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Loss of Intraocular Pressure Control With Ocusert
262
AMERICAN JOURNAL OF OPHTHALMOLOGY
turity. They suggested that a restrictive policy may be responsible for precipitating the serious form of the disorder. The hypothesis seemed to be supported by experiments in kittens, but extrapolation from the animal model was limited because no cicatricial lesions were produced in controls. The second set of animal experiments produced results that, if confirmed, threaten to overturn many accepted views. Flower and Blake," examining the effect of blocking oxygen-induced vasoconstriction with aspirin (to alter prostaglandin biosynthesis) and induced hypercarbia, were able to produce cicatricial retinopathy. For the first time a scarring lesion was produced in an experimental animal; this was probably accomplished by interfering with a change-retinal vasoconstriction--eonsidered to be the first stage of a sequence leading to retinal pathology. Most importantly, the creation of retinal scars in an animal eye answers the major criticism of nonhuman studies. If this accomplishment is reproduced by others, the results can be extended to blindness from retinopathy of prematurity with more confidence. The present uncertainties may shock those who were taught that blindness from retinopathy of prematurity is a closed and satisfactorily concluded chapter in the early history of modern neonatal medicine, but the current disbelief in the oxygen dogma is not particularly worrisome. The maxim, "Better orderly error than complex truth," is dangerous to our patients' health. WILLIAM A. SILVERMAN, M.D.
Greenbrae, California REFERENCES
1. Oxygen and retrolental fibroplasia. The questions persist. Pediatrics 60:753, 1977. 2. Phelps, D. L.: Retinopathy of prematurity. An estimate of vision loss in the United States-1979. Pediatrics 67:924, 1981. 3. - - : The role of tocopherol in oxygen-
AUGUST, 1982
induced retinopathy. Kitten mode!. Pediatrics 59(supp!. ):998, 1977. 4. Vitamin E and retrolental fibroplasia, correspondence. N. Eng!. J. Med. 306:866, 1982. 5. Phelps, D. L., and Rosenbaum, A. L.: The effect of marginal hypoxemia during the recovery period in oxygen-induced retinopathy in the kitten, abstract. CHn. Res. 30:146, 1982. 6. Flower, R. W., and Blake, D. A.: Retrolental fibroplasia. Role of prostaglandin cascade in the pathogenesis of oxygen-induced retinopathy in the newborn beagle. Pediatr, Res. 15:1293, 1981.
Loss of Intraocular Pressure Control With Ocusert Editor: Recently, the intraocular pressures of two of my patients with pigmentary glaucoma suddenly increased. One patient was being treated with Ocusert Pilo 40 and the other with Ocusert Pilo 20. The Ocuserts were still in place, but in neither case were the pupils miotic. Topically applied pilocarpine eyedrops reduced the intraocular pressures to near normal and made the pupils miotic within one hour of instillation. Both patients then said that their pupils had been returning to normal after four to five days of Ocusert use. Suspecting that the Ocuserts were defective, I returned several of the patients' used and unused units to the Alza Corporation. The response stated that, "The systems in question were within specification (i. e., functioned properly), both in total drug content and release rate." Data from the company disclosed that the release rate goes through three stages. During the first day after insertion there is a high release rate, but this decreases rapidly. What is not generally realized is that there is a small but significant decrease in the release rate that extends through day four with the Pilo 40 unit and through part of day two with the Pilo 20 unit. Thereafter the release rate has a near "zero-order pattern." Because of the decrease in release rate,
VOL. 94, NO. 2
CORRESPONDENCE
the intraocular pressures of some patients may be controlled for only the first several days of Ocusert use. Thereafter the intraocular pressure may be lost and the pilocarpine-induced miosis reversed. To ensure that the Ocusert provides adequate control, the intraocular pressure should be checked near the end of its use. Additionally, a patient should not only verify the presence of the device but can in some cases also monitor its therapeutic effect by checking his pupils. ROBERT H. DAVIS, M.D. Eugene, Oregon
