Inadvertent sclerostomy with encysted bleb following trans-scleral contact diode laser...

Clinical and Experimental Ophthalmology

2006;

34

: 81–92doi:10.1111/j.1442-9071.2006.1152.x

© 2006 Royal Australian and New Zealand College of Ophthalmologists

Letters to the Editor

Clinical Case Notes

refractory to therapy. Past medical history was notable for majordepressive disorder with suicidal and homicidal ideation. Examina-tion showed an uncorrected visual acuity of 6/45 in the right eyeand 6/12 in the left, diffuse conjunctival hyperaemia and4 mm

×

3 mm central corneal epithelial defects with surroundingring-shaped opacifications in both eyes. Despite these findings, thepatient denied pain. Topical antibiotic therapy was instituted andbandage contact lenses were placed. Cultures of corneal scrapingswere negative. One week after presentation, she returned complain-ing of intense ocular pain. Examination showed an uncorrectedvisual acuity of hand motions in the right eye and 6/15 in the left,severe contact dermatitis of the lids, 6 mm

×

6 mm central epithe-lial defects, dense ring-shaped stromal infiltrates and hypopyon inboth eyes. Once left alone in the examination room, she abruptlyleft the emergency room unannounced. She returned the next daybecause of unremitting pain and admitted to using topical propa-racaine in both eyes since the onset of her symptoms 1 monthearlier. She stated that a physician had initially given her the eyedrops and that frequent use every 30 min was no longer providingrelief. She was admitted for close observation. Repeat cultures ofcorneal scrapings were negative. On day 2 of admission, a bottleof proparacaine was noted to be missing from the room in whichthe patient had been examined. Upon repeated questioning bynursing staff, the patient surrendered the bottle that she had hiddenin her underwear. Psychiatric consultation revealed findings consis-tent with substance dependence and factitious disorder, but thepatient refused any psychiatric intervention beyond the initial con-sultation. By day 5 of admission, the patient’s pain, hypopyon andcorneal epithelial defects had resolved. Ring-shaped stromal infil-trates remained and uncorrected visual acuity was hand motions inthe right eye and 6/12 in the left (Fig. 1). The patient followed up1 week after discharge at which time her visual acuity and exami-nation were stable. She has not returned for follow up despiteattempts to contact her.

Case 2

A 21-year-old woman presented complaining of foreign-bodysensation in the right eye for 4 days. She was evaluated at anoutside emergency department at the onset of her symptoms andwas prescribed gentamicin drops. The emergency departmentphysician later informed us that anaesthetic drops were foundmissing after the patient’s visit. Her medical history was notablefor major depressive disorder with suicidal ideation. Examinationof the right eye showed an uncorrected visual acuity of 6/36, dif-fuse conjunctival hyperaemia and a 7 mm

×

6 mm corneal epithe-lial defect with an underlying ring-shaped stromal infiltrate.Examination of the left eye was within normal limits. Two weeksof fortified antibiotic therapy resulted in no improvement. Cul-tures of corneal scrapings yielded no causative organisms. Thediagnosis of anaesthetic abuse keratopathy was considered and

Anaesthetic abuse keratopathy as a manifestation of ocular Munchausen’s syndrome

A

BSTRACT

Two patients, both with a history of major depressive disorder,presented with large bilateral corneal epithelial defects and ring-shaped stromal opacities. Both were initially treated unsuccessfullywith topical antibiotic therapy for presumed infectious keratitis. Onepatient eventually admitted to topical anaesthetic abuse. In the sec-ond patient, signs of topical anaesthetic abuse and Munchausen’ssyndrome became evident. Cessation of anaesthetic use resulted inrapid resolution of the corneal epithelial defects in both patients.Anaesthetic abuse keratopathy is often a manifestation of underlyingpsychiatric illness, and psychiatric intervention is a very importantpart of management. To the authors’ knowledge, this is the firstreport of ocular Munchausen’s syndrome manifesting as anaestheticabuse keratopathy.

Key words:

anaesthetic abuse keratopathy

,

factitious disorder

,

major depressive disorder

,

Munchausen’s syndrome

,

proparacaine

.

I

NTRODUCTION

Factitious disorders represent the conscious production of signs orsymptoms of illness to achieve the sick patient role. Munchausen’ssyndrome is a severe form of factitious disorder characterized by atriad of self-inflicted illness, pathological lying and wandering fromplace to place. The ophthalmological literature contains assortedcase reports and series describing factitious disorders leading toocular sequelae.

1

One self-inflicted injury is corneal opacificationfrom repeated application of topical anaesthetics. Topical anaes-thetic abuse is easily overlooked by ophthalmologists because theclinical features mimic commonly seen conditions such as cornealabrasions and ulcers. Nevertheless, it is important to identify andtreat patients who abuse topical anaesthetics before permanentvision loss ensues. Here, we present two cases of anaesthetic abusekeratopathy and associated manifestations of psychiatric illnesses.To our knowledge, the second case represents the first report ofocular Munchausen’s syndrome manifesting as anaesthetic abusekeratopathy.

C

ASE

REPORTS

Case 1

A 19-year-old woman was referred by an outside ophthalmologistfor a 3-week history of bilateral corneal abrasions that had been

82 Letters to the Editor


she was admitted for observation. During her hospital course,an unlabelled bottle identical to that containing proparacainewas discovered in her room and was confiscated. The patientimproved and was discharged. However, she returned 1 weeklater with a new corneal epithelial defect and ring-shaped stromalopacification in the previously unaffected left eye (Fig. 2). Uncor-rected visual acuity was hand motions bilaterally. Repeat culturesof corneal scrapings were negative. Bilateral temporary tarsor-rhaphies were performed, but were rubbed open by the patient.Soon after discharge, the patient presented to a third emergencydepartment out of state for evaluation of ‘sudden painful visionloss’. One month later, the patient was emergency petitioned forpsychiatric management of self-injurious behaviour. On evalua-tion, the patient endorsed a number of symptoms of depressionincluding low mood, poor energy, disturbed sleep and diminishedvital sense. She was admitted to the psychiatric service for majordepressive disorder and factitious disorder and started on oralantidepressant medication. At no point did she acknowledgeabuse of proparacaine. At last ophthalmological follow up,5 months after presentation, examination revealed an uncorrectedvisual acuity of hand motions bilaterally with bilateral stromalring-shaped opacifications, peripheral pannus and resolved epi-thelial defects.

