682 AMERICAN JOURNAL OF OPHTHALMOLOGY June, 1989

spots were applied to the anterior chamberangle over the actively bleeding site.

During the subsequent three months, thepatient returned three times with recurrenthyphema and argon laser goniophoto­coagulation was repeated at each visit. Thepatient returned a fourth time with recurrenthyphema and gonioscopy again showed activebleeding from the wound gape. The Nd:YAGlaser was used to perform transscleral photoco­agulation to the corneosclerallimbus overlyingthe bleeding site. It was used in the free run­ning mode with pulsed energy values of 6.3 J,exposure duration of 20 msec, and maximaloffset. Three spots were applied to the corneo­scleral limbus overlying the bleeding site andthree additional spots more posteriorly (Fig­ure).

The patient has remained symptom free andwithout recurrent hyphema for eight monthspostoperatively. Her visual acuity has im­proved to 20/25 in the left eye, with intraocularpressure of 18 mm Hg.

Cataract wound neovascularization with re­current hyphema is a rare but serious cornplica­tion.! Treatments include argon lasergoniophotocoagulation and reopening the con­junctival tissue coupled with direct diathermy,cauterization, or suturing of vessels. Argonlaser treatment probably has had variable re­sults because the unpigmented sclera may notabsorb the laser energy effectively. 5 ThisNd:YAG technique may work when argon treat­ment is ineffective because the Nd:YAG laser

Figure (Kramer and associates). TransscleralNd:YAG laser treatment has been applied to thelimbal area (arrow) above the site of bleeding fromthe cataract wound. Recurrent hyphema (arrowhead)was present before treatment. Iris contraction oc­curred during treatment and caused a peaking of thepupil.

can transmit a broad band of cauterizing heat toscleral vessels without regard to pigmentation.

References

1. Beckman, H., and Sugar, H. S.: Neodymiumlaser cyclocoagulation. Arch. Ophthalmol. 90:27,1973.

2. Devenyi, R. G., Trope, G. E., Hunter, W. H.,and Badeeb, 0.: Neodymium:YAG transscleral cyclo­coagulation in human eyes. Ophthalmology 94:1519,1987.

3. Hampton, C.; and Shields, M. B.: Transscleralneodymium- YAG cyclophotocoagulation. A histo­logic study of human autopsy eyes. Arch. Ophthal­mol. 106:1121, 1988.

4. Swan, K. C: Hyphema due to wound vascular­ization after cataract extraction. Arch. Ophthalmol.89:87, 1973.

5. Swan, K. C: Late hyphema due to wound vas­cularization. Trans. Am. Acad. Ophthalmol. Otolar­yngol. 81:138, 1976.

Unilateral Pigmentary RetinopathyAssociated With OcularToxoplasmosis

Claudio Silveira, M.D.,Rubens Belfort, Jr., M.D.,Robert Nussenblatt, M.D.,Michel Farah, M.D.,Walter Takahashi, M.D.,Paulo Imamura, M.D.,and Miguel Burnier, Jr., M.D.Clinica Silveira (CS.), Departments of Ophthalmolo­gy and Pathology, Escola Paulista de Medicina (R.B.,M.F., P.!., and M.B.), Department of Ophthalmolo­gy, Faculdade de Medicina Universidade de SaoPaulo (W.T.), and National Eye Institute, NationalInstitutes of Health (R.N.).

Inquiries to Rubens Belfort, [r., M.D., Caixa Postal4086,01051-Sao Paulo, Brazil.

