doi: 10.1001/archopht.1986.01050180017001pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
doi: 10.1001/archopht.1986.01050180017001pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables.
Beekhuis, W. Houdijn;van Rij, Gabriel;Živojnović, Relja
doi: 10.1001/archopht.1986.01050180023004pmid: 3718295
Abstract To the Editor. —A letter by Paylor and Peyman reporting a case of bullous keratopathy in an aphakic patient who underwent treatment of retinal detachment with silicone oil injection was published in the December 1985 issue of the Archives.1 The authors propose a fluorescein dye test for better visualization of the silicone oil/ aqueous interface at slit lamp examination. Basically, we believe this can be a useful method to locate the anterior face of the silicone oil bubble. However, we feel that in the case of the patient who was described it is very clear that the silicone oil was not in contact with the endothelium of the cornea. Bullous keratopathy in combination with silicone oil contact to the endothelium is only seen in very late stages of silicone oil keratopathy with vascular ingrowth and gradual stromal thickening from the periphery of the cornea toward the center.2 Early References 1. Paylor RR, Peyman GA: A method to locate the silicone oil-aqueous humor interface . Arch Ophthalmol 1985;103:1782-1783.Crossref 2. Beekhuis WH, van Rij G, Živojnović R: Silicone oil keratopathy: Indications for keratoplasty . Br J Ophthalmol 1985;69:247-253.Crossref 3. Martola EL, Dohlman CH: Silicone oil in the anterior chamber of the eye . Acta Ophthalmol 1963;41:75-79.Crossref
doi: 10.1001/archopht.1986.01050180023002pmid: N/A
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract To the Editor. —The first North American Course of the Pan American Association of Ophthalmology was held in Key Biscayne, Fla, Jan 10 to 12, 1986. Although the course was designed for North American members of the association and was advertised only to them, 30% of the attendance was from Latin America, lending to the meeting a delightfully Pan American flavor.A brilliant faculty volunteered. I am told that more people volunteered to teach than could be accommodated, but then, in my opinion, Pan-American associations always attract the best.The meeting was organized into symposia, including glaucoma (the title was deceptively simple in that more new and exciting material was presented than I had heard in a glaucoma symposium in quite a while), intraocular lens implantation (organized as a dynamic round-table discussion rather than as a presentation of papers), newer forms of tumor therapy (truly enlightening), vitrectomy management of ocular trauma
Paylor, Ralph R.;Peyman, Gholam A.
doi: 10.1001/archopht.1986.01050180023005pmid: N/A
Abstract In Reply. —The purpose of our correspondence was to describe a method to locate the silicone oil-aqueous humor interface in eyes that are aphakic and contain silicone oil from an intraocular procedure. The case report was chosen only to illustrate how this method aided us in making a therapeutic decision. Although we did not intend to describe the manifestations of silicone oil keratopathy per se, in our experience corneal thickening with bullous keratopathy is not an uncommon finding with silicone oil in the anterior chamber. References 1. Paylor RR, Peyman GA: A method to locate the silicone oil-aqueous humor interface . Arch Ophthalmol 1985;103:1782-1783.Crossref
doi: 10.1001/archopht.1986.01050180023003pmid: 3718294
This article is only available in the PDF format. Download the PDF to view the article, as well as its associated figures and tables. Abstract To the Editor. —A scleral flap incision technique reduces postoperative astigmatism but can increase the incidence of hyphema during the first day after cataract surgery. Factors that decrease this occurrence are as follows: (1) The scleral flap should measure 2 to 3 mm from the limbus to the posterior flap edge. Flaps extending further posteriorly are more likely to cause hyphemas. My initial 25 to 30 scleral flaps measured 4 to 5 mm, and the incidence of hyphema was over 50%. With narrow flaps, hyphemas still occur, but at a 3% to 4% rate. (2) The lateral wound edges should be sutured securely. A suture within 2 mm of each wound extremity will assure tightness. (3) With each suture, after the needle passes through the flap, the needle should pass into the scleral bed and then posteriorly. This prevents mobility of the flap on the scleral bed. The formation of
doi: 10.1001/archopht.1986.01050180024006pmid: 3718296
Abstract To the Editor. —If it is true, as attorney Hayes says in the editorial in the December issue of the Archives,1 that "... vis à vis expert testimony. It is a physician rather than a patient who determines when and if the medical stop sign has been run" (meaning that it is physicians and not patients and their attorneys who determine if medical malpractice has occurred), then perhaps the role and the significance of the expert witness should be examined closely.It seems, from practical experience, that in those cases of malpractice, other than those in which the negligence is obvious, there are oftentimes extenuating circumstances that are almost impossible to defend against those keen and isolated standards of excellence that should prevail under all circumstances, as the expert witness would have the jury believe.In this light, thus, the expert witness can, under some circumstances, be to a malpractice References 1. Hayes JD: The plaintiff's attorney's point of view . Arch Ophthalmol 1985;103:1791-1793.Crossref
doi: 10.1001/archopht.1986.01050180024007pmid: 2424414
Abstract To the Editor. —It is clear that optic disc drusen may be observed in anomalously elevated optic discs. It has also been assumed that anomalously elevated optic discs without visible drusen nevertheless contain drusen that are "buried" below the surface of the disc, which become visible with time.1,2 If this were true, one would expect patients with anomalously elevated optic discs without visible drusen to be generally younger than patients with visible drusen. This does not appear to be the case.3Mullie and Sanders4 have used computed tomographic scanning to identify buried drusen in four optic discs of three patients with no ophthalmoscopic or fluorescein angiographic evidence of drusen; however, to my knowledge, there has never been photographic documentation of the appearance of optic disc drusen in a patient whose optic discs initially were simply anomalously elevated. I have recently seen such a patient. Report of a References 1. Miller NR: Walsh and Hoyt's Clinical Neuro-Ophthalmology , ed 4. Baltimore, Williams & Wilkins, 1982, vol 1, pp 362-363. 2. Brown G, Tasman W: Congenital Anomalies of the Optic Disc . New York, Grune & Stratton, 1983, pp 244-247. 3. Rosenberg MA, Savino PJ, Glaser JS: A clinical analysis of pseudopapilledema: I. Population, laterality, acuity, refractive error, ophthalmoscopic characteristics, and coincident disease . Arch Ophthalmol 1979;97:65-70Crossref 4. Mullie MA, Sanders MD: Computed tomographic diagnosis of buried drusen of the optic nerve head . Can J Ophthalmol 1985;20:114-117.
