The effect of nifedipine on retinal venous pressure of glaucoma patients with the Flammer-Syndrome.

PURPOSE: The purpose was to measure the retinal venous pressure (RVP) in both eyes of primary open-angle glaucoma (POAG) patients before and 3 weeks after treatment with low-dosed Nifedipine. METHODS: This retrospective study included 20 POAG patients who were treated with Nifedipine (5 mg daily) and 20 untreated control POAG patients. In both the treated and untreated control group, a distinction was made between those patients who had the Flammer-Syndrome (FS) and those who did not. The RVP was measured in all patients bilaterally at baseline and 3 weeks later by means of contact lens ophthalmodynamometry and the RVP measurements of the treated POAG patients were compared to the RVPs of the untreated POAG controls. Ophthalmodynamometry is done by applying an increasing force on the eye via a contact lens. The minimum force required to induce a venous pulsation is called the ophthalmodynamometric force (ODF). The RVP is defined and calculated as the sum of ODF and intraocular pressure (IOP) [RVP = ODF + IOP]. RESULTS: The RVP decreased significantly after 3 weeks in both eyes of patients treated with low-dosed Nifedipine compared to the untreated group (mean decrease of 12.5 mmHg (SD 12.5), P < 0.001). A larger response to therapy was found in patients with the FS compared to patients lacking the FS (mean decrease of 16.07 vs. 7.28 mmHg, confidence Interval (CI): 5.2 to 9.3 vs. 12.3 to 19.7; P < 0.001). No significant differences were accounted for in the IOP's of the patients after treatment. In the untreated control group, no significant differences were accounted for either in the RVP or the IOP after 3 weeks. CONCLUSIONS: Treatment with low-dosed Nifedipine decreases RVP in both eyes of glaucoma patients, particularly in those with the Flammer-Syndrome. This effect may be due to the partial inhibition of Endothelin-1 (ET-1) by Nifedipine.

Effect of retrobulbar versus subconjunctival anaesthesia on retrobulbar haemodynamics.

AIM: To investigate the effect of retrobulbar and subconjunctival anaesthesia on retrobulbar haemodynamics by colour Doppler imaging. METHOD: 39 patients (mean age 71 (SD 9) years; 19 females, 20 males) undergoing planned cataract surgery were included in the prospective study. Colour Doppler imaging (Siemens Sonoline Sienna, Germany) was performed before, directly after either subconjunctival (16 patients) or retrobulbar (23 patients) anaesthesia, and after cataract surgery to measure the peak systolic (PSV) and end diastolic velocities (EDV) in the ophthalmic artery (OA), central retinal artery (CRA), and central retinal vein (CRV). RESULTS: After retrobulbar anaesthesia there was a significant reduction of the PSV and of the EDV in all investigated vessels. After surgery the flow velocities increased again. Subconjunctival anaesthesia had no significant effects on retrobulbar haemodynamics. CONCLUSION: Retrobulbar anaesthesia induces a high reduction of velocity in the retrobulbar vessels in contrast with subconjunctival anaesthesia. Therefore subconjunctival anaesthesia should be preferred particularly in patients with problems of the ocular perfusion (for example, glaucoma).

Venous collateral remodeling in a patient with posttraumatic glaucoma.

PURPOSE: To photographically document venous collateral development, remodeling, and regression in a patient with traumatic glaucoma. METHODS: Consecutive fundus photographs were evaluated, labeled, and correlated with the clinical history of a patient with unilateral posttraumatic glaucoma. RESULTS: This report photographically documents the appearance, remodeling, and subsequent disappearance of collateral vessels from venous occlusion on the surface of the optic disk in an eye with increased intraocular pressure and progressive glaucomatous cupping. CONCLUSIONS: Asymptomatic chronic obstruction of a branch retinal vein on the optic disk may cause venous collaterals to develop in the absence of retinal hemorrhages or other signs of venous occlusive disease. Increased intraocular pressure, arteriolarsclerosis, and glaucomatous cupping are risk factors for these occlusions.

Solitary silent venous papillary loops and ocular hypertension.

A series of 24 eyes in 23 patients is described showing solitary silent venous papillary loops. These loops are usually associated with a considerable degree of ocular hypertension, presenting when this hypertension is being investigated. They are silent, usually with no previous ocular history, single with a large diameter, affecting veins at the optic disc and not extending into the vitreous. The optic disc is cupped, but usually not more than 0.6 disc diameter, there is good central vision and either a full visual field or only early field loss. Fluorescein angiography shows the loops to be competent with no evidence of any other retinal vascular abnormality. Rarely loss of central vision may occur due to progression to advanced glaucoma. The condition is distinct from prepapillary vascular arterial papillary loops, neovascularization at the optic disc and optociliary shunt vessels. It is also distinct from the venous collateral vessels which develop at the optic disc after acute central or branch retinal vein occlusion. These collaterals are usually multiple, the accompanying ocular hypertension is of lesser degree, cupping of the disc and field loss are usually much more advanced and, while visual acuity may be normal, it is often grossly reduced. On fluorescein angiography all these cases of venous collaterals after retinal vein occlusion showed evidence of other retinal vascular dysfunction. Solitary silent venous papillary loops appear to develop from venules on the optic disc as a bypass to a low grade venous occlusion which is seldom clinically manifest. They form a distinct entity with a good prognosis if the accompanying ocular hypertension is carefully controlled.