A specific form of glaucoma secondary to uveitis —- Glaucoma ciliary syndrome Glaucoma ciliary syndrome (GCS), also known as glaucoma ciliary crisis, is a specific form of anterior uveitis with glaucoma, mainly seen in young adults aged 20-50 years, characterized by non-granulomatous uveitis with marked IOP elevation. It is characterized by non-granulomatous uveitis with markedly elevated intraocular pressure, with an acute onset, mostly monocular, recurrent, and associated with exertion, especially mental fatigue and stress; the mechanism of occurrence is a prostaglandin-mediated inflammatory response. The mechanism of inflammation is prostaglandin-mediated inflammation. The clinical manifestations of inflammation are mild, the local congestion is very mild, and the IOP is elevated, usually with little effect on vision. Glaucomatous ciliary syndrome is a recurrent form of monocular glaucoma combined with ciliary cystitis. Originally described by Posner and Schlossmann, it is characterized by unilateral, recurrent episodes of mildly reduced visual acuity, moderately elevated intraocular pressure, an open atrial angle, and a small amount of grayish KP, hence the name Posner-Schlossmarm syndrome. It has been reported mostly since 1948 as a separate eye disease and has been studied in various aspects. Epidemiology Glaucoma ciliary syndrome can occur in any region and of any race and is a rare disease, about which the incidence and prevalence are not known and which accounts for a low percentage of the overall uveitis. The age of onset of the disease is 11 to 69 years, but it occurs mostly in young adults. Patients tend to have monocular involvement, with a few patients presenting with bilateral involvement, but the manifestations can be asynchronous. The pathogenesis of the disease is based on clinical and experimental studies, which have demonstrated that the disease is due to increased atrial fluid production and decreased atrial fluid flow coefficient. PGS increases the vasodilatation of the uvea and increases the permeability of the blood-atrial water barrier, leading to increased atrial water production and anterior segment inflammation. The decreased atrial fluid fluency coefficient may be related to the constraint of catecholamines by PGS. It is well established that endogenous catecholamines, especially norepinephrine, act on alpha receptors and are important mediators in regulating and promoting atrial fluid efflux. Animal studies have shown that in the presence of increased PGE, the release of norepinephrine from sympathetic nerve endings is significantly inhibited in many organs; at the same time, PGS acts on the receptors and directly antagonizes the biological effects of norepinephrine, thus depriving the organ of the normal physiological functions maintained by norepinephrine. When glaucomatous ciliary dyskinesia strikes, the filtration curtain loses its normal regulation due to increased PGS in the atrial fluid, possibly through its dual inhibitory effect of norepinephrine, leading to a decrease in the fluency coefficient. Moreover, when IOP is significantly elevated, mechanical compression of the filter curtain, in turn, increases the resistance to atrial fluid drainage, resulting in a significant increase in IOP. The pathogenesis of the disease may also be complicated by the finding that cyclic guanosine monophosphate (GMP) and calcium ions can affect IOP, and that there is an intricate relationship between PGS, cAMPGMP, Ca, and catecholamines. The disease can be combined with bilateral primary open-angle glaucoma, suggesting that there are other factors. In particular, the attacks are often emotionally stressful, possibly due to autonomic nervous system dysregulation, and sympathetic excitation may also be an important factor in the excitation. Clinical manifestations 1, monocular onset and recurrent attacks in the same eye, occasionally both eyes are involved. 2. Episodes of elevated intraocular pressure are recurrent, with intervals of several months to 1~2 years. IOP can be as high as 5.33~8.0kPa (40~60mmHg), and the duration of each episode of high IOP is usually 1~14 days, which can recover on its own, a few continue for a month, and rarely for two months. 3. There are no conscious symptoms during the attack, only mild discomfort, and even at the peak of the attack, there are no obvious symptoms such as headache and eye pain like acute angle-closure glaucoma. 4, vision is generally normal, such as corneal edema, then blurred vision. 5. The pupil is slightly enlarged during the attack and the response to light is present. Although there are repeated episodes of mild ciliary cystitis, post-iris adhesions never occur. 6. Each episode presents with mild ciliary cystitis often within 3 days of the onset of hypertension, with a few cells floating in the atrial fluid and often negative atrial flash. The posterior corneal wall deposits often appear within 3 days after the attack and are grayish white, small or large and flat, suede shaped, usually no more than 25, set in the lower l/3 of the cornea or hidden in the atrial trabecular meshwork. They disappear within a few days to a month after the IOP returns to normal. KP may or may not reappear when IOP fluctuates, so a full detailed examination should be performed. 7. There are no inflammatory cells in the vitreous. 8, The anterior chamber angle is open in the high IOP state, and there is no peripheral iris anterior adhesion. 9, The fundus is generally normal. If coexisting with primary open angle glaucoma, glaucomatous optic nerve and visual field damage may occur. However, in acute attacks of the disease, there may be an enlargement of the dark shadow of the blood vessels. 10. The “C” value is low in the high IOP state, and the “C” value and IOP return to normal in the interval and are negative for various excitation tests. This disease can coexist with primary open angle glaucoma. Treatment Glaucoma ciliary syndrome is a self-limiting eye disease, but can recur. Topical corticosteroids applied during episodes can control the progression of inflammation. High IOP requires oral carbonic anhydrase inhibitors. The administration of anti-inflammatory pain inhibits PG biosynthesis and may achieve partial hypotensive effect in the treatment of this syndrome. Flufenamic acid not only inhibits PG biosynthesis, but also directly counteracts the biological effects of PG, so it is better than anti-inflammatory pain. Topical application of epinephrine and thimerosal also helps to lower IOP. Surgery is not recommended for glaucomatous ciliary dyskinesia syndrome because surgery cannot prevent its recurrence. However, it should be closely monitored and followed up for a long time. If it is combined with primary or secondary open-angle glaucoma, surgery should be considered if the visual function is at risk.