D

ISCUSSION

This series presents two cases of bilateral anaesthetic abuse kerat-opathy with significant visual morbidity. In the second case, thethree classic features of Munchausen’s syndrome (self-inflicted ill-ness, pathological lying and wandering from place to place) arepresent. Anaesthetic abuse keratopathy has been well characterizedin the ophthalmic literature and should be included in the differ-ential diagnosis of ring-shaped stromal infiltrates and non-healingepithelial defects.

2,3

In addition to the salient features ofMunchausen’s syndrome, risk factors for anaesthetic abuse mayinclude recent corneal trauma, surgery or infection, access to top-ical anaesthetic and symptoms and signs that do not correlate withclinical history. Ophthalmologists should educate patients, primaryand emergency caregivers and pharmacists about the potential forpermanent visual loss in cases of anaesthetic abuse as the cornealtoxicity of topical anaesthetics has been well described.

4,5

In man-aging anaesthetic abuse keratopathy, one should repeat cornealcultures at appropriate intervals to evaluate for superinfection.Finally, in the setting of confirmed anaesthetic abuse, ophthalmol-ogists should consider obtaining early psychiatric consultation toassist in the management of this potentially devastating syndrome.

Figure 1.

Case 1. Dense ring-shaped stromal infiltrates werepresent in the right (a) and left (b) eyes 2 weeks after cessation oftopical anaesthetic use.

a

b

Figure 2.

Case 2. A dense stromal infiltrate was present in theright eye 1 month after presentation (a). By that time, a dense ring-shaped stromal infiltrate and prominent epithelial defects haddeveloped in the left eye (b).

a

b

Letters to the Editor 83


Husam Ansari

MD,*

Daniel C

Garibaldi MD*

and

Albert S

Jun MD

The Wilmer Eye Institute, Johns Hopkins University School of Medicine,Baltimore, Maryland, USA

Received 27 Feb 2005; accepted 23 June 2005.

R

EFERENCES

1. Rosenberg PN, Krohel GB, Webb RM

et al.

Ocular Mun-chausen’s syndrome.

Ophthalmology

1986;

93

: 1120–3.2. Rocha G, Brunette I, Le Francois M. Severe toxic keratopathy

secondary to topical anesthetic abuse.

Can J Ophthalmol

1995;

30

: 198–202.3. Varga JH, Rubinfeld RS, Wolf TC

et al.

Topical anesthetic abusering keratitis: report of four cases.

Cornea

1997;

16

: 424–9.4. Judge AJ, Najafi K, Lee DA

et al.

Corneal endothelial toxicityof topical anesthesia.

Ophthalmology

1997;

104

: 1373–9.5. Moreira LB, Kasetsuwan N, Sanchez D

et al.

Toxicity of topicalanesthetic agents to human keratocytes

in vivo

.

J Cataract RefractSurg

1999;

25

: 975–80.

*

These authors contributed equally to this work.

OphthalmologistsDecember 20053368384Letter to the Editor Letter to the EditorLetter to the Editor

Letters to the Editor

Clinical Case Notes

Congenital rubella cataract: a timely reminder in the new millennium?

A

BSTRACT

Maternal infection with rubella in the first trimester is an importantcause of congenital cataract. Any injury affecting the foetus followingmaternal rubella infection in the phase of organogenesis results incongenital defects collectively termed as congenital rubella syndrome(CRS). Although rubella embryopathy is a less common cause forcongenital cataract than in the past, it is still seen. The number ofcases reduced to one in 1997 after which there were no new casestill 2002. However, there have been two new cases of CRS in 2003.Herein another one in early 2004 is reported. Outbreaks of CRSwill continue until the percentage of susceptible individuals is reducedto a minimum through immunization. The majority of rubella casesin Australia are confined to young female immigrants, many comingfor marriage. We must continue to immunize children, identify andimmunize vaccine failures and susceptible women before theybecome pregnant, and to screen pregnant women so they can bevaccinated after delivery.

Key words:

Australia

,

cataract

,

congenital rubella syndrome

.

I

NTRODUCTION

Maternal infection with the rubella virus in the first trimester is animportant cause of congenital cataract. The infective virus may becultured from the lens for up to 3 years and accounts for the pro-gression of the opacity. The cataract is often bilateral and is of thelamellar, nuclear, membranous or mature type. Infection early inpregnancy is associated with a worse cataract. Other ocular features

include nystagmus, strabismus, microphthalmos, corneal opacities,retinopathy, glaucoma and a small pupil that is difficult to dilate.Foetal infection occurs transplacentally during maternal viraemia,but the mechanism of foetal damage is poorly understood. Thefoetal defects observed in congenital rubella syndrome (CRS) arelikely secondary to vasculitis resulting in tissue necrosis withoutinflammation. Another mechanism is direct viral damage of infectedcells. These are the result of chromosomal breakage or productionof mitosis inhibiting proteins.

1

Any injury affecting the foetus fol-lowing maternal rubella infection in the first trimester or the phaseof organogenesis results in congenital defects collectively termedas CRS. The classical triad consists of sensorineural hearing loss,ocular abnormalities and congenital heart disease.

1

C

ASE

REPORT

An Indonesian premature neonate born in Australia at 36 weeks ofgestation presented to us in early 2004 with bilateral progressivecongenital lamellar dense cataracts at the age of 2 days. The babywas small for dates with a birthweight of 2025 g and a ‘failure tothrive’ in the nursery. He was born of parents with a consanguinousmarriage. The two older siblings had no ocular or systemic prob-lems. Examination revealed bilateral microphthalmos with micro-cornea (8 mm horizontal diameter) (Fig. 1). There was bilateralhearing impairment – auditory evoked potential testing (90% deaf-ness right, 70% deafness left).

