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Abstract #6108 Published in IGR 2-2

Hemorrhage of the optic disk in normal-tension glaucoma (comment) (editorial)

Shields MB
American Journal of Ophthalmology 2000; 129: 796-797


This editorial deals with disc hemorrhages provoked by a paper of Ishida et al. Splinter hemorrhages typically occur in the inferotemporal or superotemporal margin of the optic nerve head. They come and go, and their accumulated incidence may be as high as 33% in normal tension glaucoma and 10% in patients with open-angle glaucoma. In fact, in the Ishida paper, the incidence is even higher than 33%. What is the mechanism leading to bleeding? Does it represent a primary vascular disorder or is it the result of mechanical shearing? Or is it caused by IOP? What is the meaning of the presence of a hemorrhage for the management of glaucoma? Ishida et al. followed 70 patients for an average of 5.6 years. Of the two end points: mean defect deterioration of more than 3 dB, or point-wise depression of 10 dB or more in two contiguous points/5 dB in three contiguous points, the focal loss was the more sensitive indicator of visual field change. Of the 70 eyes, 32 had at least one disc hemorrhage. Visual field progression was found in 45% of cases without hemorrhage and in 81% in cases with hemorrhage, and in all 23 cases (30%) of eyes with recurrent hemorrhages. In most cases, the disc hemorrhages preceded visual field loss by 1.5 years. Interestingly, the location of the disc hemorrhage was only correlated with the field defect in two of three eyes. Does the presence of a disc hemorrhage present a pressure-dependent or a pressure-independent mechanism? Other causes of disc hemorrhages should be excluded, such as ischemic optic neuropathy, papillitis, central retinal vein occlusion, diabetic retinopathy, and posterior vitreous detachment. Vascular or hematological abnormalities may also be found, such as small vessel disease, recent blood loss, recent medical reduction of systemic blood pressure, anemia or other blood disorders. The author considers a pressure-independent neuroprotective agent, indicating that he definitely feels that a pressure-independent mechanism is operating. The only approved neuroprotector is a calcium channel blocker. He feels it may be reasonable to try a therapeutic trial of a calcium channel blocker in some patients.


Classification:

9.2.2 Other risk factors for glaucoma (Part of: 9 Clinical forms of glaucomas > 9.2 Primary open angle glaucomas)



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