Measurement of venous outflow pressure in the central retinal vein to evaluate intraorbital pressure in Graves' ophthalmopathy: a preliminary report.

PURPOSE

To evaluate the intraorbital pressure in patients with Graves' ophthalmopathy (GO) in relation to the intraocular pressure (IOP) and proptosis and to find out whether optic nerve compression is predictable.

METHODS

The venous outflow pressure (VOP) in the central retinal vein was measured by the perviously described technique of oculodynamometry.1 Since the central retinal vein passes through the orbit, the VOP cannot be lower than the intraorbital pressure if outflow is to be guaranteed. The IOP was measured either in primary position or with slight chin elevation to avoid restriction of the globe. Fifty-seven patients underwent a complete ophthalmologic examination, including VOP measurements, Hertel exophthalmometry and visual fields.

RESULTS

The IOP in primary position ranged between 10 and 29 mmHg and in most (n=54) cases the VOP was 0-4 mmHg higher than the IOP. These patients had neither scotomas nor visual deterioration during an observation period of up to 2 years. In those cases (n=3) where the difference between IOP and VOP was 35 mmHg, the patients developed scotomas and visual deterioration and had to be treated (high-dose steroids or orbital decompression). The elevation in VOP did not correlate with the degree of proptosis. In one unilateral case, treatment of high IOP (32 mmHg) with dorzolamide drops led to a decrease in visual acuity of two lines, inferior field depression and relative afferent pupillary defect. The difference between IOP and VOP was 10 mmHg. Stopping treatment normalized visual function, the IOP rose to its original level and the difference between IOP and VOP was 4 mmHg.

CONCLUSION

The increased IOP in GO is not caused by primary glaucoma but by elevated intraorbital pressure. The difference between IOP and VOP must be <5 mmHg to guarantee normal perfusion. We interpret these findings to suggest that loss of visual acuity and visual field defects may not only be caused by optic nerve compression at the apex but also by deterioration of optic nerve head perfusion.