doi: 10.1001/archopht.1986.01050180025010pmid: 3487304
Abstract To the Editor. —The report by Donoso and associates1 in the January 1986 issue of the Archives, which shows an association between morphologically distinctive zones and staining by a monoclonal antibody in four cases of uveal melanoma, deserves further discussion. In their article, Donoso et al1 state, "The clinical significance of antigenic and cellular heterogeneity in uveal melanomas, as illustrated in our study, is uncertain and highly speculative but warrants further investigation." I agree that the conclusions of this report are "uncertain and highly speculative," but readers of the Archives should be aware of the extensive investigations into this topic that have already been published.2-4The antibody that Donoso and coworkers1 used, MAb8-1H, has similar staining characteristics to another antimelanoma monoclonal antibody, ME491.2-3 In fact, both monoclonal antibodies recognize an epitope of the same melanoma-associated antigen retained in formalin-fixed, paraffinembedded tissues.3 The staining characteristics of ME491 were studied on a series References 1. Donoso LA, Shields JA, Augsburger JJ, et al: Antigenic and cellular heterogeneity of primary uveal malignant melanomas . Arch Ophthalmol 1986;104:106-110.Crossref 2. Folberg R, Donoso LA, Herlyn M, et al: An antimelanoma monoclonal antibody and the histopathology of uveal melanomas . Arch Ophthalmol 1985;103:275-279.Crossref 3. Donoso LA, Folberg R, Edelberg K, et al: Tissue distribution and biochemical properties of an ocular melanoma-associated antigen . J Histochem Cytochem 1985;33:1190-1196.Crossref 4. Folberg R, Donoso LA, Herlyn M, et al: Antigens in ocular and cutaneous melanoma . Am J Ophthalmol 1984;96:394-395. 5. Flocks M, Gerende JH, Zimmerman LE: The size and shape of malignant melanomas of the choroid and ciliary body in relation to prognosis and histologic characteristics . Trans Am Acad Ophthalmol Otolaryngol 1955;59:740-758. 6. Gamel JW, McLean IW, Greenberg RA, et al: Computerized histologic assessment of malignant potential: A method for determining the prognosis of uveal melanomas . Hum Pathol 1982; 10:893-897.Crossref 7. Fidler IJ, Gersten DM, Hart IR: Biology of cancer invasion and metastasis . Adv Cancer Res 1978;28:149-250.
Finkelstein, Daniel;Kimball, Allyn
doi: 10.1001/archopht.1986.01050180025008pmid: 3718297
Abstract To the Editor. —In their case-control study, "Risk Factors of Branch Vein Occlusion," Johnston et al, in the December 1985 issue of the Archives,1 state that systemic hypertension is a risk factor, with 60% of cases studied being hypertensive as compared with 47% of controls (P =.011). The answer to the several important methodological questions that follow would be helpful in assessing their claim: (1) Was hypertension determined comparably in the retrospective cases vs the prospective controls; ie, how often was the determination made by patient history vs blood pressure measurement in cases vs controls? When the assessment was performed by blood pressure measurement, how was blood pressure measured (eg, one or more readings, by whom, under what patient conditions, and using a random zero manometer)? In patients with branch retinal vein occlusion, how often was hypertension diagnosed by the internist based primarily on the existence of a new References 1. Johnston RL, Brucker AJ, Steinmann W, et al: Risk factors of branch retinal vein occlusion . Arch Ophthalmol 1985;103:1831-1832.Crossref
Steinmann, William C.;Brucker, Alexander J.;Johnston, Randolph L.;Holmes, John H.
doi: 10.1001/archopht.1986.01050180025009pmid: N/A
Abstract In Reply. — We appreciate the comments by Drs Finkelstein and Kimble since they deal with important methodologic issues we addressed on conducting the study analysis.The measures for determining hypertension are described in the text. The proportions for cases and controls defined as hypertensive using the three criteria were similar, and thus could not exert a possible bias (90% in both cases and controls were diagnosed on the basis of past history). In no patient was a new diagnosis of hypertension made after the diagnosis of the retinal occlusive event, thus excluding the probability of expectation bias for this condition.As stated, there was no significant difference by age between cases and controls. Both mean age as well as distribution by five- or ten-year age groups (using x2 with Yates correction for these categorical data) were not significantly different between groups. Hence, no further adjustment was made for References 1. Schlesselman JJ: Case-Control Studies Design Conduct Analysis . New York, Oxford University Press Inc, 1982.
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