The mother gave a history of a febrile rash early in the firsttrimester while visiting family in Indonesia. At that point she didnot know she had conceived. She had been vaccinated againstrubella as a schoolgirl and had been living in Australia for 6 years.The mother’s serum polymerase chain reaction carried out after thebaby’s birth had tested positive for rubella. This fact, coupled withthe size of the baby and ophthalmic findings, made suspicions pointto a CRS with rubella cataract. Bilateral lens extraction with ante-rior vitrectomy was carried out at 4 weeks of age. Rubella virus wasgrown from lens culture and polymerase chain reaction wasstrongly positive for rubella. Salt and pepper retinopathy was seenpostoperatively once the medium was clear. He was prescribedaphakic paediatric contact lenses. When last seen at 6 months of

Figure 1.

Dense rubella cataract with microphthalmos in the casereported.



age the examination revealed wandering nystagmus with poor fix-ation. The eyes appeared quiet. Rehabilitation with intraocularlenses is planned in the near future.

D

ISCUSSION

This is the third case of CRS in Australia in the last 2 years, whichnow has a low index of suspicion in Australia.

2

Paediatric cataract is a major cause of childhood blindness allover the world with an estimated incidence of 2.2 per 10 000 birthsin Australia. In 1941, a Sydney ophthalmologist, Norman McAlisterGregg, correctly identified the link between congenital cataracts ininfants and maternal rubella early in pregnancy. Although rubellaembryopathy is a less common cause for congenital cataract thanin the past, it is still seen.

3

So great is the menace of CRS in the developing world thatstudies in India identify the incidence of childhood cataract due torubella to be 4.6–25% of all paediatric cataracts. A cataract in achild less than 1 year of age, with a nuclear morphology, has a 75%positive predictive value for CRS.

4

Any sick infant with congenitalcataract should be investigated for CRS.

After the introduction of rubella vaccination in 1970, there wasa rapid fall in the incidence of congenital infection. Between 1993and 1997 there were 20 cases of CRS, with the number graduallydiminishing to just one case in 1997. There were no cases of CRSafter 1997 till 2002. This was probably a result of vaccination.Although it is also a possibility that there could have been under-reporting of CRS and it was also probably a matter of chance thatno previously immunized woman in Australia contracted wild virusas did the mother of the reported infant. It seemed that locallyacquired infection causing CRS was a thing of the past in Australiauntil two infants were born with congenital rubella defects inQueensland in 2003, following an upsurge in rubella infection in2001–2002,

2

In Australia infant vaccination with measles, mumps, rubella(MMR) was introduced in 1989 to interrupt circulation of the virusin young children, and in 1994–95 the adolescent school-basedrubella vaccination programme was changed to MMR for both boysand girls. A peak incidence rate in young male adults in 1995reflected the lack of immunization in this cohort. The impact ofchanging the second dose of MMR vaccine to 4 years of age in1998 will require careful monitoring.

5

In most instances, the individuals involved in these outbreakshave no history of rubella immunization. In addition, most of theoutbreaks have been reported among persons who emigrated fromcountries where rubella is not included in the routine immunizationschedule or after previously vaccinated mothers were exposed towild virus during pregnancy. The number of reported cases is highin countries where routine rubella immunization either is not avail-able or was recently introduced. Although the burden of CRS isnot well characterized in all countries, more than 100 000 cases areestimated to occur each year in developing countries alone.

1

Care is to be taken to limit prevention of outbreaks from personsinfected with rubella. All persons who have contact with patientsinfected with rubella or children with CRS (e.g. caregivers, house-hold contacts, medical personnel, laboratory workers) should beimmune to rubella to prevent rubella outbreaks. Isolation of allpatients is imperative. Droplet precautions and standard precau-tions are recommended for 7 days after the onset of rash in patientswith postnatally acquired rubella infections. Contact isolation is

indicated for all children with proven or suspected congenitalrubella infection until they are aged at least 1 year unless nasopha-ryngeal swab and urine cultures after age 3 months are repeatedlynegative for rubella virus. Some authorities suggest that an infantshould be considered infectious until two cultures of clinical spec-imens obtained 1 month apart are negative for rubella virus. Rubellavaccine is the most effective preventive strategy for rubella infec-tion. MMR vaccine is especially recommended for all adults at riskof rubella infection (e.g. college students, military recruits andhealthcare personnel). Last but most importantly, all post-pubertalwomen without documentation of immunity should be vaccinatedunless they are known to be pregnant because vaccine viruses cancross the placenta barrier. Every prospective mother consideringpregnancy needs to be aware of the need to check their immunitywell before they become pregnant and should have a rubella titredone. History of vaccination is not enough. Women receiving thevaccine should be counselled not to become pregnant within3 months of vaccine administration. As vaccination is not 100%effective in inducing lifelong immunity to rubella, ascertainingrubella immunity is a routine part of antenatal screening regardlessof previous vaccination status.

1,2,5

Outbreaks of rubella and CRS will continue until the percentageof susceptible individuals is reduced to a minimum through immu-nization. The majority of rubella cases in Australia are confinedto young female immigrants. The Department of Health has aresponsibility to these new immigrants and the next generation ofAustralians. The birth of a baby with congenital rubella is both apersonal and a community tragedy. We must continue to immunizechildren, to identify and immunize vaccine failures and other sus-ceptible women before they become pregnant, and to screen preg-nant women so they can be vaccinated after delivery. Effectivesurveillance of rubella and CRS is also needed. Continued vigilancewill be the price of freedom from congenital rubella.

Sapna Sharan

DNB (Ophth)

,

1

Shanel Sharma

MB BS

2

andFrank A Billson

FRANZCO

1

1

Save Sight Institute, University of Sydney, Department ofOphthalmology, Sydney Eye Hospital, and

2

Department ofOphthalmology, Prince of Wales Hospital, Sydney,

New South Wales, Australia

Received 23 January 2005; accepted 6 April 2005.

R

EFERENCES

1. American Academy of Paediatrics.

2000 Red Book. Report of theCommittee on Infectious Diseases

, 25th edn. Elk Grove Villiage:American Academy of Paediatrics, 2000.

2. Forrest JM, Burgess M, Donovan T. A resurgence of congenitalrubella in Australia?

Commun Dis Intell

2003;

27

: 533–5.3. Wirth MG, Russell-Eggitt IM, Craig JE, Elder JE, Mackey DA.

