abstractsis 2 March 2004.


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br j ophthalmol 87 postscript · 1 buratto l, ed. phacoemulsification: principles and technique....

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