Glaucoma-cyclitis syndrome

Introduction to glaucoma and ciliary body syndrome Glaucoma ciliary inflammatory syndrome (hereinafter referred to as cyanotic-ciliary syndrome), also known as Posner-SchlMsman syndrome, is a recurrent monocular glaucoma with ciliary inflammatory disease characterized by unilateral, recurrent, and low vision. Decreased, moderate intraocular pressure, open angle, a small amount of gray-white KP, the disease occurs in 20 to 50 years old, more than 50 years old are rare, more than 60 years old are more rare. basic knowledge The proportion of illness: 0.032% Susceptible people: no specific population Mode of infection: non-infectious Complications: primary open angle glaucoma pigmented glaucoma

Causes of glaucoma and ciliary body syndrome

(1) Causes of the disease

The cause of the disease is not well understood. Some people think that it may be related to allergic factors, focal infection, hypothalamic disorder, autonomic dysfunction, abnormal ciliary vascular nervous system reaction and abnormal anterior chamber angle. The concentration of prostaglandin (PG), especially PGE, increased significantly.

(two) pathogenesis

In recent years, according to clinical and experimental studies, it is proved that the disease is caused by increased water production and a decrease in the fluency coefficient of aqueous humor. It is also found that the content of prostaglandins (PGS) in the aqueous humor is significantly increased when the disease occurs, and the disease is reduced to normal after the disease is relieved. PGS can make uveal vasodilatation, increase the permeability of blood-aqueous barrier, lead to increased aqueous humor production and anterior segment inflammation. The decrease of aqueous humor flow coefficient may be related to the inhibition of catecholamine by PGS, and the endogenous catecholamine has been confirmed. In particular, norepinephrine acts on alpha receptors and is an important mediator for regulating and promoting the excretion of aqueous humor. Animal experiments have shown that in the case of increased PGE, the release of norepinephrine from sympathetic nerve endings in many organs is significantly inhibited; It can act on the receptor and directly antagonize the biological effects of norepinephrine, so that the organ loses the normal physiological function maintained by norepinephrine. When glaucomatous ciliary body inflammation occurs, it may pass due to the increase of PGS in the aqueous humor. Its dual inhibitory effect of norepinephrine causes the filter curtain to lose its normal regulation, resulting in a decrease in the fluency coefficient and When significantly increased, mechanical compression of the filter curtain, and increased drainage resistance, resulting in a significant increase in intraocular pressure, recently discovered cyclic guanosine monophosphate (GMP), calcium ions can affect intraocular pressure, and PGS, cAMP GMP, There is an intricate relationship between Ca and catecholamines, so the pathogenesis of this disease may be complicated. This disease can be combined with primary open angle glaucoma, indicating that there are other factors, especially when the episode is often in emotional stress. It may be an autonomic nervous system disorder, and sympathetic excitation may also be an important factor in the stimulation.

Glaucoma ciliary inflammatory syndrome prevention

In the early stage of the disease, the patient should return to the clinic every few days, and then review it every week until the condition recovers. The acute attack usually resolves after several hours to several weeks. In addition, the possibility of chronic open angle glaucoma in both eyes should be guarded.

Complications of glaucoma and ciliary body syndrome Complications: primary open angle glaucoma pigmented glaucoma

Primary open angle glaucoma

This type of patient is bilateral glaucoma, one of which is blue-cyan syndrome, the latter is always ipsilateral, but the other eye has a clear primary open angle glaucoma: high intraocular pressure, aqueous humor flow coefficient Low, the drinking water test is positive, the optic disc sag and visual field defect appear in the follow-up, the blue-ciliary syndrome eye can also coexist with the primary open-angle glaucoma, when the onset of intraocular pressure rises for a long time, poor response to drug treatment It is difficult to control and is not easy to relieve. This type of glaucoma should be treated with both. It should be avoided as much as possible. The local corticosteroid treatment time should not be too long to avoid hormonal glaucoma.

