Preliminary research of the clinical pathways of glaucomatous optic nerve damage in cases with glaucomatocyclitic crisis: A retrospective study.

Abstract

To investigate the clinical pathways via which the glaucomatous optic nerve damage (GOND) occurred in cases with glaucomatocyclitic crisis (also called Posner-Schlossman syndrome, PSS). A retrospective study was conducted, 59 PSS patients with confirmed GOND were screened out from 190 PSS cases and followed up for a period of 5 ± 3.3 years. Clinical data were retrospectively analyzed systematically and dynamically, including intraocular pressure and its dynamic change, appearance of fundus, visual field and the state of anterior chamber angle in initial and later period during the episodes and intermission of PSS. Based on the clinical data, a classification and standard for the clinical pathways of GOND were established, and the clinical pathway of GOND in each patient was classified accordingly. There are at least 4 clinical pathways of GOND in PSS patients, namely: Type A: GOND was simply caused by the accumulation effect of high IOP during many attacks of PSS itself. Type B: GOND was resulted from the combined action of PSS itself and another type of secondary open-angle glaucoma. The recurrent inflammation during the episodes of PSS damaged the trabecular meshwork, which can cause elevation of IOP during the intermission of PSS. Type C: PSS combined with primary open angle glaucoma (POAG). Type D: PSS combined with primary angle-closure glaucoma (PACG). Base on the clinical gateways of GOND classification above, the cases of type A, B, C, and D were 27, 6, 19, and 7 respectively. The staging of visual field damage in cases with GOND from different clinical pathways showed a significant difference (Person chi-square χ2 test, χ2 = 7.211, P = .007). There are at least 4 clinical pathways of GOND in PSS patients, and each clinical pathway corresponds to different clinical features and different treatment principles. It is extremely important to correctly discriminate the pathways of GOND in PSS patients.