Aetiology of congenital and paediatric cataract in an Australianpopulation.

Br J Ophthalmol

2002;

86

: 782–6.4. Eckstein M, Vijayalakshmi P, Killedar M, Gilbert C, Foster A.

Aetiology of childhood cataract in south India.

Br J Ophthalmol

1996;

80

: 628–32.5. Sullivan EM, Burgess MA, Forrest JM. The epidemiology of

rubella and congenital rubella in Australia, 1992–1997.

CommunDis Intell

1999;

23

: 209–14.



Ocular coherence tomography findings with retained submacular perfluoron

A

BSTRACT

Herein a case of retained perfluorocarbon liquid beneath the macula,following surgical repair of a complicated retinal detachment, isreported. The ocular coherence tomography findings were helpfulin distinguishing retained perfluorocarbon liquid from residual sub-retinal fluid, macular cyst or cystoid macular oedema.

Key words:

ocular coherence tomography

,

perfluoron

,

subretinal

.

I

NTRODUCTION

Retained subretinal perfluorocarbon liquid (PFO) has beenreported, but generally does not cause problems for the patientunless it localizes beneath the macula. If the retained bubbles arevisually symptomatic, they can be removed via a subretinalcannula.

Herein we report a case of retained PFO beneath the macula,following surgical repair of a complicated retinal detachment.

C

ASE

REPORT

A 63-year-old man presented with a combined schisis-rhegmatog-enous retinal detachment. He underwent three vitreoretinal surgi-cal procedures in an attempt to reattach his retina. The surgicalinterventions included a large inferior relaxing retinectomyto remove unresectable proliferative vitreoretinopathy (PVR),removal of subretinal membranes, PFO (Perfluoron – Alcon, FortWorth, TX, USA) to flatten the retina, extensive endolaser photo-coagulation and silicone oil injection. Following surgery, his retinawas attached with finger counting vision but he noted significantdistortion of his central vision. On examination, he had four small‘bubbles’ beneath his macula (Fig. 1). The macula was draggedinferiorly due to the inferior PVR changes. Ocular coherencetomography (OCT) testing (Stratus OCT – Carl Zeiss Meditec,Dublin, CA, USA) revealed three cystic spaces in the central mac-ula in the subretinal space (Fig. 2). There was no thickening orfibrosis of the surrounding retina and the overlying retina wascompressed between the PFO and overlying silicone oil. An addi-tional surgical procedure was performed, removing the subretinalPFO with a Lewis subretinal 33-gauge cannula (Synergetics, Inc,St. Charles, MO, USA), while leaving the silicone oil in place.

Although the PFO was removed and the macula flattened, therewas no improvement in visual acuity. The retina remained attached.However, there was slightly less distortion in the patient’s vision.The patient declined any further testing or intervention.

D

ISCUSSION

Retained subretinal PFO has been reported, but generally does notcause problems for the patient unless it localizes beneath the mac-ula.

1,2

If the retained bubbles are visually symptomatic, they can beremoved via a subretinal cannula. Often these eyes have limitedvision potential due to the complexity of their underlying disease,

in which case the bubbles can be left in place. The OCT can beused to differentiate between retained subretinal PFO at the maculaand residual subretinal fluid. The former produces distinctive bub-bles beneath the retina whereas residual subretinal fluid produces adome-shaped elevation of the retina.

To become trapped beneath the retina, the PFO must gainaccess to the subretinal space, usually through a retinal break or anedge of a relaxing retinotomy. This can occur during fluid–airexchange and can be avoided by careful aspiration of PFO at theretinotomy edge or at the retinal break as the air level descendsbelow this point. Membrane peeling under PFO is another wayPFO can gain access to the subretinal space. During peeling, trac-tion is applied to the retina, creating a suction force, drawing PFOinto the subretinal space, through either a retinal break or theedge of a retinotomy. Often during such complicated vitrectomysurgery, the view is suboptimal and small amounts of trapped sub-retinal PFO can be easily missed. Although rinsing the vitreouscavity with balanced salt solution is useful in removing residualPFO in the vitreous cavity, this technique will not remove subreti-nal PFO.

Figure 1.

Colour fundus photograph of the left eye showing fourperfluorocarbon liquid bubbles beneath the macula, which has beendragged inferiorly due to proliferative vitreoretinopathy.

Figure 2.

Ocular coherence tomography scan of the left maculashowing three subretinal cystic spaces with no fibrosis or scarringof the underlying retinal pigment epithelium or overlying retina.



A small-gauge subretinal cannula is the optimal method ofremoving subretinal PFO. The only alternatives would be creationof a larger retinotomy or redetachment of the retina. One advan-tage of a small-gauge cannula is that the procedure can be per-formed without removing the silicone oil, reducing the risk ofredetachment. However, of greater importance is the decision ofwhether or not to even attempt removal, based on the long-termvisual prognosis. Eyes with complicated macula-off retinal detach-ments may not have the visual potential to warrant such interven-tion, as evidenced by the results of this case. This patient had onlyminimal improvement in his symptoms following PFO removal,indicating that his symptoms were primarily due to his macula-offdetachment, subsequent PVR, retinal rotation and traction.

Brian C Joondeph

MD FACS

and

Hoang Nguyen

BS CRA

Retinal Alliance, Denver, Colorado, USA

Received 14 February 2005; accepted 1 June 2005.

R

EFERENCES

1. Saatci AO, Kocak N. Retained submacular perfluorodecalin.

Can J Ophthalmol

2003;

38

: 293–6.2. Ciardella PA, Langton K, Chang S. Intra ocular dispersion of

perfluorocarbon liquids in silicone oil.

Am J Ophthalmol

2003;

136

: 365–7.

Inadvertent sclerostomy with encysted bleb following trans-scleral contact diode laser cyclophotocoagulation

A

BSTRACT

A 22-year-old woman underwent 360

°

trans-scleral contact diodelaser cyclophotocoagulation for refractory glaucoma. Conjunctivalburns and scleral thinning were noticed inferonasally at the last laserapplication. Intraocular pressure in the first week was normal. Sixmonths later the patient presented with encysted filtering bleb andhigh intraocular pressure. Ultrasound biomicroscopy revealed a fullthickness sclerostomy. This report suggests that inadvertent scleros-tomy may present with encysted bleb months after trans-scleralcontact diode laser cyclophotocoagulation.