Traumatic Expulsion of an Intraocular Lens Editor: In February 1981, I examined an 81year-old man whose best corrected visual acuity was 6/60 (20/200) in both eyes because of cataracts. He underwent an extracapsular procedure in the left eye with implantation of a Shearing posterior chamber intraocular lens on March 4, 1981. He did well postoperatively and all the sutures were finally cut four months after surgery in order to relieve astigmatism. On July 21, 1981, healing appeared to be good and there was no evidence of any wound dehiscence or filtering bleb. His best corrected visual acuity in the left eye was 6/12 (20/40). On Aug. 25, he was in an automobile accident. The only injury he sustained was a contusion of the left eye that resulted in a hyphema and scleral laceration. He told a physician at that time that his intraocular lens had come out. He found it and wrapped it in a handkerchief which he later lost. When he was operated on that evening, it was learned that the iris had prolapsed through the old cataract wound from the 10 o'clock to the 12 o'clock position. The posterior capsule was large-
263
ly intact in the inferior half of the eye, but the superior half was ruptured and there was some vitreous in the wound. The prolapsed iris was excised and anterior vitrectomy performed along with removal of the rest of the posterior capsule and resuturing of the cataract wound. Postoperatively the patient had mild corneal edema and a vitreous hemorrhage. Both cleared up gradually during the next few weeks. As of March 9, 1982, his eye had healed well without any evidence of increased intraocular pressure, cystoid macular edema, retinal tears, retinal detachment, or any other problems. The patient was taking no drugs. His visual acuity was 6/12 (20/40) in the left eye and the only sign of previous surgery was a large superior sector iridectomy. CLARK R. COBBLE, M.D. Danville, Virginia
Retroview of the Iris Editor: I have discovered that the posterior surface of the iris can be viewed with the slit lamp in patients with posterior chamber intraocular lenses. With the patient placed in the usual position at the slit lamp and the eyes in the right gaze position, the slit beam of the biomicroscope is passed from the left at approximately 30 degrees off-center. When the observer focuses behind the intraocular lens, it is possible to view the back surface of the left side of the iris. Two images corresponding to front and back surface reflections from the intraocular lens can be observed. The more posterior reflection covers a larger area, but one restricted to the peripupillary region (Figure). The only significant abnormality of the posterior iris surface that I have observed so far is some areas of loss of pigment, presumably resulting from previous sur-
AMERICAN JOURNAL OF OPHTHALMOLOGY
turity. They suggested that a restrictive policy may be responsible for precipitating the serious form of the disorder. The hypothesis seemed to be supported by experiments in kittens, but extrapolation from the animal model was limited because no cicatricial lesions were produced in controls. The second set of animal experiments produced results that, if confirmed, threaten to overturn many accepted views. Flower and Blake," examining the effect of blocking oxygen-induced vasoconstriction with aspirin (to alter prostaglandin biosynthesis) and induced hypercarbia, were able to produce cicatricial retinopathy. For the first time a scarring lesion was produced in an experimental animal; this was probably accomplished by interfering with a change-retinal vasoconstriction--eonsidered to be the first stage of a sequence leading to retinal pathology. Most importantly, the creation of retinal scars in an animal eye answers the major criticism of nonhuman studies. If this accomplishment is reproduced by others, the results can be extended to blindness from retinopathy of prematurity with more confidence. The present uncertainties may shock those who were taught that blindness from retinopathy of prematurity is a closed and satisfactorily concluded chapter in the early history of modern neonatal medicine, but the current disbelief in the oxygen dogma is not particularly worrisome. The maxim, "Better orderly error than complex truth," is dangerous to our patients' health. WILLIAM A. SILVERMAN, M.D.
Greenbrae, California REFERENCES
1. Oxygen and retrolental fibroplasia. The questions persist. Pediatrics 60:753, 1977. 2. Phelps, D. L.: Retinopathy of prematurity. An estimate of vision loss in the United States-1979. Pediatrics 67:924, 1981. 3. - - : The role of tocopherol in oxygen-
AUGUST, 1982
induced retinopathy. Kitten mode!. Pediatrics 59(supp!. ):998, 1977. 4. Vitamin E and retrolental fibroplasia, correspondence. N. Eng!. J. Med. 306:866, 1982. 5. Phelps, D. L., and Rosenbaum, A. L.: The effect of marginal hypoxemia during the recovery period in oxygen-induced retinopathy in the kitten, abstract. CHn. Res. 30:146, 1982. 6. Flower, R. W., and Blake, D. A.: Retrolental fibroplasia. Role of prostaglandin cascade in the pathogenesis of oxygen-induced retinopathy in the newborn beagle. Pediatr, Res. 15:1293, 1981.