Retinitis pigmentosa frequently has heredi­tary predisposition. However, pigmentary reti­nopathy simulating retinitis pigmentosa canresult from previous retinal inflammatory dis­eases such as syphilis, rubeola, other viralentities, and onchocerciasis. 1 Our seven pa­tients with bilateral recurrent ocular toxoplas­mosis developed a fundus appearance simulat­ing unilateral retinitis pigmentosa. They hadnonrecordable electroretinograms as a late re­sult of the inflammatory ocular disease. Noneof the patients had ocular trauma, retinal de-

Vol. 107, No.6 Letters to the Journal 683

Fig. 1 (Silveira and associates). Composite retinalpicture with bilateral ocular toxoplasmosis and uni­lateral pigmentary and vascular changes identical toretinitis pigmentosa. The electroretinogram wasnonrecordable.

tachment, or uveal effusion. All patients hadpositive serologic findings for toxoplasmosis,and clinical findings typical of ocular toxoplas­mosis, with a necrotizing retinochoroiditisoften associated with satellite lesions (Fig. 1).Other known causes of focal retinochoroiditis,such as syphilis and tuberculosis, were ex­cluded.

The patients ranged in age from 23 to 59years; five were women and two were men. Allpatients had bilateral ocular toxoplasmosis andunilateral pigmentary retinopathy simulatingretinitis pigmentosa. This disturbance was sec­torial in four of the patients and affected allquadrants of the retina in the other three. Twoof them had unilateral pigmentary retinopathyfor more than five years. Four of the sevenpatients had the active retinochoroiditis typicalof ocular toxoplasmosis more than 15 yearspreviously and developed unilateral pigmen­tary retinopathy after the uveitis disappeared.One patient, who was first seen at 17 years ofage, had had bilateral ocular toxoplasmosisscars for several years (Fig. 2). Three years laterunilateral pigmentary retinopathy simulatingretinitis pigmentosa was noted, but the patientmade no mention of any further episode ofretinochoroiditis. In at least two patients theocular manifestations of toxoplasmosis wereprobably acquired because siblings had the typ­ical necrotizing retinal scars caused by the toxo­plasmic infection of the retina."

Four of the seven patients were examinedwhile the toxoplasmosis was active, years be­fore the appearance of the pigmentary retinop­athy. Constricted visual fields without periph­eral islands as well as an extinguished

Fig. 2 (Silveira and associates). Family with oculartoxoplasmosis in the mother and three siblings. Thesecond affected sibling has bilateral toxoplasmosisand unilateral pigmentary retinopathy simulatingretinitis pigmentosa (arrow). The fully blackenedsymbols denote bilateral ocular toxoplasmosis andthe half blackened symbols denote unilateral oculartoxoplasmosis.

electroretinogram were noted in the eyes offour patients with findings simulating retinitispigmentosa. The contralateral eyes had normalelectroretinograms and the visual field defectscorresponded to the retinochoroidal scars. Theelectroretinograms and visual fields of the re­maining three patients could not be obtained.

Ocular toxoplasmosis has been associatedwith Fuchs' heterochromic cyclitis." and Fuchs'heterochromic cyclitis has been reported inassociation with retinitis pigmentosa. 4,5 It is notclear how Toxoplasma gondii infections can leadeither to clinical findings typical of Fuchs' het­erochromic cyclitis or to pigmentary retinopa­thy. The reasons for the presence of oculartoxoplasmosis in both eyes and the retinal pig­ment epithelial changes identical to retinitispigmentosa as well as a nonrecordable electro­retinogram in only one eye of the patients areunknown. This unilateral condition has alsobeen reported in the association betweenFuchs' heterochromic cyclitis and ocular toxo­plasmosis. The mechanism may be related tobiochemical changes triggered by the toxoplas­mic retinochoroiditis. However, these retinalchanges may be related to secondary autoim­mune responses either to retinal or choroidalantigens or to severe vascular compromiseleading to perturbation of the retinal pigmentepithelium.

References

1. Heckenlively, J. R.: Simplex retinitis pigmento­sa. Nonhereditary pigment retinopathies. In Retini­tis Pigmentosa. Philadelphia, J. B. Lippincott, 1988,pp.188-197.

684 AMERICAN JOURNAL OF OPHTHALMOLOGY June, 1989

2. Silveira, C. 5., Belfort, R., Jr., Burnier, M., j-..and Nussenblatt, R.: Acquired toxoplasmosis infec­tion as the cause of toxoplasmic retinochoroiditis infamilies. Am. J. Ophthalmol. 106:362, 1988.