Key words: encysted bleb, inadvertent sclerostomy, trans-

scleral contact diode laser cyclophotocoagulation.

INTRODUCTION

Trans-scleral diode laser cyclophotocoagulation has emerged as aneffective treatment for controlling intraocular pressure (IOP) andpain in refractory glaucoma. Contact method (trans-scleral contactdiode laser cyclophotocoagulation [TCDLC]) is more commonthan non-contact because of the ease of application, reducedenergy requirement and greater efficacy. One of the uncommoncomplications reported with TCDLC is the development of aninadvertent sclerostomy.1,2

We report a patient with uveitic glaucoma who, 6 months fol-lowing TCDLC, presented with a full thickness encysted filteringbleb associated with an inadvertent sclerostomy.

CASE REPORT

A 22-year-old woman presented with a history of recurrent attacksof pain and redness for the previous 2 years, associated with dimi-nution of vision in the left eye. The best-corrected visual acuity was6/6 in the right eye and counting finger close to face with accurateprojection in the left eye. There was a left divergent squint. Slit-lamp examination revealed diffuse corneal haze, old keratic precip-itates and iris bombe in the left eye. There were no anterior cham-ber cells or flare. A complicated cataract was present. No areas ofscleral thinning were seen. The posterior segment could not bevisualized. The right eye was normal. The IOP was 18 mmHg inthe right eye and 44 mmHg in the left. There was no history ofjoint pain or any other systemic disorder. Erythrocyte sedimenta-tion rate was normal, and rheumatoid factor and anti-nuclear anti-body test were negative. A diagnosis of quiescent uveitis withsecondary glaucoma was made.

Peripheral Nd:YAG iridotomy was performed to relieve the irisbombe. Postoperatively the patient received topical timolol maleate0.5% twice daily (BD), betamethasone 1% four times a day (QID)and systemic acetazolamide 250 mg BD to control the IOP andpostoperative inflammation. One week later the IOP was reducedto 32 mmHg. Considering the poor visual status and refractorynature of glaucoma, she was advised to have TCDLC for furthercontrol of IOP in the left eye. A 360° TCDLC (810 nm) wasperformed in her left eye under peribulbar block, using 1500mW,avoiding the 3 and 9 o’clock meridians (the power was kept justbelow the level at which a ‘popping’ sound was heard) for 2 s perspot (3 J energy) with a fibreoptic flat-tipped cyclophotocoagula-tion probe (Nidek DC 3000, Nidek, Tokyo, Japan). The probe wasplaced such that its anterior edge approximated the surgical limbus.Forty such spots were placed, at one spot width distance. Powersettings were kept constant throughout the procedure. At the lastlaser spot application inferonasally, a conjunctival burn occurred.Slit-lamp examination showed scleral thinning in the same area.Seidel’s test was negative.

The patient was prescribed topical betamethasone 1% eye dropQID, ciprofloxacin 0.3% eye drop QID, tropicamide 1% eye dropTDS and timolol maleate 0.5% BD. The next day the IOP was16 mmHg. At 1-week follow up, the conjunctival defect around thearea of scleral thinning had healed and Seidel’s test was negative.The patient was advised to return after 1 month but did not.

The patient presented again 6 months after TCDLC with aninferonasal swelling in the left eye. She had noticed the swelling3 months following the laser, but presented when she felt that theswelling had become cosmetically disfiguring. On examinationthere was an inferior scleral ectasia extending from 5 o’clock to 6o’clock with overlying cystic bleb in the left eye (Fig. 1). The IOPin the left eye was 28 mmHg without any antiglaucoma medication.The anterior chamber was shallow; her visual acuity was maintainedto finger counting close to face with accurate projection. Ultra-sound biomicroscopy (Paradigm Medical Industries, Salt Lake City,UT, USA) showed a full thickness defect 1.5–2 mm from the limbuswith direct communication between the posterior chamber and theconjunctival cyst (Fig. 2). The conjunctival bleb was excised andthe scleral defect was repaired with 8-0 monofilament nylon suture.



Following this the IOP was 20 mmHg with topical timolol maleate0.5% BD.

DISCUSSION

Anterior segment inflammation, pupillary distortion and conjuncti-val burns are a few of the well-documented complications ofTCDLC.1,2,3 We have previously reported inadvertent sclerostomyin two of 30 eyes after TCDLC in a prospective study.1 Both eyesshowed unrecordable low IOPs in the first week, but in due coursespontaneous healing of the sclera and the overlying conjunctivaleading to closure of the sclerostomy.

Sabri and Vernon reported scleral perforation followingTCDLC in an eye with pre-existing scleral thinning, whichrequired surgical closure of the defect.2 The present case had noevidence of scleral thinning before laser. The patient developed aconjunctival burn and scleral thinning during application of the lastlaser spot inferonasally. The IOP was normal in the immediate post-laser period, but the patient presented with increased IOP 6 monthslater. It is possible that a very small scleral defect occurred duringTCDLC that was not visible on slit-lamp and was initially missedas the IOP remained normal. This defect might have enlarged laterleading to a subconjunctival bleb, which in due course becameencysted leading to a further rise of IOP.

Inadvertent sclerostomy is more common with flat-tippedprobes compared with round-tipped probes used for TCDLC.3,4

Causes of inadvertent sclerostomy include heating and carboniza-tion of the tissue debris at the probe tip leading to extra energybeing transmitted to the sclera or mechanical pressure applied incontact method especially in eyes with a staphyloma or thinsclera.2,5 Noecker et al. noted cracks and disruption of the probetips on scanning electron microscopy after repeated use of thesame probe.6 We had used the same probe earlier in five cases andthere is the possibility that probe tip damage resulting in excessiveenergy delivery to the sclera may have resulted in the inadvertentsclerostomy. Inadvertent application of laser twice to the same sitemay also result in sclerostomy; however, this did not occur in ourcase.

The present case highlights that inadvertent sclerostomy fol-lowing TCDLC may have a delayed presentation.

