Rate of visual field loss in progressive glaucoma.

OBJECTIVE: To investigate the rate of visual field (VF) loss in progressive glaucoma. SETTING: Outpatient department, nonreferral base. METHODS: A cohort of 34 patients with normal-pressure glaucoma (NPG), 68 patients with primary open-angle glaucoma (POAG), and 125 patients with ocular hypertension (OHT) were followed up for an average of 9 years. Visual fields were obtained annually with automated perimetry. The rate of VF loss as a percentage per year was calculated. RESULTS: Twenty-three eyes with NPG, 31 with POAG, and 10 with OHT showed progression of VF loss. The mean (+/-SD) rates of VF deterioration were 3.7%+/-3.3% per year in NPG, 2.5%+/-1.8% in POAG, and 2.3%+/-1.3% in OHT converting to POAG, and did not differ significantly. No difference in the rate of VF loss was found between eyes with and without optic disc hemorrhages (2.7%+/-2.9% and 3.1%+/-2.1%, respectively). The rate of VF loss was not related to the initial VF status. The rate of VF loss between the superior and inferior hemifields was correlated in patients with NPG (r(s) = 0.67, P = .04). Comparison of visual field loss with linear regression analysis showed significant slopes in only 37.5% of eyes with progression, which had a progression rate of 4.2%+/-3.0%. CONCLUSIONS: The rate of VF loss did not differ between patients with NPG and POAG. The rate of deterioration was related neither to initial VF status nor to the presence of disc hemorrhages. Linear regression is applicable only in a portion of the patients who have progression of VF loss.

[Four new drugs for glaucoma: apraclonidine, brimonidine, dorzolamide and latanoprost]. / Vier nieuwe geneesmiddelen bij glaucoom: apraclonidine, brimonidine, dorzolamide en latanoprost.

Glaucoma is in most of cases initially treated with drugs, viz. beta-blocking agents, miotics, sympathicomimetics and carbonic anhydrase inhibitors. The therapy of first choice is a beta-blocking agent, but in approximately 50% of the patients treated the effect becomes inadequate with time and combination therapy is necessary. Recently, four new antiglaucomatous agents have become available: apraclonidine, brimonidine, dorzolamide and latanoprost. Apraclonidine, an alpha 2-adrenergic agonist, is indicated for brief episodes of postlaser rise of the intraocular pressure. Longer treatment may lead to tolerance. Brimonidine, another alpha 2-adrenergic agonist, is indicated for long-term treatment of glaucoma; tolerance does not often occur. Dorzolamide is a local carbonic anhydrase inhibitor which lacks the systemic side effects seen after oral administration of carbonic anhydrase inhibitors. Latanoprost, a prostaglandin F2 alpha-derivative induces an effective decrease of the intraocular pressure if administered as monotherapy and has a good efficacy when combined with other drugs lowering the intraocular pressure. The new antiglaucomatous agents are a welcome addition to the pharmacotherapy, since in many cases they make it possible to postpone or avoid surgery.

Deterioration of visual fields in patients with glaucoma with and without optic disc hemorrhages.

OBJECTIVE: To evaluate visual field deterioration in patients with glaucoma with and without optic disc hemorrhages (DHs). DESIGN: A prospective study at quarterly base involving annual perimetry; mean follow-up of 9 years. SETTING: Outpatient department, nonreferral basis. PATIENTS: Sixty-eight patients with primary open-angle glaucoma, 34 with normal pressure glaucoma (NPG), and 125 with ocular hypertension. RESULTS: Visual field deterioration occurred in 32%, 32%, and 6% of the patients without DHs who had NPG, primary open-angle glaucoma, or ocular hypertension, respectively, while visual field deterioration occurred in 80%, 89%, and 14% of patients with DH, respectively. Cox proportional hazards ratio(CHR) for deterioration in patients with vs patients without DHs was 5.4 for NPG (P<.01) and 3.6 for primary open-angle glaucoma (P<.01). In patients with NPG and DHs, ipsilateral eyes with DHs deteriorated in 58%, while contralateral eyes without DHs deteriorated in 11% (CHR, 8.9; P<.04). For primary open-angle glaucoma and ocular hypertension, progression did not differ between eyes with DHs and contralateral eyes without DHs. Mean (+/-SD) interval between DHs and ipsilateral visual field deterioration was 3.1+/-1.7 years. No difference in the proportion of eyes progressing after single or recurrent DHs was noted. The position of DHs was related to the site of the visual field loss in 44% of the eyes. CONCLUSIONS: The presence of DHs increased the risk of visual field deterioration. Disc hemorrhages were indicative only of deterioration in ipsilateral eyes in patients with NPG.