2. Pigmented glaucoma

There are three main types of pathogenesis of pigmented glaucoma:

1 glaucoma is only related to the mechanical obstruction of the pigment discharge channel;

2 In addition to pigmentation, the iris cornea angle has congenital anomalies in the structure;

3 pigmented glaucoma is a pigmentation dispersion syndrome in patients with primary open angle glaucoma, glaucoma-ciliary body syndrome and pigmented glaucoma are two different diseases, but Both can cause increased intraocular pressure, optic nerve damage and glaucoma visual field defects. Robinson first reported that one case occurred in the same patient. After 20 years of follow-up, the patient had a recurrent glaucoma-ciliary body syndrome in the right eye at 37 years old. The typical manifestations of the left corneal endothelium and trabecular meshwork have fine pigmentation. During the follow-up, the right eye optic disc depression gradually becomes larger, the visual field shows a nasal side step, and after 10 years, the left intraocular pressure increases, KP(-), room flash (- ), Krukenberg's fusiform pigmentation is visible on the trabecular mesh, and the aqueous humor flow coefficient is reduced to 0.1. It has been found that those with pigmentary glaucoma in the primary glaucoma family have spindle-like pigmentation, and the corticosteroid test is highly reactive. It shows that there is a genetic relationship between pigmented glaucoma and open-angle primary glaucoma. The cyanotic syndrome is also related to the primary open-angle glaucoma. Eye and Glaucoma - syndrome with cyclitis is understandable.

Can also be complicated by corneal edema, mild ciliary body inflammation.

Symptoms of glaucoma and ciliary body syndrome Common symptoms Increased intraocular pressure, high intraocular pressure, high intraocular pressure, green eye pressure, sudden and rapid increase of ciliary congestion visual field defect

It occurs mostly in young adults, with monocular onset and repeated attacks in the same eye. Occasionally, both eyes are affected, and the visual acuity is generally normal. If the corneal edema is obvious, the visual appearance is blurred. The clinical manifestations of the cyanotic syndrome are as follows:

1, single eye disease and repeated episodes of the same eye, occasionally affected by both eyes, Li Zhihui et al (1982) reported 93 cases of binocular involvement in 9 cases accounted for 10%.

2, paroxysmal intraocular pressure increased and repeated attacks, interval can be several months to 1 to 2 years, intraocular pressure can be as high as 5.33 ~ 8.0kPa (40 ~ 60mmHg), the duration of each episode of high intraocular pressure is generally 1 ~ 14 Days, they can recover on their own, a few last for one month, and rarely last for two months.

3, there is no self-conscious symptoms at the time of onset, only mild discomfort, even at the peak of the attack, there are no obvious symptoms such as headache, eye pain and other symptoms like acute angle-closure glaucoma.

4, normal vision, such as corneal edema, blurred vision.

5, the pupil during the attack is slightly larger, the reaction to light exists, although repeated episodes of mild ciliary body inflammation, but no post-iris adhesions.

6, each episode of mild ciliary body inflammation, mild ciliary congestion, corneal epithelial edema, a small amount of gray and white KP, the larger is sheep fat KP, generally no more than 25, more Located under the cornea, or in the trabecular meshwork, the intraocular pressure disappears several days or weeks after the normal pressure, the KP may reappear or not appear when the intraocular pressure fluctuates, the floating matter in the aqueous humor occasionally, the flash is weakly positive, the anterior chamber is not Shallow, the corner of the room is open, the pupil is slightly open, and the reaction to light exists. The iris has no front and the posterior adhesion, and the vitreous has no inflammatory cells.

Often appear within 3 days after the onset of high intraocular pressure, a small number of cells floating in the aqueous humor, often flash negative in the aqueous humor, the posterior wall of the cornea often appears within 3 days after the onset, grayish white, small or large and flat, showing sheep fat It usually does not exceed 25, and it is located at l/3 below the cornea or concealed on the trabecular meshwork of the angle. After the intraocular pressure returns to normal, it disappears within a few days to one month. When the intraocular pressure fluctuates, it may reappear or not appear KP. Therefore, it should be thoroughly examined in detail.

7, no viable cells in the vitreous.

8, the anterior chamber angle is open under high intraocular pressure, no peripheral anterior adhesion.

9, the general fundus is normal, if glaucoma optic nerve and visual field damage may occur when coexisting with primary open angle glaucoma, but in the acute attack of this disease may appear vascular shadow enlargement, severe cases, long-term recurrent episodes, or each episode Long duration, often glaucomatous optic disc and visual field changes under high intraocular pressure.

10. The "C" value is low under high intraocular pressure. The "C" value and intraocular pressure in the intermittent period return to normal and are negative for various excitation tests. This disease can coexist with primary open angle glaucoma. Li Zhihui Etc. (1982) reported that the incidence rate was 31%. In addition to paying attention to the clinical features of this disease, it is also necessary to pay attention to whether there is primary open angle glaucoma at the same time to avoid delay in treatment.