Viney Gupta MD, Parul Sony MD andRamanjit Sihota MD FRCS

Rajendra Prasad Centre for Ophthalmic Sciences, All India Institute ofMedical Sciences, New Delhi, India

Received 9 February 2005; accepted 12 May 2005.

REFERENCES

1. Agarwal HC, Gupta V, Sihota R. Evaluation of contact versusnon contact diode laser cyclophotocoagulation for refractoryglaucoma using similar energy setting. Clin Experiment Ophthalmol2004; 32: 33–8.

2. Sabri K, Vernon SA. Scleral perforation following trans-scleralcyclodiode. Br J Ophthalmol 1999; 83: 501.

3. Bhola RM, Prasad S, McCormick AG, Rennie IG, Talbot JF,Parsons MA. Pupillary distortion and staphyloma followingtransscleral contact diode laser cyclophotocoagulation: aclinicopathologic study of three patients. Eye 2001; 15: 453–7.

4. Beadles KA, Smith MF. Inadvertent sclerostomy during trans-scleral Nd:YAG cyclophotocoagulation. Am J Ophthalmol 1994;118: 669–71.

5. Stolzenburg S, Kresse S, Muller-Stolzenberg NW. Thermalside reactions during in vitro contact cyclophotocoagulationwith continuous wave Nd:YAG laser. Ophthalmic Surg 1990; 21:356–9.

6. Noecker RJ, Kelly T, Patterson EL. Scanning electronmicroscopy of IRIS diode laser G-probes after repeat cyclo-photocoagulation treatments. Invest Ophthalmol Vis Sci 2000;41: S578.

Figure 1. Slit-lamp photograph showing the conjunctival cystinferonasally (arrowheads indicate the extent).

Figure 2. Ultrasound biomicroscopy showing the full thicknesssclerostomy (white arrow). B, encysted bleb, S, sclera.



Letter to the EditorClinical Case Notes

Traumatic optic nerve avulsion and central retinal artery occlusion following rugby injury

ABSTRACT

Optic nerve avulsion (ONA) secondary to finger gouging is a rarecomplication. A case is reported of a 14-year-old boy who had anacute loss of vision after being poked in his left eye during a gameof rugby union. He was later diagnosed with ONA, and this wasassociated with central retinal artery occlusion, which was rarelyreported in the literature. His progress was complicated by a delayedonset of neovascular glaucoma. This is the first report of ONAsecondary to a rugby injury and highlights the need for clinicians tobe aware of the potential for loss of sight from gouging.

Key words: athletic injuries, football, glaucoma, neovascular,

optic nerve injuries, retinal artery occlusions.

INTRODUCTION

Optic nerve avulsion (ONA) is defined as a rupture of the opticnerve at the disc margin but without damage to the optic sheathand is an uncommon form of traumatic optic neuropathy. ONA hasbeen infrequently reported since its first description by His in1856.1 The following case describes an adolescent patient with arare combination of ONA associated with central retinal arteryocclusion (CRAO) complicated by neovascular glaucoma (NVG).To our knowledge, ONA secondary to a rugby injury has not beenpreviously described. This case highlights the potential for severevision loss resulting from finger gouging.

CASE REPORT

A 14-year-old schoolboy presented with acute vision loss (Fig. 1)immediately following finger gouging of his left eye (LE) whileplaying rugby. Visual acuity (VA) was bare light perception LE.External eye examination 24 h later revealed periorbital bruisingand oedema with microscopic hyphaema. A relative afferent pupil-lary defect LE was noted. Intraocular pressure (IOP) was 16 mmHgLE. Dilated fundus examination LE revealed preretinal and subret-inal haemorrhage surrounding the optic disc, but no evidence ofretinal detachment. There was evidence of CRAO with sparing ofthe cilioretinal artery (Fig. 1). Fundus fluorescein angiography con-firmed CRAO (Fig. 2). Computed tomography revealed no fractureor abnormality of the optic nerve.

A diagnosis of ONA complicated by CRAO was made. Thepatient was treated with a 3-week course of tapering systemicsteroid. Subsequently, the preretinal and subretinal haemorrhagesettled. VA remained at bare light perception LE only. On followup at 12 months, the IOP had risen to 44 mmHg LE with evidenceof rubeosis of the iris and angle. Gonioscopy showed the angle LEto be open with new vessels observed throughout the whole anglebut no evidence of peripheral anterior synechiae formation. Thecup to disc ratio was 0.7 LE and 0.25 right. The IOP was controlledmedically with guttae timolol LE. The rubeosis resolved with pan-retinal photocoagulation within 2 weeks.

DISCUSSION

Several mechanisms had been postulated to explain ONA. Theyincluded direct trauma to the globe, sudden marked increase in IOPthat forces the nerve out of the scleral canal, shearing forces fromacute globe rotation and focal or diffuse vasospasm in the opticnerve. All resulted in tearing of the fibres at the level of the laminacribrosa.2 In this patient, an acute rotation of the globe was thelikely mechanism. The anatomy of the optic nerve head mayexplain why such a devastating injury can occur despite no associ-ated injury to the globe. Nerve fibres at the disc have minimalsupportive connective tissue as they traverse the brittle laminacribrosa. They are therefore susceptible to tears from shearing

Figure 1. Fundus photograph in the left eye showed preretinalhaemorrhage obscuring the optic disc and retinal oedema nasal tothe optic disc. Nasally, subretinal haemorrhage was present. Centralretinal artery occlusion with sparing of the cilioretinal artery isshown.

Figure 2. Fluorescein angiogram in the left eye showed centralretinal artery occlusion with capillary non-perfusion. There wasintact capillary perfusion in the distribution of the cilioretinal artery.Preretinal haemorrhage produced blocked hypofluorescence.



forces as the globe rotates suddenly due to forceful entry of thefingers into the orbit.

