Hartmann K, Meyer-Schwickerath R
Department of Strabismus and Neuroophthalmology, University Eye Hospital, Aachen, Germany.
Strabismus. 2000 Sep;8(3):187-93.
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.
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.
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.
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.
评估格雷夫斯眼病（GO）患者的眶内压与眼压（IOP）及眼球突出的关系，并探究视神经压迫是否可预测。
采用先前描述的眼血流动力学测量技术测量视网膜中央静脉的静脉流出压（VOP）。由于视网膜中央静脉穿过眼眶，若要保证血液流出，VOP不能低于眶内压。在第一眼位或轻微抬头位测量IOP，以避免眼球受限。57例患者接受了全面的眼科检查，包括VOP测量、Hertel眼球突出计测量和视野检查。
第一眼位的IOP在10至29 mmHg之间，大多数（n = 54）病例中VOP比IOP高0至4 mmHg。在长达2年的观察期内，这些患者既没有暗点也没有视力下降。在那些IOP与VOP差值为35 mmHg的病例（n = 3）中，患者出现了暗点和视力下降，必须接受治疗（高剂量类固醇或眼眶减压）。VOP升高与眼球突出程度无关。在一例单侧病例中，用多佐胺滴眼液治疗高眼压（32 mmHg）导致视力下降两行、下方视野缺损和相对传入性瞳孔障碍。IOP与VOP的差值为10 mmHg。停止治疗后视觉功能恢复正常，IOP升至原来水平，IOP与VOP的差值为4 mmHg。
GO患者眼压升高不是由原发性青光眼引起的，而是由眶内压升高所致。IOP与VOP的差值必须<5 mmHg才能保证正常灌注。我们认为这些发现表明视力丧失和视野缺损可能不仅是由眶尖处的视神经压迫引起的，还可能是由视神经乳头灌注恶化引起的。
