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We performed filtration surgery with a unidirectional, pressure-sensitive valve implant in 40 eyes with neovascular glaucoma. The device consisted of an open Supramid tube (outside diameter 0.58 mm, inside diameter 0.38 mm) sealed to a Silastic tube with a slit valve. The Supramid tube was inserted at the corneoscleral limbus 1 to 4 mm into the anterior chamber and the Silastic portion was located under a lamellar scleral flap. Twenty-seven of 40 eyes (68%) had a postoperative IOP less than or equal to 24 mm Hg with a mean follow-up of 13.8 months. Ten of these 27 eyes required postoperative medical therapy to achieve this level of IOP control. The glaucoma valve implant failed to return IOP to normal in 13 of the 40 eyes (32%), 11 of these as a consequence of scarring of the external bleb.

Filtration surgery was performed with a pressure-sensitive, unidirectional valve implant in 79 eyes with neovascular glaucoma. The device consisted of an open Supramid tube (outside diameter 0.58 mm) sealed to a Silastic tube with a slit valve. The Supramid tube was inserted at the corneoscleral limbus 1 to 4 mm into the anterior chamber. The Silastic portion was located under a scleral flap. Of the 79 eyes, 53 had postoperative intraocular pressures less than or equal to 24 mm Hg after a mean follow-up period of 23.7 +/- 10.9 months. Bleb revision for external scarring was required in ten of these 53 eyes and postoperative medical therapy was required in 26. The valve implant failed to control intraocular pressure in 26 of the 79 eyes. Failure was secondary to scarring of the external bleb in 18 eyes and to closure of the internal Supramid tube in five eyes. Mortality during the follow-up period was high: 12 of the 53 successfully treated patients and five of the unsuccessfully treated patients died.

Prostaglandin E1 administered into the third ventricle of rabbits produced increased intraocular pressure and body temperature. Similar responses were observed after third ventricle instillation of arachidonic acid, a precursor of prostaglandin E2. Increase of body temperature occurred with lower doses of prostaglandin E1 and arachidonic acid while the intraocular pressure response required larger amounts of these drugs. Pretreatment with aspirin rectal suppositories had no effect on the third ventricle responses induced by prostaglandin E1. Aspirin pretreatment before third ventricle instillation of arachidonic acid blocked the increases of intraocular pressure and temperature.

We determined the cross-sectional natural history of retinopathy by prospective study of 461 insulin-dependent juvenile-onset diabetics. In so doing, we compared the sensitivity of ophthalmoscopy, photography, and fluorescein angiography in detecting retinopathy. Photography was far more reliable than ophthalmoscopy in detecting early retinopathy and equivalent to angiography. Retinopathy was not present at diagnosis of diabetes. After a lag period, the prevalence of retinopathy rose in sigmoidal fashion, reaching 50% at just over seven years duration, and asymptotically approaching 90% at 17--50 years. Proliferative retinopathy was first seen at 13 years duration, and its prevalence rose to 26% at 26--50 years. From the natural history we computed the dimensions of a proposed clinical trial to test the effect of tight metabolic control in prevention of retinopathy.

Argon laser trabeculoplasty was performed in one eye of 57 phakic patients with primary open-angle glaucoma. The eyes received a mean of 78 +/- 7 treatments over 360 degrees to the anterior trabecular meshwork. The power was titrated to produce blanching without bubble formation. Increased intraocular pressure (range +1 to +22 mmHg) occurred in 30 of the 57 (53%) eyes 1 hour after treatment. Eight (14%) of these eyes had a clinically significant elevation defined by all of three criteria: (1) an intraocular pressure greater than 30 mmHg, (2) greater than a 30% increase over the mean prelaser intraocular pressure, and (3) greater than a 10 mmHg increase over the peak prelaser diurnal intraocular pressure curve. These eight patients received either oral glycerine or acetazolamide. A rebound increase in intraocular pressure requiring repeat medical treatment occurred in four of the eight eyes. Two additional eyes without a pressure elevation 1 hour after treatment showed a later elevation. This was first detected 4 hours postoperatively in one eye and 7 hours after treatment in another eye. The 1-hour postoperative measurement detected most patients with clinically significant increased intraocular pressure (8 of 10 eyes) but these required continued observation for rebound increases. Patients with advanced glaucomatous visual field loss should also be followed closely to detect late increases in intraocular pressure (2 of 10 eyes).

