Glaucomatous optic neuropathy (GON) is morphologically characterized by an almost pathognomonic loss of neuroretinal rim, a deepening of the optic cup, thinning of the peripapillary retinal nerve fiber layer, development and enlargement of parapapillary beta zone, focal and diffuse thinning of the retinal arterioles, and optic disc hemorrhages (DHs). After Stephan Drance had alerted the scientific community to the association of DHs with GON, numerous studies have examined the prevalence and incidence of disc hemorrhages in eyes with GON and their associations with other morphological and psychophysical parameters. These investigations revealed that the DHs, although being highly significantly associated with the presence and progression of GON, are not pathognomonic for GON but can occur in a variety of disorders and diseases including posterior vitreous detachment from the optic nerve head, that the number and size of detected DHs is significantly higher in so-called normal-pressure glaucoma than in high-pressure glaucoma, that they remain ophthalmoscopically visible for about one to three months, and that they indicate with a high probability a progression of the glaucomatous process at the site of the DH in eyes with GON, to mention only few of the findings. All these studies were limited in the sense that they assessed the ophthalmoscopically visible DHs. DHs smaller than the spatial resolution of their ophthalmoscopical detectability remained undetected. Since however the event leading to the hemorrhage, such as a vessel break, may be more important than the size of the bleeding, the limitation of the ophthalmoscopical detectability of the DHs might have led to a marked bias in the whole discussion of the pathogenesis of glaucomatous DHs and their importance for GON. To cite an example, the lower intraocular pressure in eyes with normal-pressure glaucoma as compared to eyes with high-pressure glaucoma leads to an higher transmural pressure difference in the retinal arterioles of eyes with normal-pressure glaucoma, so that a vessel break leads to a larger DH in eyes with normal-pressure glaucoma. Due to their larger size, the DHs in eyes with normal-pressure glaucoma remain longer detectable so that the frequency of their ophthalmoscopical detection is higher.
To overcome these limitations of the preceding studies, Ahnul Ha and colleagues used a customized image-compensation software to enhance stereo disc photographs to detect micro-DHs defined by a size of less than 0.01-mm2 and being undetectable on conventional stereo disc photographs. Among 107 eyes with primary open-angle glaucoma and with macro-DHs, the authors found micro-DHs prior to the macro-DHs in 37% of the eyes, with a median time lag between both hemorrhages of 13.6 months. During a follow-up of 7.1 ± 0.8 years, a perimetric progression of GON was detected in 54% of the eyes with micro-DHs and in 28% of the 68 eyes without micro-DHs (P = 0.008).
During a follow-up of 7.1 ± 0.8 years, a perimetric progression of GON was detected in 54% of the eyes with micro-DHs and in 28% of the 68 eyes without micro-DHs (P = 0.008).
The differences between the micro-DHs positive group and the micro-DH-negative group in the cumulative perimetric progression probability (P = 0.001) and in the overall visual field deterioration rate (−1.01 ± 0.58 vs. −0.78 ± 0.49 dB/year; P = 0.029) were signific
The technique applied by Ha and colleagues and the findings may open a new avenue for a more precise detectability of DHs in eyes with glaucoma, for a better understanding of the etiology of DHs in the process of GON, and for a better clinical diagnosis of the presence and progression of GON.