is slightly than greater than 250 �m. This findingprompted us to analyze the residual stromal bed thicknessin keratectasia cases after LASIK in the literature. Fromthe pachymetry, flap, and ablation data in previouslypublished cases, we calculated residual stromal bed thick-ness in 57 eyes that ranged from 113 to 353 �m.1–6 In 28(49%) of 57 eyes, residual stromal bed thickness wasgreater than 250 �m.1–6 To calculate the residual stromalbed thickness, the flap thickness is assumed to be thelabeled plate depth, which may be subject to error. In ourcases and in the literature, inaccuracies in presumed flapdepth could lead to overestimation of calculated residualstromal bed thickness. This potential source of error isinherent in the procedure and is included in planning theresidual stromal bed thickness. It is also possible that the250-�m target thickness for the residual stromal bed is toolow, especially since this number was derived from assump-tions of the tangential elastic modulus of the normalcornea rather than experimental data.1 Regardless ofwhether the technique for calculating the residual stromalbed or the derived number is at fault, our data and theliterature show that the calculated residual stromal bed of250 �m does not prevent keratectasia. A prospective studyto directly measure residual stromal bed thickness imme-diately after LASIK is needed to determine the actualthickness that precludes keratectasia.

REFERENCES

1. Ozdamar A, Aras C, Ustundag C, Bahcecioglu H, Ozkan S.Corneal iron ring associated with iatrogenic keratectasia aftermyopic laser in situ keratomileusis. J Cataract Refract Surg2000; 26:1684–1686.

2. Lafond G, Bazin R, Lajoie C. Bilateral severe keratoconusafter laser in situ keratomileusis in a patient with forme frustekeratoconus. J Cataract Refract Surg 2001;27:1115–1118.

3. Argento C, Cosentino MJ, Tytiun A, Rapetti G, Zarate J.Corneal ectasia after laser in situ keratomileusis. J CataractRefract Surg 2001;27:1440–1448.

4. Jabbur NS, Stark WJ, Green WR. Corneal ectasia afterlaser-assisted in situ keratomileusis. Arch Ophthalmol 2001;119:1714–1716.

5. Lyle WA, Jin GJC. Laser in situ keratomileusis with the VISXStar laser for myopia over �10.0 diopters. J Cataract RefractSurg 2001;27:1812–1822.

6. Pallikaris IG, Kymionis GD, Astyrakakis NK. Corneal ectasiainduced by laser in situ keratomileusis. J Cataract Refract Surg2001;27:1796–1802.

7. Hogan MJ, Alvarado JA, Weddell JE. Histology of the humaneye, an atlas and textbook. Philadelphia: W.B. Saunders,1971:89.

Recurrence of Retinoblastoma12 Years After BrachytherapyHiroshi Goto, MD, Akiko Kousaka, MD,Shigeru Takano, MD, and Masahiko Usui, MD

PURPOSE: To report a case of retinoblastoma that re-curred 12 years after brachytherapy.DESIGN: Interventional case report.METHODS: A 2-month-old boy presented in December1983 with bilateral retinoblastoma and was treated withbilateral 198Au plaque radiotherapy, photocoagulation,and cryotherapy. He maintained a visual acuity of 20/200 in both eyes. In December 1995, he had a suddendecrease of vision in the right eye and vitreous hemor-rhage with fluffy opacification.RESULTS: In January 1996, cytopathologic examinationof large keratic precipitates in the right eye demonstratedcells consistant with retinoblastoma. The right eye wasenucleated and diffuse retinoblastoma was noted his-topathologically. Systemic chemotherapy was given, andthere has been no local recurrence or extraocular metas-tasis for 5 years.CONCLUSIONS: This case emphasizes that long-term fol-low-up is essential for managing retinoblastoma aftereye-preserving conservative therapy. (Am J Ophthal-mol 2002;134:773–775. © 2002 by Elsevier ScienceInc. All rights reserved.)

CONVENTIONAL THERAPIES FOR RETINOBLASTOMA,

including eyeball enucleation, external beam radio-therapy, brachytherapy, laser photocoagulation, and cryo-therapy, have achieved favorable survival rates.1 Inaddition, more than 50% of patients with retinoblastomaare managed with chemoreduction.2 Shields and associ-ates3 reported recurrence rates of retinoblastoma treatedwith plaque radiotherapy combined with other treatmentsof 17% at 1 year and 20% at 4 years and a mean intervalto recurrence of 8 months. We describe a case of retino-blastoma that recurred 12 years after brachytherapy.