In our case, the ONA was associated with CRAO, which is rare.3

However, other previously described abnormalities of the retinalvasculature included tortuosity, attenuation, vessels ending abruptlyat the avulsion, arteriolar occlusion and segmentation of the bloodcolumn. There had been only a single report of ONA complicatedby NVG.4 In our case, the NVG was delayed and likely to beassociated with retinal hypoxia following CRAO.5

Optic nerve avulsion from finger gouging in sports has beeninfrequently reported in association with basketball,2 but not rugby.In rugby union, multiple players are involved and often entangledin a pile-up in an attempt to gain possession of the ball and thismay lead to missed observations of foul acts such as gouging fromreferees. Although reports of gouging are sparse in the literature,this case highlights the need for clinicians to be aware of thepotential for gouging to cause sight-threatening globe and opticnerve damage.

Colin CW Chong MB BS2,3 andAndrew A Chang PhD FRANZCO1,2,3

1Vitreoretinal Unit, Sydney Eye Hospital, 2Sydney Retina Clinic andDay Surgery, and 3Save Sight Institute, University of Sydney, Sydney,

New South Wales, AustraliaReceived 9 May 2005; accepted 4 July 2005.

REFERENCES

1. Buchwald HJ, Otte P, Lang GE. Evulsion of the opticnerve following blunt bulbar trauma. Case report andreview of the literature. Klin Monatsbl Augenheilkd 2003;220: 303–8.

2. Friedman SM. Optic nerve avulsion secondary to a basketballinjury. Ophthalmic Surg Lasers 1999; 30: 676–7.

3. Noro M, Ishikawa A, Nakanome Y et al. A case of evulsion ofthe optic nerve. Nippon Ganka Gakkai Zasshi 1990; 94: 1177–80.

4. Bouchet JP, Tapiero B, Riss I et al. Avulsion of the optic nerveand neovascular glaucoma. Bull Soc Ophtalmol Fr 1989; 89:1153–4.

5. Duker JS, Sivalingam A, Brown GC et al. A prospective studyof acute central retinal artery obstruction. The incidence ofsecondary ocular neovascularization. Arch Ophthalmol 1991;109: 339–42.

Negative electroretinograms in pericentral pigmentary retinal degeneration

ABSTRACT

The clinical presentation and electrophysiological findings aredescribed of three consecutive cases with pericentral pigmentaryretinal degeneration. The responses to bright flashes after dark adap-tation showed negative waveform shape in all cases. Rod responseswere strongly reduced compared with cone responses. Cone elec-troretinograms elicited by long-duration stimuli showed greater lossof the on-response than the off-response. The ratio of the on-

response amplitude to off-response amplitude of these patients(0.52 ± 0.12; mean ± SD, n = 6) was significantly smaller than thatof normal subject (0.83 ± 0.21; mean ± SD, n = 8) (Mann–WhitneyU-test, P < 0.01). The electrophysiological findings of these casessuggest a greater defect of inner retinal function, especially in trans-mission between photoreceptors and depolarizing bipolar cells.

Key words: negative electroretinograms, off-response, on-

response, pericentral pigmentary retinal degeneration.

INTRODUCTION

Multiple names (i.e. peripapillary, arcuate, annular, sectorial, seg-mental, etc.) have been used by investigators when referring topericentral pigmentary retinal degeneration. It is a rare conditionof the fundus characterized by areas of chorioretinal degenerationwith pigment migration and ring-shaped bony spicule formationaround the macula, leaving central vision unimpaired.1,2

Herein, we report the electrophysiological features of threeconsecutive cases with pericentral pigmentary retinal degeneration.

Figure 1. Case 1. Forty-eight-year-old Japanese woman withvisual acuity of 6/6 in both eyes complained of mild night blindness.(a) Fundus and (b) fluorescein angiographic examination showedcircinate chorioretinal atrophy surrounding the macula, large num-ber of bony spicule formation and bull’s eye macula appearance. (c)Goldmann perimetry demonstrated symmetric ring scotoma.

a

b

c



CASE REPORTS AND ELECTROPHYSIOLOGICAL TECHNIQUES

Case 1 and Case 2 were both 48-year-old Japanese women whoseconditions were diagnosed as retinitis pigmentosa at the age of 45and 41, respectively. Case 3 was a 67-year-old Japanese man whowas referred to our clinic with a 3-year history of night blindness.These cases were unrelated. Family history was unremarkable ineach case. None of the patients recalled taking medication knownto be retinotoxic. Their visual acuity was 6/7.5 or better. However,they all complained of mild night blindness. The diagnosis ofpericentral pigmentary retinal degeneration was based on typicalfundus and fluorescein angiographic findings. These showed sym-metrical retinal pigment epithelial atrophy with choriocapillar atro-phy around the optic nerve with bony spicule pigment formation(Figs 1–3).1,2 Goldmann perimetry also demonstrated symmetricarcuate or ring scotoma in all cases.

The method for recording full-field electroretinograms (ERGs)has been described in detail elsewhere.3 In brief, ERGs were

recorded using a contact lens electrode with built-in white light-emitting diodes (LEDs) (LW-l02, TOMEY, Nagoya, Japan). In thissystem, three high-brightness white LEDs are incorporated into acontact lens electrode (unipolar), and serve as the source for thestimulus and the background. After 30 min of dark adaptation, arod response was elicited by a flash of 0.0096 cd-s/m2 (80 cd/m2

× 0.12 ms). A mixed rod and cone response was elicited by a brightflash of 200 cd-s/m2 (20 000 cd/m2 × 10 ms), and this response wasrecorded after 30 min of dark adaptation. After 10 min of lightadaptation, a single flash cone response was elicited by a flash of 3cd-s/m2 (6000 cd/m2 × 0.5 ms) on a steady background illuminationof 25 cd/m2. A 30-Hz flicker response was elicited by a square waveof 50% duty cycle (600 cd/m2 and 25 cd/m2). Photopic on- and off-responses were elicited by a long-duration flash (100 ms) of 360 cd/m2 on a steady background illumination of 40 cd/m2. A singleresponse was used for a mixed rod and cone response, but 4–32responses were averaged for other responses to improve the signal/noise level.