Cumulative incidence of patients with disc hemorrhages in glaucoma and the effect of therapy.

PURPOSE: In this longitudinal study, the cumulative incidence of patients with glaucoma and disc hemorrhages was investigated. A possible effect of glaucoma therapy on the incidence rate of disc hemorrhages was evaluated. METHODS: A group consisting of 68 patients with primary open-angle glaucoma (POAG), 34 with normal-pressure glaucoma, and 125 with suspected glaucoma (mean follow-up, 7.3 +/- 2.5 years; range 3-13 years) was observed closely with quarterly examinations. RESULTS: In normal-pressure glaucoma, the cumulative incidence of patients with disc hemorrhages was 35.3%, which was significantly higher than for those with POAG (10.3%; P < 0.01) and for those with suspected glaucoma (10.4%; P < 0.001). The mean follow-up period before a first disc hemorrhage was detected was 2.5 +/- 2.8 years. In the bleeders, recurrent disc hemorrhages were observed in 67% of the patients with normal-pressure glaucoma, 29% of those with POAG, and 54% of glaucoma suspects. In normal-pressure glaucoma, therapy had no effect on the incidence rate of disc hemorrhages. In glaucoma suspects, a significant reduction of the incidence rate of disc hemorrhages per year (0.11 +/- 0.04) was observed during episodes with therapy compared with episodes without (0.43 +/- 0.15; P < 0.05). A concept of two populations (i.e., one with disc hemorrhages and the other never having them) seems to be valid for normal-pressure glaucoma, but not for POAG and suspected glaucoma. CONCLUSION: The cumulative incidence of initial disc hemorrhages increases with time in POAG and suspected glaucoma, but reaches a limit in normal-pressure glaucoma. Glaucoma therapy may reduce the incidence rate of all, initial and recurrent, disc hemorrhages in patients with high pressures, but not in patients with normal-pressure glaucoma.

Effects of endotoxemia on systemic plasma loss and hematocrit in rats.

Endotoxemia in rats increases plasma extravasation but does not result in continuously rising hematocrit. These contradictory observations led us to design a study in anesthetized rats (C, control rats, n = 10; E, endotoxin rats, n = 10) in which we continuously measured in blood hematocrit (conductivity cell) and changes in concentration of 125I-HSA (human serum albumin) and 51Cr-labeled red cell (51Cr-RBC; multichannel analyzer) in an extracorporeal circuit. In two additional series of experiments we measured in blood samples changes in protein concentration (series II, C: n = 7, E: n = 7) and uptake of intraperitoneally injected 125I-HSA and 51Cr-RBC (reflecting lymph flow rate; series III, C: n = 6, E: n = 7). Endotoxemia was induced by infusion (iv, 0.2 ml/100 g.hr) of Escherichia coli endotoxin (20 mg/kg) from t = 0 to t = 60 min; controls received saline. Experiments ended at t = 120 (series I and II) or 150 min (series III). The endotoxemia resulted in a marked rise of serum lactate (by ca 500% at t = 120); heart rate increased and central venous pressure decreased (by ca 20 and -95% at t = 120, respectively). All rats showed characteristic changes in hematocrit during endotoxemia: an increase from t = 20 to t = 45 (by ca 9%) followed by a decrease to preshock values or less at t = 120. The 51Cr activity per microliter blood cells did not change, indicating that there was no red cell mobilization. Protein concentration and 125I-HSA activity also showed a temporary increase during endotoxemia, but 125I-HSA activity per gram protein was decreased. Peritoneal uptake of 125I-HSA and 51Cr-RBC was significantly increased during endotoxemia (by 200%). We conclude that fluid extravasation during endotoxemia is temporary, mainly concerns plasma water, and is compensated by mechanisms like reabsorption and increased lymph flow, resulting in restoration of plasma volume.