Developing a spatial framework of common ecological regions for the conterminous United States.

In 1996, nine federal agencies with mandates to inventory and manage the nation's land, water, and biological resources signed a memorandum of understanding entitled "Developing a Spatial Framework of Ecological Units of The United States." This spatial framework is the basis for interagency coordination and collaboration in the development of ecosystem management strategies. One of the objectives in this memorandum is the development of a map of common ecological regions for the conterminous United States. The regions defined in the spatial framework will be areas within which biotic, abiotic, terrestrial, and aquatic capacities and potentials are similar. The agencies agreed to begin by exploring areas of agreement and disagreement in three federal natural-resource spatial frameworks--Major Land Resource Areas of the US Department of Agriculture (USDA) Natural Resources Conservation Service, National Hierarchy of Ecological Units of the USDA Forest Service, and Level III Ecoregions of the US Environmental Protection Agency. The explicit intention is that the framework will foster an ecological understanding of the landscape, rather than an understanding based on a single resource, single discipline, or single agency perspective. This paper describes the origin, capabilities, and limitations of three major federal agency frameworks and suggests why a common ecological framework is desirable. The scientific and programmatic benefits of common ecological regions are described, and a proposed process for development of the common framework is presented.

Macular corneal dystrophy type II: multiple studies on a cornea with low levels of sulphated keratan sulphate.

We investigated an individual macular corneal dystrophy (MCD) type II cornea from a 42-year-old woman with markedly reduced antigenic keratan sulphate levels. A characteristic 4.6 A X-ray reflection was evident, and the mid-stroma contained 30% less sulphur than normal. Close packing of collagen was restricted to the superficial stroma. Abnormally large proteoglycan filaments were noted throughout the extracellular matrix and Descemet's membrane's posterior non-banded zone, but not its anterior banded zone. Small, collagen-associated stromal proteoglycans were susceptible to digestion with chondroitinase ABC, but not keratanase I or N-glycanase. On occasion, collagen fibrils ranged in size from 20 nm to 58 nm, with preferential diameters of 34 nm and 42 nm. Corneal guttae were evident, as were numerous endothelial inclusions, most probably due to intracellular fibrillogranular vacuoles similar to those found in the stroma. The endothelium expressed reduced anti-keratan sulphate labelling.

Spontaneous detachment of Descemet's membrane. Case report and literature review.

Detachment of Descemet's membrane is an unusual cause of postoperative corneal edema. The typical detachment is small and usually limited to the area near the limbal wound. These peripheral detachments usually heal without sequelae as endothelium spreads over the area and secretes a new Descemet's membrane. We report an unusual case of spontaneous, extensive central separation of Descemet's membrane occurring 3 weeks following uncomplicated extracapsular cataract extraction with posterior chamber lens implant. Attempted reattachment of the membrane with intracameral air was only partially successful, but 12 weeks later the detachment spontaneously resolved with recovery of vision to 20/30. An anatomic predisposition may be implicated, because the fellow eye exhibits the diffuse thickening of Descemet's membrane. Descemet's detachment is a rare but potentially reversible cause of corneal edema following cataract surgery and should not be confused with early-onset pseudophakic bullous keratopathy.

Management of pseudophakic bullous keratopathy.

The incidence of pseudophakic bullous keratopathy, now the most common indication for penetrating keratoplasty, is increasing. Since over one million intraocular lenses were implanted in 1986, a large number of eyes are at risk. The etiology of pseudophakic bullous keratopathy is varied and depends in great part on the surgical technique used for cataract extraction. Given the magnitude and changing patterns of intraocular lens usage, a review of pseudophakic bullous keratopathy is appropriate.

Comparison of intraocular irrigating solutions in pars plana vitrectomy.

