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Fleck Retina in Kjellin's Syndrome: Reply
Vol. 99, No. 6
Correspondence
sive accumulation of normal products resulting from a defect in their degradation in various tissues (including the brain and retinal pigment epithelium) is more likely. ELIAS I. TRABOULSI, M.D.
Beirut, Lebanon
Reference 1. Meredith, T. A., Wright, J. D., Gammon, J. A., Fellner, S. K., Warshaw, B. 1., and Maio, M.: Ocular involvement in primary hyperoxaluria. Arch. Ophthalmol. 102:584, 1984.
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EDITOR:
Dr. Traboulsi believes that the ocular findings in Kjellin's syndrome resemble those seen in patients with primary hyperoxaluria. Patients with hyperoxaluria have many fine, refractile intraretinal crystals,I.2 occasionally with intense surrounding hyperpigmentation! and unique, black geographic macular lesions.! In contrast, the patients we described had fewer and nonrefractile deposits at the level of the retinal pigment epithelium. These differences clearly separate the crystalline retinopathy of oxalosis from the fleck retina of Kjellin's syndrome. The flecks in our patients did not appear to be refractile on contact lens biomicroscopy and so we doubt that they represented crystalline material. Although the deposits resemble lipofuscin, their composition remains unknown.
739
(Am. J. Ophthalmol. 98:723, Dec. 1984), by A. K. Vine. Avulsed retinal vessels without retinal breaks in cases unrelated to other diseases of the ocular fundus constitute an uncommon, distinct clinical entity. I believe, however, that the data cited, that is, one case in a total of 1,325 patients with vitreous hemorrhage secondary to an avulsed retinal blood vessel, do not reflect the real picture of the condition and I consider that the condition is not as rare as suggested. This view was substantiated by six cases of avulsed retinal vessels with vitreous hemorrhage, without break and without any concomitant other fundus disease. 1 This study also disclosed something which, to the best of my knowledge, had not hitherto been described, that is, that the vessel sometimes ruptures completely with the result that its detached peripheral end floats about freely within the vitreous cavity, whereas in other instances the classic pattern of the avulsed vessel subjected to vitreous traction was found. Therapeutic management in our cases, depending on the size of the avulsed vessel, consisted of the combination of a scleral buckle and laser treatment, laser application and vitrectomy, or laser application alone. In five of our six cases there was no recurrence of the hemorrhage after follow-up periods of ten months to eight years. PROF. G. P. THEODOSSIADIS
Athens, Greece
Reference
SAMUEL G. FARMER, M.D.
Iowa City, Iowa
References 1. Zak, T. A., and Bunde, R.: Primary hereditary oxalosis retinopathy. Arch. Ophthalmol. 101:78, 1983. 2. Meredith, T. A., Wright, J. D., Gammon, J. A., Fellner, S. K., Warschaw, B. 1., and Maio, M.: Ocular involvement in primary hyperoxaluria. Arch. Ophthalmol. 102:584, 1984.
Avulsed Retinal Veins Without Retinal Breaks EDITOR:
I would like to coment on the interesting article, "Avulsed retinal veins without retinal breaks"
1. Chatzoulis, D., Theodossiadis, G. P., Apostolopoulos, M., and Koutsandrea, c.: Rezidivierende Claskorperblutungen infolge eines in die Glaskorperhohle hereingezogenen Netzhautgefiisses. Klin. Monatsbl. Augenheilkd. 183:256, 1983.
_ _ _ _ _ _ _ Reply
_
EDITOR:
I thank Dr. Theodossiadis for his comments. I agree that an avulsed retinal vein without a retinal break is not rare. In my discussion I pointed out that avulsed retinal veins without retinal breaks could account for some of the unexplained hemorrhages in reported large series of vitreous hemorrhages. Dr. Theodossiadis appears to have had better success with therapeutic measures which were unsuccessful in treating avulsed retinal vessels with
Correspondence
sive accumulation of normal products resulting from a defect in their degradation in various tissues (including the brain and retinal pigment epithelium) is more likely. ELIAS I. TRABOULSI, M.D.
Beirut, Lebanon
Reference 1. Meredith, T. A., Wright, J. D., Gammon, J. A., Fellner, S. K., Warshaw, B. 1., and Maio, M.: Ocular involvement in primary hyperoxaluria. Arch. Ophthalmol. 102:584, 1984.
_ _ _ _ _ _ _ Reply
_
EDITOR:
Dr. Traboulsi believes that the ocular findings in Kjellin's syndrome resemble those seen in patients with primary hyperoxaluria. Patients with hyperoxaluria have many fine, refractile intraretinal crystals,I.2 occasionally with intense surrounding hyperpigmentation! and unique, black geographic macular lesions.! In contrast, the patients we described had fewer and nonrefractile deposits at the level of the retinal pigment epithelium. These differences clearly separate the crystalline retinopathy of oxalosis from the fleck retina of Kjellin's syndrome. The flecks in our patients did not appear to be refractile on contact lens biomicroscopy and so we doubt that they represented crystalline material. Although the deposits resemble lipofuscin, their composition remains unknown.
739
(Am. J. Ophthalmol. 98:723, Dec. 1984), by A. K. Vine. Avulsed retinal vessels without retinal breaks in cases unrelated to other diseases of the ocular fundus constitute an uncommon, distinct clinical entity. I believe, however, that the data cited, that is, one case in a total of 1,325 patients with vitreous hemorrhage secondary to an avulsed retinal blood vessel, do not reflect the real picture of the condition and I consider that the condition is not as rare as suggested. This view was substantiated by six cases of avulsed retinal vessels with vitreous hemorrhage, without break and without any concomitant other fundus disease. 1 This study also disclosed something which, to the best of my knowledge, had not hitherto been described, that is, that the vessel sometimes ruptures completely with the result that its detached peripheral end floats about freely within the vitreous cavity, whereas in other instances the classic pattern of the avulsed vessel subjected to vitreous traction was found. Therapeutic management in our cases, depending on the size of the avulsed vessel, consisted of the combination of a scleral buckle and laser treatment, laser application and vitrectomy, or laser application alone. In five of our six cases there was no recurrence of the hemorrhage after follow-up periods of ten months to eight years. PROF. G. P. THEODOSSIADIS
Athens, Greece
Reference
SAMUEL G. FARMER, M.D.
Iowa City, Iowa
References 1. Zak, T. A., and Bunde, R.: Primary hereditary oxalosis retinopathy. Arch. Ophthalmol. 101:78, 1983. 2. Meredith, T. A., Wright, J. D., Gammon, J. A., Fellner, S. K., Warschaw, B. 1., and Maio, M.: Ocular involvement in primary hyperoxaluria. Arch. Ophthalmol. 102:584, 1984.
Avulsed Retinal Veins Without Retinal Breaks EDITOR:
I would like to coment on the interesting article, "Avulsed retinal veins without retinal breaks"
1. Chatzoulis, D., Theodossiadis, G. P., Apostolopoulos, M., and Koutsandrea, c.: Rezidivierende Claskorperblutungen infolge eines in die Glaskorperhohle hereingezogenen Netzhautgefiisses. Klin. Monatsbl. Augenheilkd. 183:256, 1983.
_ _ _ _ _ _ _ Reply
_
EDITOR:
I thank Dr. Theodossiadis for his comments. I agree that an avulsed retinal vein without a retinal break is not rare. In my discussion I pointed out that avulsed retinal veins without retinal breaks could account for some of the unexplained hemorrhages in reported large series of vitreous hemorrhages. Dr. Theodossiadis appears to have had better success with therapeutic measures which were unsuccessful in treating avulsed retinal vessels with