Loss of Intraocular Pressure Control With Ocusert Editor: Recently, the intraocular pressures of two of my patients with pigmentary glaucoma suddenly increased. One patient was being treated with Ocusert Pilo 40 and the other with Ocusert Pilo 20. The Ocuserts were still in place, but in neither case were the pupils miotic. Topically applied pilocarpine eyedrops reduced the intraocular pressures to near normal and made the pupils miotic within one hour of instillation. Both patients then said that their pupils had been returning to normal after four to five days of Ocusert use. Suspecting that the Ocuserts were defective, I returned several of the patients' used and unused units to the Alza Corporation. The response stated that, "The systems in question were within specification (i. e., functioned properly), both in total drug content and release rate." Data from the company disclosed that the release rate goes through three stages. During the first day after insertion there is a high release rate, but this decreases rapidly. What is not generally realized is that there is a small but significant decrease in the release rate that extends through day four with the Pilo 40 unit and through part of day two with the Pilo 20 unit. Thereafter the release rate has a near "zero-order pattern." Because of the decrease in release rate,
VOL. 94, NO. 2
CORRESPONDENCE
the intraocular pressures of some patients may be controlled for only the first several days of Ocusert use. Thereafter the intraocular pressure may be lost and the pilocarpine-induced miosis reversed. To ensure that the Ocusert provides adequate control, the intraocular pressure should be checked near the end of its use. Additionally, a patient should not only verify the presence of the device but can in some cases also monitor its therapeutic effect by checking his pupils. ROBERT H. DAVIS, M.D. Eugene, Oregon
Traumatic Expulsion of an Intraocular Lens Editor: In February 1981, I examined an 81year-old man whose best corrected visual acuity was 6/60 (20/200) in both eyes because of cataracts. He underwent an extracapsular procedure in the left eye with implantation of a Shearing posterior chamber intraocular lens on March 4, 1981. He did well postoperatively and all the sutures were finally cut four months after surgery in order to relieve astigmatism. On July 21, 1981, healing appeared to be good and there was no evidence of any wound dehiscence or filtering bleb. His best corrected visual acuity in the left eye was 6/12 (20/40). On Aug. 25, he was in an automobile accident. The only injury he sustained was a contusion of the left eye that resulted in a hyphema and scleral laceration. He told a physician at that time that his intraocular lens had come out. He found it and wrapped it in a handkerchief which he later lost. When he was operated on that evening, it was learned that the iris had prolapsed through the old cataract wound from the 10 o'clock to the 12 o'clock position. The posterior capsule was large-
263
ly intact in the inferior half of the eye, but the superior half was ruptured and there was some vitreous in the wound. The prolapsed iris was excised and anterior vitrectomy performed along with removal of the rest of the posterior capsule and resuturing of the cataract wound. Postoperatively the patient had mild corneal edema and a vitreous hemorrhage. Both cleared up gradually during the next few weeks. As of March 9, 1982, his eye had healed well without any evidence of increased intraocular pressure, cystoid macular edema, retinal tears, retinal detachment, or any other problems. The patient was taking no drugs. His visual acuity was 6/12 (20/40) in the left eye and the only sign of previous surgery was a large superior sector iridectomy. CLARK R. COBBLE, M.D. Danville, Virginia
Retroview of the Iris Editor: I have discovered that the posterior surface of the iris can be viewed with the slit lamp in patients with posterior chamber intraocular lenses. With the patient placed in the usual position at the slit lamp and the eyes in the right gaze position, the slit beam of the biomicroscope is passed from the left at approximately 30 degrees off-center. When the observer focuses behind the intraocular lens, it is possible to view the back surface of the left side of the iris. Two images corresponding to front and back surface reflections from the intraocular lens can be observed. The more posterior reflection covers a larger area, but one restricted to the peripupillary region (Figure). The only significant abnormality of the posterior iris surface that I have observed so far is some areas of loss of pigment, presumably resulting from previous sur-