The diagnosis of this disease is mainly based on the following typical clinical features: 1 elevated intraocular pressure and no proportion of symptoms, patients often have significant increase in intraocular pressure, but usually asymptomatic or only mild symptoms; 2 elevated intraocular pressure and Signs are not proportional, although the patient's intraocular pressure rise is sudden, and the degree of intraocular pressure rise can cause serious ocular tissue damage, but patients generally do not have acute ocular features of acute angle-closure glaucoma, such as ciliary congestion. , corneal edema, optic nerve damage, visual field defects, etc.; 3 elevated intraocular pressure is not proportional to the severity of iridocyclitis, iridocyclitis can be due to exudate, cell blockage angle, post-iris adhesion and other mechanisms Causes elevated intraocular pressure, but the disease of iridocyclitis is mild, does not cause post-irisal adhesions, elevated intraocular pressure is particularly significant, and elevated intraocular pressure can occur before the appearance of signs of inflammation; 4 single eye involvement, although this The disease can affect both eyes, but the patient typically presents with monocular involvement; 5 characteristic KP, which is typically characterized by a small number, a special distribution (bottom pupil area), and a slow regression (increased eye pressure, anterior chamber flash) Hui fades slowly); 6 repeated attacks; 7 angle of the eye is open when the intraocular pressure is elevated; 8 living body ultrasound microscopy can detect ciliary body swelling and exudation.

Examination of glaucoma and ciliary body syndrome

1. History: whether there is any use of mydriatic agents, systemic anticholinergic drugs or exercise, history of previous episodes, or corneal or systemic diseases;

2. Slit lamp inspection;

3. Anterior chamber keratoscopy;

4. Assess the optic nerve;

5. Retinal examination;

6. Aqueous cytology can detect inflammatory cells;

7. The tonometer measures the intraocular pressure, estimates the condition, and can also determine the fluency coefficient and the patency ratio of the aqueous humor. The gonioscopic examination can understand the occlusion of the angle of the anterior chamber and the angle of the anterior chamber. The fundus examination can present glaucomatous optic disc for long-term patients. Changes, ultrasound biomicroscopy can detect ciliary body swelling and exudation, fluorescein iris angiography can detect iris vascular lesions.

Diagnosis and diagnosis of glaucoma and ciliary inflammatory syndrome

diagnosis:

Diagnosis can be based on the cause, symptoms and related tests.

Differential diagnosis:

Glaucoma ciliary inflammatory syndrome is easily misdiagnosed as other diseases, and should be differentiated from acute angle-closure glaucoma, Fuchs syndrome and acute iridocyclitis.

1. Acute angle-closure glaucoma

Acute angle-closure glaucoma showed a sudden increase in intraocular pressure. The patient had red eyes, eye pain, headache, decreased vision, rainbow vision, nausea, vomiting and other obvious symptoms. The examination revealed ciliary congestion, corneal edema, and dilated pupils. It has a vertical oval shape, a shallow anterior chamber, a narrow or closed corner, and no KP. These features contribute to the identification of the two.

2. Fuchs syndrome

Although Fuchs syndrome is usually manifested as unilateral involvement, there is no post-iris adhesion, it is easy to cause complicated cataract, and the intraocular pressure is elevated, but the onset is more concealed or slow, and the increase of intraocular pressure is mostly mild to moderately elevated. High, its KP is often star-shaped, diffuse distribution, pupil area distribution or triangular distribution below, iris has different degrees of depigmentation, Koeppe nodules are easy to appear, mild vitreous opacity can also occur, according to these characteristics, generally not It is difficult to distinguish the two.

3. Idiopathic anterior uveitis

Idiopathic anterior uveitis is divided into acute and chronic types. The former has multiple onset, sudden redness, eye pain, photophobia, and tearing. KP is dusty and distributed under the cornea. Anterior chamber glint and a large number of anterior chamber inflammatory cells may have post-iris adhesions, intraocular pressure is generally not high or slightly decreased, occasionally elevated intraocular pressure may occur; the latter is slow onset, KP is dusty or sheep fat, Located in the lower cornea, anterior chamber glint and anterior chamber inflammatory cells are usually more obvious, prone to post-iris adhesion, anterior iris adhesion, complicated cataract, elevated intraocular pressure mainly related to inflammation or occlusion of the angle of the horn, post-iris adhesion, according to These clinical features are generally not difficult to distinguish between idiopathic anterior uveitis and glaucoma ciliary inflammatory syndrome.

4. Neovascular glaucoma

5. Inflammatory open angle glaucoma

6. Other

Such as herpes simplex virus or herpes zoster viral keratitis.

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