A 2-month-old boy was referred to us in December 1983to rule out retinopathy of prematurity. Ocular fundusexamination revealed no evidence of retinopathy of pre-maturity, but detected multiple intraocular tumors in botheyes (Figure 1). A diagnosis of bilateral retinoblastoma wasmade based on the ocular manifestations and computedtomography. No remarkable family histories were present,and genetic analysis was not performed. Plaques with198Au were implanted on the sclera of both eyes andremoved 1 week later, resulting in 50-Gy irradiation.Retinal photocoagulation and cryotherapy were subse-quently added. After these combination therapies, theintraocular tumors gradually regressed and chorioretinalscars remained. Periodical ophthalmic follow-up was con-tinued, and the infant’s visual acuity was maintained at20/200 in both eyes.

Accepted for publication July 1, 2002.From the Department of Ophthalmology, Tokyo Medical University,

Tokyo, Japan.Inquiries to Hiroshi Goto, MD, Department of Ophthalmology, Tokyo

Medical University, 6-7-1 Nishi-shinjuku, Shinjuku-ku, Tokyo 160-0023,Japan; fax: (�81) 3-3346-9170; e-mail: goto1115@tokyo-med.ac.jp

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Twelve years after these treatments, visual acuity in theboy’s right eye suddenly decreased to hand motions and hevisited us in December 1995. Although diffuse vitreoushemorrhage with disseminated fluffy opacification in hisright eye was observed, detailed fundus findings wereunknown. In January 1996, large keratic precipitates andmoderate cell infiltration in the anterior chamber werenoted (Figure 2, top). No significant changes were presentin his left eye except diffuse chorioretinal atrophy. Ultra-sonography, magnetic resonance imaging, and computedtomography revealed no evidence of intraocular tumor.However, cytopathologic examination of the aqueous hu-mor collected by paracentesis demonstrated tumor cellsconsistent with retinoblastoma in the right eye (Figure 2,top). His right eye was enucleated in February 1996, andhistopathologic examination demonstrated flat and diffuseinfiltration of tumor cells with occasional rosette formationand foci of calcification (Figure 2, bottom). The tumorcells infiltrated into the vitreous cavity and anteriorchamber, whereas the optic nerve was spared. Combinedchemotherapy with vincristine sulfate, etoposide, and car-boplatin was given postoperatively. No local recurrence orexraocular metastasis was found for 5 years.

Iodine 125 (I125) plaque radiotherapy is currently themost common brachytherapy for intraocular neoplasms inthe United States,3 but its use has been prohibited by lawin Japan. However, 198Au has been authorized for brachy-therapy for more than 25 years, and its clinical use isallowed in Japan. The small size and short half-life of198Au make it safe and permanently applicable to variousorgans.4

Recurrence of retinoblastoma generally occurs at theedge of or within the scar, whereas new tumors usually

arise far from the primary site after conservative therapy.5It was difficult to demonstrate histologically whether thediffuse tumor in the present case was a recurrent or de novotumor. Long-term periodic follow-up is essential to man-aging patients with retinoblastoma after eye-preservingconservative therapy.

REFERENCES

1. Shields CL, Potter PD, Himelstein BP, et al. Chemoreductionin the initial management of retinoblastoma. Arch Ophthal-mol 1996;114:1330–1338.

2. Shields CL, Shields JA, Needle M, et al. Combined chemore-duction and adjuvant treatment for intraocular retinoblas-toma. Ophthalmology 1997;104:2101–2111.

3. Shields CL, Shields JA, Cater J, et al. Plaque radiotherapy forretinoblastoma. Long-term tumor control and treatment com-plications in 208 tumors. Ophthalmology 2001;108:2116–2121.

4. Yasumoto M, Shibuya H, Hoshina M, et al. External and

FIGURE 1. Fundus photograph demonstrating multiple retino-blastomas adjacent to the optic disk in the right eye.

FIGURE 2. (Top) Slit-lamp biomicroscope showing large ker-atic precipitates at the periphery and posterior subcapsularcataract. Note the accumulation of tumor cells consistent withretinoblastoma in aqueous humor collected by paracentesis(inset). (Bottom) Histopathological examination, right eye,demonstrating flat and diffuse infiltration of retinoblastoma(arrow). Note the foci of calcification in the tumor (inset).

AMERICAN JOURNAL OF OPHTHALMOLOGY774 NOVEMBER 2002

interstitial radiotherapy in the treatment of oropharyngealsquamous cell carcinoma. Br J Radiol 1995;68:630–635.

5. Hadjistilianou T, Greco G, Frezzotti R. Recurrent and newtumors during conservative treatment of bilateral retinoblas-toma. Ophthalmic Paediatr Genetics 1991;12:79–84.