A prospective, randomized, masked clinical study was conducted to examine the effects of pars plana vitrectomy on the corneal endothelium comparing Balanced Salt Solution (BSS) to BSS-Plus as an intraocular irrigating solution. Seventy-one patients were followed for at least six months. A significant 6.9% decrease in endothelial cell density was observed among all patients at six months postoperatively, compared to preoperative values, using the contralateral eye as a control. However, no significant difference in endothelial cell loss was found between BSS and BSS-Plus eyes. Both aphakic eyes and those undergoing lensectomy (with vitrectomy) showed a significantly greater reduction of endothelial cell density at six months compared to phakic eyes. No significant difference in corneal thickness was observed at six months postoperatively compared to preoperative values. For the one-year duration of our study BSS was as efficacious in preserving the integrity of the corneal endothelium as was BSS-Plus.

Fluorophotometry in juvenile-onset diabetes: long-term follow-up.

Sequential ocular fluorophotometry was performed on 59 patients with juvenile-onset, insulin-dependent diabetes mellitus. Elevated vitreous fluorescein concentrations (greater than or equal to 6 ng per ml) occurred at study entry in 76% of the 59 patients and in 70% of the 46 diabetic patients without retinopathy. None of the 27 control subjects had a vitreous reading of this magnitude. At the conclusion of the study, 10 of the 46 patients originally without retinopathy developed Grade 1 retinopathy. In addition, 6 of the original 13 patients with retinopathy showed progression of their disease. A high (greater than or equal to 12 ng per ml) vitreous fluorescein concentration which occurred in 17 patients was associated with the presence as well as progression of diabetic retinopathy. A similar association was found for a simultaneous high vitreous and aqueous (greater than or equal to 100 ng per ml) fluorescein concentration.

Sodium hyaluronate use during lens expression in extracapsular cataract surgery in rabbits.

Albino rabbits were used to compare the effects of filling the anterior chamber with balanced salt solution or sodium hyaluronate prior to lens expression in an extracapsular surgical technique. No significant differences were found between the two utilizing periodic slit lamp examinations, measurements of intraocular pressure, corneal thickness or corneal endothelial cell density. Sodium hyaluronate maintained a deeper anterior chamber and simplified lens expression.

Sequential vitreous fluorophotometry in diabetes mellitus: a five-year prospective study.

Fifty-nine patients with juvenile-onset, insulin-dependent diabetes mellitus were followed for 5 years with sequential retinal photographs and ocular fluorophotometry. Very good metabolic control with a mean hemoglobin A1C level of 8.8% was maintained with conventional twice daily insulin injections. The incidence of retinopathy during the initial 10 years of the disease was considerably lower than that in previously reported series. The incidence of the development of retinopathy within the first 5 to 7 years of diabetes was 0 compared to a previous predicted incidence of 44%. It was possible to separate patients with diabetes mellitus without visible retinopathy from a group of normal control subjects. In this group of patients high hemoglobin A1C levels and thickened capillary basement membranes were not predictive of the development of progression of retinopathy. High vitreous fluorescein values and simultaneously high aqueous and vitreous fluorescein values were indicative of the presence of retinopathy or were harbingers of the development or progression of retinopathy. Disease duration was the single most important factor in determining the prevalence of retinopathy.

Quantitative vitreous fluorophotometry in insulin-treated cystic fibrosis patients.

A series of 22 patients with cystic fibrosis (CF) of similar clinical severity (9 with normal carbohydrate tolerance and 13 with insulin-treated fasting hyperglycemia) was examined with quantitative vitreous fluorophotometry. All of the CF patients studied had normal fundi on ophthalmoscopy, fundus photographs, and fluorescein angiography. Mean vitreous fluorescein concentration in the CF patients whose hyperglycemia was treated with insulin (11.79 ng/ml) was significantly higher than in CF patients with normal carbohydrate tolerance (6.98 ng/ml, P less than 0.005). Thus, CF patients with fasting hyperglycemia demonstrate a breakdown of the blood-retinal barrier. When CF patients with fasting hyperglycemia were compared with age- and sex-matched type I diabetics, there was no significant difference in mean vitreous fluorescein accumulation. Thus, breakdown of the blood-retinal barrier, one of the earliest detectable functional abnormalities that may be associated with the microangiopathy of diabetes mellitus, also occurs with equal frequency and severity in the diabetes secondary to pancreatic fibrosis associated with CF.