Figure 2. Case 2. Forty-eight-year-old Japanese woman withvisual acuity of 6/7.5 in both eyes complained of mild night blind-ness. (a) Fundus and (b) fluorescein angiographic examinationshowed chorioretinal atrophy around the optic disc and radiatingfrom the optic disc, small number of bony spicule formation andfaint bull’s eye macula appearance. (c) Goldmann perimetry dem-onstrated symmetric ring scotoma.

a

b

c

Figure 3. Case 3. Sixty-seven-year-old Japanese man with visualacuity of 6/6 in both eyes complained of mild night blindness. (a)Fundus and (b) fluorescein angiographic examination showed sym-metrical chorioretinal atrophy around the optic disc and radiatingfrom the optic disc, bony spicule formation and faint bull’s eyemacula appearance. (c) Goldmann perimetry demonstrated sym-metric arcuate scotoma.

a

b

c



Statistical comparisons were made by Mann–Whitney U-test.P-values <0.05 were considered statistically significant.

RESULTS

The ERGs recorded from the three cases are shown in Fig. 4 andTable 1. The responses to bright flashes after dark adaptationshowed an expected loss of a-wave amplitude but an unexpectedlylarge reduction in the b-wave, leading to a negative waveform shapein all cases. Rod responses were strongly reduced compared withcone responses. Cone ERGs elicited by long-duration stimulishowed greater loss of the on-response than the off-response. Theratio of the on-response amplitude to off-response amplitude inCase 1 was 0.56 in the right eye and 0.72 in the left eye. It was0.38 and 0.45 in Case 2, 0.47 and 0.54 in Case 3, respectively. Themean of the ratios of three patients was 0.52 ± 0.12 (mean ± SD,n = 6). Six women and two men were tested as age-matched con-trols. Their ages ranged from 45 to 70 years, mean 56 ± 10. Theirmean age did not differ significantly from the patients. The resultsof the cases were smaller than that of the normal subjects(0.83 ± 0.21, n = 8) (P < 0.01).

DISCUSSION

We present here the electrophysiological findings in three cases ofpericentral pigmentary retinal degeneration. Sakanaka et al.4 alsoreported 20 cases of pericentral type posterior retinitis pigmentosa.From their fundus photographs, some of their cases seem to be thesame disease as our cases. They found that seven cases out of the20 patients (35%) showed negative waveform to a bright flash inthe dark-adapted state (negative ERG). This previous report sup-ports our findings. Negative ERGs have also been reported in casesof X-linked juvenile retinoschisis, congenital stationary night blind-ness, central retinal artery occlusion, birdshot chorioretinopathyand melanoma-associated retinopathy.5 Some cases of photorecep-tor dystrophy (rod-cone/cone-rod) were also found to have

Figure 4. The responses to bright flashes showed negativewaveform shape in all cases. Rod responses were strongly reducedcompared with cone responses. Cone responses elicited by long-duration stimuli showed greater loss of the on-response than theoff-response. (The horizontal calibration line designates 25 ms.The vertical line designates 100 µV for flash, rod, cone and flicker,and 25 µV for on- and off-responses.)

Control

Bright Flash RL

Scotopic

Photopic

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148

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6/6

86.0

72.0

0.84

13.5

11.4

25.0

45.0

0.56

20.5

52.0

123.

5L

6/6

88.3

55.5

0.63

14.2

5.4

22.5

31.3

0.72

25.5

51.0

124.

02

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7.5

197.

314

3.0

0.72

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480

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8.7

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negative ERGs.5 In 1989 we also reported several cases of bull’s eyemaculopathy and otherwise normal fundus with negative ERG.6

Cone dystrophy, congenital stationary night blindness, Batten’s dis-ease and retinitis pigmentosa were excluded. In 1993 Cideciyan andJacobson7 reported seven cases of typical retinitis pigmentosa withnegative ERG. They also found that their patients had a dispropor-tionate reduction of the ‘on’ compared with the ‘off’ component.Although the clinical features are definitely different from thesepreviously reported cases, the electrophysiological findings of thecurrent cases are very similar to these cases suggesting a greaterdefect of inner retinal function, especially in transmission betweenphotoreceptors and depolarizing bipolar cells.8

The definite mechanism leading to this unusual dysfunction inthese patients is not known. Further physiological and geneticinvestigations are required to separate this disorder from othertypes of retinal degenerations, as currently the diagnosis is mainlydetermined by the fundus examination.

Kazuki Hotta MD,1 Mineo Kondo MD,2

Makoto Nakamura MD,2 Junko Hotta MD,1

Hiroko Terasaki MD,2 Yozo Miyake MD2 andTetsuo Hida MD3

1Department of Ophthalmology, Kameda Medical Center, Chiba,2Department of Ophthalmology, Nagoya University School of Medicen,

Nagoya, and 3Kyorin Eye Center, Kyorin University School ofMedicen, Tokyo, Japan

Received 31 January 2005; accepted 4 July 2005.

REFERENCES

1. Hayasaka S, Fukuda K, Tsuchiya M, Mizuno K. Pericentralpigmentary retinal degeneration. Jpn J Ophthalmol 1985; 29:161–9.

2. Noble KG. Peripapillary (pericentral) pigmentary retinaldegeneration. Am J Ophthalmol 1989; 108: 686–90.

3. Kondo M, Piao CH, Tanikawa A, Horiguchi M, Miyake Y. Acontact lens electrode with built-in high intensity white light-emitting diodes. A contact lens electrode with built-in whiteLEDs. Doc Ophthalmol 2001; 102: 1–9.

4. Sakanaka S, Murayama K, Adachi E. Clinical and electrophys-iological studies on posterior retinitis pigmentosa. Nippon GankaGakkai Zasshi 1996; 100: 50–4.

5. Koh AH, Hogg CR, Holder GE. The incidence of negativeERG in clinical practice. Doc Ophthalmol 2001; 102: 19–30.

6. Miyake Y, Shiroyama N, Horiguchi M et al. Bull’s-eye macul-opathy and negative electroretinogram. Retina 1989; 9: 210–15.

7. Cideciyan AV, Jacobson SG. Negative electroretinograms inretinitis pigmentosa. Invest Ophthalmol Vis Sci 1993; 34: 3253–63.

8. Miyake Y, Yagasaki K, Horiguchi M, Kawase Y. On- and off-responses in photopic electroretinogram in complete andincomplete types of congenital stationary night blindness. JpnJ Ophthalmol 1987; 31: 81–7.

Inadvertent sclerostomy with encysted bleb following trans-scleral contact diode laser...

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