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Primary Angle-Closure Glaucoma

Chunhui Jiang, MD, PhD and Xinghuai Sun, MD, PhD

Glaucoma is a multifactorial optic neuropathy, and vascular factors have been suggested as being significant contributors to the development and progression of primary open-angle glaucoma (POAG),^1,2 normal-tension glaucoma, and ocular hypertension. On the other hand, another distinct type of glaucoma, primary angle-closure glaucoma (PACG), may cause bilateral blindness and remains the predominant form of glaucoma in East Asia.³ Using optical coherence tomography angiography (OCTA), retinal perfusion in PACG eyes was studied. Here we present our results of 2 separate studies carried out on 2 different groups of PACG eyes. In the first study, we examined the perfusion of the peripapillary area in a group of acute PACG eyes that had just recovered from an acute attack, and also compared them with a group of POAG eyes with similar visual field damage. The second study focused on the change in perfusion at different parts of the fundus, the disc, and macular regions, by measuring the retinal perfusion in another group of PACG eyes.

REDUCED PERFUSION IN ACUTE PRIMARY ANGLE-CLOSURE GLAUCOMA

A group of PACG eyes that had just recovered from an acute attack was recruited. OCTA was examined with a spectral domain OCT system (Avanti RTVue XR, Optovue Inc) using AngioVue OCTA software version 2015.1.0.90. Optic disc (4.5 × 4.5 mm) OCTA scans were acquired. The peripapillary region was defined as a 700-μm-wide elliptical annulus extending outward from the optic disc boundary (Figure 33-1A). The boundary of measurement was set from internal limiting membrane (ILM) to the outer border of the retinal nerve fiber layer (NFL). The system automatically provided the vessel area density of the peripapillary area. The vessel area density was defined as the proportion of the total area occupied by vessels.^4,5 Compared to normal controls, the PACG eyes showed significantly reduced retinal perfusion in the peripapillary area (mean reduction 14.5%; Figures 33-1A and 33-1B; Table 33-1). Yet the PACG group demonstrated almost normal retinal nerve fiber layers in the peripapillary area. One possible explanation is that vascular changes precede damage of the NFL in PACG eyes, but there could be other explanations. For example, high intraocular pressure (IOP) during an acute attack could cause ischemic optic neuropathy leading to optic nerve edema.^6,7 On the other hand, earlier studies found that increasing IOP could have resulted in significant retrodisplacement of the lamina through which the optic nerve passes, which might cause direct damage to the nerve fibers, as well as compromise blood flow.^8–10 These changes might also lead to optic nerve edema. The presence of edema in the disc area was supported by the discovery that after controlling for IOP, the NFL in the PACG group still decreased during follow-up.6,7 The decrease in NFL thickness during follow-up could be caused either by the subsiding of edema or by damage due to reduced perfusion.

As reduced perfusion has also been recorded in POAG eyes, we thought it might be interesting to compare the 2 types of glaucoma to see if they involve a similar change in retinal perfusion. Using the same system and software as above, a group of POAG eyes with similar glaucoma damage was recruited. Compared to POAG eyes, the perfusion in PACG eyes seemed to be evenly reduced. In POAG eyes, on the other hand, perfusion was much lower in the inferior temporal area than in other parts of the eye (Table 33-2). This is in accordance with the frequent superonasal visual field damage in POAG eyes,¹¹ and despite a similar mean deviation in the visual field results, the PACG group had a much smaller pattern standard deviation (P = 0.001). The reason for the different changes in perfusion and visual field in these two types of glaucoma was not fully understood. Here is a possible explanation. Hayreh¹² pointed out that in the peripapillary choroid, the obliteration caused by high IOP was usually more marked in the superior and inferior parts and less in the temporal and nasal. As the disc and peripapillary area also receives blood flow from the choroid,¹³ although we did not measure choroid perfusion this time, vessels in a different part of the disc area might respond differently to high IOP. As in POAG eyes, the IOP was usually moderately elevated, and the difference in vessels could be demonstrated. However, in PACG eyes, the IOP at the acute attack could far exceed the normal level, so all vessels might be affected. Future studies that include measurement of choroid blood flow might be able to tell us more. However, in a group of eyes with more severe glaucoma, Sihota et al¹⁴ observed a different pattern. In their study, POAG eyes showed diffuse damage on fluorescein angiography, while chronic PACG eyes demonstrated sectoral damage.14 The reason for the difference between the studies is not fully understood, but different methods used to study perfusion, different types of glaucoma, and differences in the severity of optic nerve damage might all be contributing factors.

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