Central corneal endothelial cell density and central corneal thickness in ocular hypertension and primary open-angle glaucoma.

In order to assess the effect of increased intraocular pressure on the corneal endothelium, we classified 254 patients into four groups: Group 1, those with normal intraocular pressures; Group 2, those with untreated ocular hypertension; Group 3, those with treated ocular hypertension; and Group 4, those with primary open-angle glaucoma. One eye of each patient underwent specular microscopy and pachymetry. The eyes in the four groups did not differ significantly as to central corneal endothelial cell density or central corneal thickness. These measurements were not related to sex, race, or intraocular pressure (P greater than .12 in all cases). Increasing age was associated with a decrease in central corneal endothelial cell density (P = .0001), but was not associated with a change in central corneal thickness (P = .22). There was no significant relationship between the use of topical ocular hypotensive medications and central corneal endothelial cell density (P = .38) or central corneal thickness (P = .07) in patients with ocular hypertension or primary open-angle glaucoma. Neither uncomplicated peripheral iridectomy nor trabeculectomy produced significant changes when preoperative measurements were compared to measurements made 12 weeks postoperatively (P greater than .30 in all cases). Two eyes with flat anterior chambers following trabeculectomy had substantial decreases in central corneal endothelial cell density.

Fluorometric studies on the blood-retinal barrier in experimental animals.

Fluorophotometry was used to evaluate the blood-ocular barrier in rats following streptozocin-induced diabetes, experimental systemic hypertension, sodium iodate treatment, diet-induced galactosemia, and aldose reductase inhibitors. After administration of intravenous (IV) fluorescein sodium, diabetes, hypertension, or sodium iodate treatment resulted in an increased vitreous accumulation of IV fluorescein. Accumulation of dextran-labeled fluorescein (3,000 and 19,000 molecular weight [mol wt]) was not increased in diabetic or sodium iodate-treated animals. However, 3,000-mol wt dextran-labeled dye accumulated in the vitreous of hypertensive rats. The disappearance of fluorescein injected into the vitreous was significantly delayed in diabetic and sodium iodate-treated rats, whereas this rate was normal in hypertension animals. Galactosemia did not alter vitreous fluorophotometric measurements. Pretreatment for systemic effects with aldose reductase inhibitors did not correct the vitreous fluorophotometric measurements of diabetic rats.

Reversal of abnormalities in ocular fluorophotometry in insulin-dependent diabetes after five to nine months of improved metabolic control.

Abnormalities in ocular fluorophotometry occur in human and experimental diabetes mellitus. To determine the reversibility of these abnormalities, we studied prospectively 11 intensively treated and 25 conventionally treated insulin-dependent diabetics (IDD) preselected because of abnormal vitreous fluorophotometry. Among the 25 IDD treated conventionally with one or two insulin injections daily, hemoglobin A1C concentrations remained elevated and fluorescein concentration, 1 h after the intravenous injection of fluorescein (7 mg/kg), did not change significantly in either the anterior chamber or the posterior vitreous. Among 11 IDD treated intensively with home blood glucose monitoring and pumped subcutaneous insulin or three or more injections daily, hemoglobin A1C fell dramatically (10.4 +/- 0.7% to 7.5 +/- 0.2%) and anterior chamber fluorescein concentration decreased (73.9 +/- 7.7 to 49.5 +/- 5.3 ng/ml). Two patients with proliferative retinopathy showed no improvement in their massive vitreous fluorescein accumulation and subsequently required photocoagulation. In the nine subjects without proliferative retinopathy, vitreous fluorescein accumulation decreased in eight (10.6 +/- 0.7 to 6.5 +/- 0.5 ng/ml) and was normal in six after 1 yr. The only subject with increasing vitreous fluorescein accumulation also had concurrent worsening of background retinopathy. These studies support the hypothesis that moderate abnormalities in ocular fluorophotometry are due to reversible changes in ocular tissues, such as retinal pigment epithelium. Fluorescein leakage emanating from the advanced vascular or retinal abnormalities of proliferative retinopathy were not reversed with the degree and duration of metabolic control achieved in the present study. The long-term significance of the reversal of moderate abnormalities in fluorophotometry is not clear at the present time.