Intravenous desmopressin, a synthetic antidiuretic hormone, resulted in a dose-dependent increase in intraocular pressure (IOP) in rabbits. IOP was increased 3.6 +/- 0.8 mm Hg 6 hr following injection of desmopressin 200 mUnits/kg with the increase lasting over 10 hr. IOP returned to baseline 24 hr after the injection. Systemic blood pressure, plasma osmolarity and arterial blood gases were not altered by desmopressin. The increased IOP was not associated with alterations in measured outflow facility or episcleral venous pressure. Five hours after desmopressin injection, calculated aqueous humor flow was increased approximately 57%. Aqueous humor ascorbate measurements for calculation of flow to diffusion ratios and anterior chamber fluorophotometry also were consistent with an increased rate of aqueous humor formation as the mechanism for the IOP elevation. Desmopressin administration did not increase aqueous humor protein or aqueous humor cyclic AMP concentration. Systemic pretreatment with indomethacin only partially blocked the IOP increase. Systemic pretreatment with demeclocycline completely blocked the desmopressin-induced increase in IOP.

Forty patients classified as high responders (GG) to dexamethasone testing (intraocular pressure greater than 31 mm Hg) without visual field loss were subjected to plasma cortisol suppression testing. After a five-year follow-up adequate data were available on 35 patients. Eighteen responded to 1.0 mg of dexamethasone-diphenylhydantoin suppression testing in a similar fashion to patients with primary open-angle glaucoma while 17 responded in a similar fashion to subjects classified as low (NN, intraocular pressure less than 20 mm Hg) and intermediate (NG, intraocular pressure 20 to 31 mm Hg) responders to dexamethasone testing. Eight of the 35 patients developed glaucomatous visual field loss during the follow-up period. These eight patients were not more sensitive to suppression of plasma cortisol than the 27 patients maintaining normal visual fields. Thus, plasma cortisol suppression testing failed to predict the development of primary open-angle glaucoma in GG responders.

Hyperthermia increased intraocular pressure (Po) by approximately 5 mm Hg in rabbit eyes. This increase was not associated with changes in plasma osmolarity, blood lactate, or pH. Episcleral venous pressure (Pv) decreased from a baseline of 11 +/- 1 mm Hg(mean +/- SEM) to 8 +/- 1 mm Hg after one hour of hyperthermia. Outflow facility (c) as measured by tonography remained unchanged. Aqueous humor flow [c(Po - Pv)] as estimated by tonography increased by about 126%. The elevation of intraocular pressure was not prevented by aspirin pretreatment nor altered by unilateral optic nerve transection.

The first four automated visual field examinations of 20 patients with clinically stable chronic open-angle glaucoma who had previously undergone manual perimetry were studied for the presence of a learning effect on mean sensitivity, number of disturbed test locations, total loss, and short-term fluctuation. A learning effect, if present, would manifest itself as an improvement in the visual field as patients become more experienced with the test. There was no apparent effect of patient experience on the mean sensitivity, total loss, or the number of disturbed test locations. There was a significant (P less than 0.0001) decrease in short-term fluctuation as measured by the root mean square between the first and second visual field examinations. These results indicate that a learning effect did not play an important role in the clinical interpretation of automated perimetry in patients with glaucoma who have previous experience with manual perimetry. In most cases, it was not necessary to obtain more than one "baseline" examination unless a patient demonstrated unusually high short-term fluctuation or had visual field defects inconsistent with the rest of the clinical examination.