3. De Abreu, M. T., Belfort, R., Jr., and Hirata, P.:Fuchs' heterochromic cyclitis and ocular toxoplasmo­sis. Am. J. Ophthalmol. 93:739, 1982.

4. Francois, J., and Mastilovic, B.: L'hetero­chromie de Fuchs' associee aux heredo-degeneres­cences chorioretiniennes, Ann. Oculist. 94:385, 1961.

5. Galixto, N., and Maia, J. A. c. Fuchs' hetero­chromic cyclitis. 22nd Concilium Ophthalmol. Paris,Acta 2:503, 1974.

Correspondence

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Everyeffort will be made to resolvecontroversies betweenthe correspondents and the authors of the article beforepublication.

The Expanding OphthalmologicSpectrum of Lyme Disease

EDITOR:In the article "The expanding ophthalmo­

logic spectrum of Lyme disease," by ThomasM. Aaberg (Am. J. Ophthalmol. 107:77, Janu­ary 1989), Dr. Aaberg summarized the sug­gested antibiotic regimens for each stage ofLyme disease and for the age groups that areinfected. We suggest that corticosteroid thera­py be considered, either alone or in combina­tion with antimicrobial treatment, for the sub­acute or chronic ocular manifestation of Lymedisease after primary infections, at least insome patients.

We previously described a girl who had hadseveral episodes of Lyme arthritis and hadbeen treated with aspirin and two courses ofparenteral penicillin G in the three years pre­ceding her first ocular symptom of photopho­bia.' This symptom remitted spontaneouslyafter four months. We first saw her five yearsafter her first attack of Lyme arthritis, whenshe had bilateral keratitis. Presuming that thekeratitis was caused by Lyme disease, wetreated her with topical applications of pred­nisolone acetate with an excellent response. A

recurrence in one eye was similarly treated.She has had no recurrences in more than 18months.

It is difficult to determine which patientsshould be treated with corticosteroids. Thereis precedent for the use of corticosteroids inanother spirochetal infection of the eye, syph­ilitic interstital keratitis, in which an immuno­logic reaction is thought to play an importantrole. This kera titis bears similarities to thekeratitis of Lyme disease. We are not certain ifthe inflammatory component of Lyme kerati­tis indicates that there are still living spiro­chetes, which would be an indication for anti­microbial treatment, or is purely animmunologic reaction. The excellent clinicalresponse to prednisolone alone in our patientsuggests that corticosteroids should be con­sidered in treatment.

Although corticosteroids are not commonlyused to treat other forms of Lyme disease,other anti-inflammatory agents in conjunctionwith antibiotics are used to treat synovitis.Nonsteroidal anti-inflammatory drugs arecommonly used in the treatment of Lyme ar­thritis. These may be preferred over cortico­steroids because they have a lesser risk ofinterfering with host defenses against infec­tion. Their role in the treatment of the ocularmanifestations of Lyme disease has yet to beexplored.

It is difficult to determine if and when corti­costeroid therapy might prove to be effectivein treating the inflammatory component ofthe reaction. However, in our treatment ofone patient with relapsing bilateral keratitisthat first appeared three years after the initialepisode of Lyme arthritis and long after sev­eral therapeutic courses of antibiotics, our de­cision to instill topical corticosteroid eyedropswithout specific therapy has resulted in nofurther attacks." The decision to use suchtherapy was based on a partial similarity ofthe condition to syphilitic interstitial keratitis(although no corneal vacularization was pres­ent) and on the possibility that the diseaseprocess in the chronic stage might be parallelto that of syphilis. Both diseases are the re­sult of infection by spirochetes with commoncharacteristics. We previously suggested thatthe keratitis was more likely caused by anantigen-antibody reaction than by an infec­tion.! We further stated that, as in syphilis,complications in the form of episodic recur­rences may be " ... related to persistence ofthe antigen, either in living sequestered or­ganisms or fragments of organisms in treatedpatients."!