The natural history of retinopathy in insulin-dependent juvenile-onset diabetes.

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.

Reversal of neuropathic and gastrointestinal complications related to diabetes mellitus in adolescents with improved metabolic control.

Two adolescents with insulin-dependent diabetes mellitus developed unusually severe diabetic neuropathy which responded to intensive measures to achieve improved metabolic control. Employing home blood glucose monitoring and either frequent insulin injections or a portable insulin infusion pump, painful peripheral neuropathy and autonomic gastrointestinal neuropathy improved after five and 12 months of therapy, respectively. During this period of time, abnormal ocular fluorophotometry, an early change in the eye of diabetic patients, also returned to normal. These patients demonstrate the reversibility of unusually severe neuropathy and early ocular changes in adolescents with diabetes when treated with intensive measures designed to improve metabolic control.

Penetrating keratoplasty for pseudophakic bullous keratopathy. Visual results.

Thirty-six patients with pseudophakic bullous keratopathy had penetrating keratoplasties with one immediate graft failure and two subsequent rejections. Fifty-four percent of the patients saw 20/40 or better, and 79% saw 20/80 or better. These results are much better than reported for aphakic bullous keratopathy. Endothelial counts in the other eyes showed that 17% of these patients have unexpectedly very low cell counts, which were not appreciated on slitlamp examination and were probably a contributing factor to their corneal decompensation.

Aphakic keratoplasty: visual acuity and optical errors.

Sixty-four consecutive patients with aphakic penetrating keratoplasty and penetrating keratoplasty combined with intracapsular cataract extraction were reviewed in a prospective fashion with a minimum of a one-year follow-up. Five were lost to follow-up. There were seven graft failures at the end of one year. Five of these were from 11 patients who underwent second operations because of failed grafts. Visual acuity was 20/80 or better in 29 of the patients. Pathology accounted for decreased visual acuity in all of those with visual acuity less then 20/80. Problems wre macular degeneration in 11 of the 23 patients with poor visual acuity (48%); marked cystoid macular edema in four patients (17%), advanced glaucoma in three patients (13%) and amblyopia in three patients (13%). Graft size had no significant effect on visual acuity. In terms of the final refractive error and astigmatism, there were no significant differences seen in those in whom a larger donor was used compared with those in whom a donor the same size as the recipient opening was used. Aphakic penetrating keratoplasty has shown outstanding technical success with poor visual acuity representing a difficulty in screening for non-corneal pathology. With an otherwise normal eye, the chances for excellent optical success are very good at the present time with modern techniques in aphakic penetrating keratoplasty.

Fluorophotometry and the blood-ocular barrier in experimental systemic hypertension.

Fluorophotometry was used to evaluate alterations in the blood-ocular barrier to fluorescein in rats with experimental hypertension. One hour after intravenous injection of fluorescein, 16.6 mg/kg, concentrations in the anterior chamber were increased from mean normotensive values of 135 micrograms/mL to 299 micrograms/mL (P = .005) in animals with severe hypertension. Fluorescein concentrations in the vitreous also were increased from 50 micrograms/mL in normotensive rats to 109 micrograms/mL (P = .005) in hypertensive animals. With increasing duration of systemic pressures above 160 mm Hg, anterior chamber fluorescein concentrations rose from base-line of 135 micrograms/mL to 210 micrograms/mL after one to four weeks of hypertension, and to 394 micrograms/mL after five to eight weeks (P = .005). Similarly, vitreous concentrations increased from baseline of 50 micrograms/mL to 76 micrgrams/mL and 136 micrograms/mL (P = .005) after the shorter and longer periods of hypertension. Control of hypertension with return of systolic pressure to below 120 mm Hg caused a reversal of the abnormal fluorescein permeability.