Primary Adrenal Lymphoma WithChoroidal MetastasesLisa S. Schocket, MD, Nasreen A. Syed, MD,and Stuart L. Fine, MD

PURPOSE: To describe a 71-year-old man with bilateralprimary adrenal lymphoma with metastases to the choroid.DESIGN: Interventional case report.METHODS: A 71-year-old man presented with decreasedvisual acuity in his left eye secondary to an exudativeretinal detachment. Abdominal computed tomographyand percutaneous biopsy revealed non-Hodgkin large-celllymphoma involving both adrenal glands.RESULTS: Ocular and adrenal lesions resolved after sixcycles of chemotherapy with cytoxan, adriamycin, vin-cristine, and prednisone. Seven years after his initialdiagnosis, the patient reported no recurrence of eitherocular or systemic lymphoma.CONCLUSIONS: To our knowledge, this is the first casereport of bilateral primary adrenal lymphoma with appar-ent metastases exclusively to the eye. (Am J Ophthal-mol 2002;134:775–776. © 2002 by Elsevier ScienceInc. All rights reserved.)

AN INTERVENTIONAL CASE REPORT OF BILATERAL PRI-

mary adrenal lymphoma with apparent metastasesexclusively to the eye that presented with blurred vision isdescribed.

A 71-year-old man had a 4-month history of decreasedvision that began in the left eye. Ocular examinationrevealed a visual acuity of 20/30 in the right eye and20/100 in the left eye. Amsler grid was normal in the righteye, but showed diffuse central distortion in the left eye.Slit-lamp biomicroscopy revealed a clear vitreous in theright eye, but a turbid, acellular vitreous in the left eye.Dilated fundus examination in the right eye was normal,but disclosed an exudative/infiltrative detachment involv-ing the posterior pole and inferior retina in the left eye(Figure 1).

The exudative detachment with a yellow infiltrate inthe subretinal space suggested the possibility of a choroidalmetastasis, intraocular non-Hodgkin lymphoma, or anamelanotic melanoma. Further questioning revealed a 4-

to 8-week history of severe bronchitis, low-grade fever,night sweats, and decreased appetite with an unintentional15- to 20-pound weight loss. Subsequent physical exami-nation demonstrated a healthy man. Laboratory data weresignificant for mild anemia (hemoglobin 12 g/dl) andslightly elevated lactate dehydrogenase ([LDH] 280 U/l).

An abdominal computed tomogram (CT) demonstratedlarge, lobulated, poorly defined masses in the region ofboth adrenal glands. The morphology was consistent withlymphadenopathy, but the location was unusual (Figure 2,left). Percutaneous CT-guided biopsy specimens revealedlarge lymphoid cells with immunoblastic features (Figure 2,right), supporting the diagnosis of large-cell lymphoma,B-cell phenotype. Laboratory data led to the diagnosis ofadrenal insufficiency, and corticosteroids were started.

Visual acuity in the right eye subsequently decreased to20/50. Examination revealed a detachment of the rightmacula with a suggestion of an infiltrative componentunder the retinal pigment epithelium. Ultrasonography inboth eyes demonstrated lesions with moderate reflectivity.Six cycles of chemotherapy with cytoxan, adriamycin,vincristine, and prednisone were initiated. A follow-upabdominal CT 4 months after his diagnosis showed noevidence of residual lymphoma. In addition, adrenal func-tion and LDH normalized. Seven and a half years after hisdiagnosis, the patient’s visual acuity was 20/20 in botheyes, and regular medical surveillance has disclosed noevidence of recurrent systemic disease.

Intraocular non-Hodgkin’s lymphoma has been classi-fied into two clinically distinct forms: (1) non-Hodgkin’slymphoma of the central nervous system and (2) systemicnon-Hodgkin’s lymphoma. Non-Hodgkin’s lymphoma ofthe central nervous system is more common and tends toaffect the vitreous and retina. In contrast, patients withsystemic disease tend to present with symptoms of theirunderlying malignancy.1 Freeman and associates2 foundthat, in patients with visceral involvement, visceral symp-toms preceded ocular symptoms in 57% of cases. Ocularinvolvement in such cases is due to invasion through thechoroidal circulation, so the uveal tract tends to beaffected.3

The occurrence of non-Hodgkin’s lymphoma in boththe adrenals and the eye is unique for several reasons. First,when it involves the adrenals, the disease is usually alsopresent in the retroperitoneal space or the kidney.4 In thiscase, the kidneys and the retroperitoneum were free ofany detectable disease. Second, primary adrenal non-Hodgkin’s lymphoma is extremely rare; fewer than 15cases have been reported in the last 50 years.5 Thedevelopment of primary adrenal non-Hodgkin’s lymphomais possible because hematopoietic tissue, a tissue necessaryfor the development of the disease, can exist in theadrenals. Third, even when the disease infiltrates theadrenal glands, adrenal insufficiency, as recognized in ourpatient, is rare.6 Finally, a MEDLINE search revealed noprevious reports of bilateral primary adrenal non-

Accepted for publication June 17, 2002.From the Department of Ophthalmology, Scheie Eye Institute, Uni-

versity of Pennsylvania School of Medicine, Philadelphia, PennsylvaniaInquiries to Lisa S. Schocket, MD, Scheie Eye Institute, University of

Pennsylvania, 51 N 39th St, Philadelphia, PA 19104; e-mail: lschocket@yahoo.com

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