Inflammation-related glaucoma

Introduction to inflammation-related glaucoma Inflammation-associated glaucoma is a secondary glaucoma that often combines both angle-closure and open-angle. Closed-angle glaucoma is a common type of glaucoma caused by the closure of the patient's anterior chamber angle and the blockage of aqueous humor in the eye. Open-angle glaucoma generally refers to primary open-angle glaucoma, in which glaucomatous optic neuropathy and corresponding visual field defects occur without obvious cause and the anterior chamber angle is open, which may eventually lead to blindness. basic knowledge The proportion of illness: the incidence rate is about 0.005%-0.007% Susceptible people: no special people Mode of infection: non-infectious Complications: intermediate uveitis

Inflammation-related glaucoma etiology

(1) Causes of the disease

Eye inflammation that causes glaucoma includes herpes simplex keratitis, herpes zoster keratitis and uveitis, scleritis and superficial scleritis, uveitis, and the like.

(two) pathogenesis

Here we discuss the pathogenesis of uveitis caused by uveitis, and glaucoma caused by other inflammations has similarities.

Inflammation of uveal tissue can alter the dynamics of aqueous drainage, including inflammatory tract occlusion of the trabecular meshwork, peripheral pre-irisal adhesion or pupillary block, and steroid glaucoma. The clinical course can be acute, chronic or recurrent, even in stable inflammation. Secondary glaucoma can occur during the period, and the symptoms can be light or heavy.

In clinical practice, intraocular pressure may be normal, decreased or increased during uveitis, because inflammation can not only change the drainage resistance of aqueous humor, but also change the rate of aqueous humor production. When the secretion of aqueous humor is reduced, it is often accompanied by The drainage drainage resistance increases, sometimes this effect can develop in the opposite direction, which shows that the outflow resistance increases and the intraocular pressure can be normal or decreased. For example, the characteristics or intensity of inflammation change, the rate of aqueous humor returns to normal, and the discharge resistance remains high. The intraocular pressure will inevitably increase; on the contrary, if the drainage resistance of the aqueous humor is normal and the intraocular inflammation reduces the rate of aqueous humor production, the intraocular pressure is reduced, and the secondary glaucoma of uveitis can be expressed as an open angle. And closed angle glaucoma, the mechanism of increase in intraocular pressure is as follows:

Open angle glaucoma

(1) trabecular meshwork inflammation and inflammatory substances block trabecular meshwork: inflammatory response of trabecular meshwork and its function in acute inflammatory phase, leading to trabecular meshwork swelling and endothelial cell dysfunction, inflammatory debris accumulated in trabeculae In the drainage channel of the net or other aqueous humor, including cellulose, white blood cells and macrophages, these are formed and adhered together, and some are decomposed by proteases, accumulate in the trabecular meshwork or adjacent to the Schlemm tube, and block the aqueous drainage channel. Caused by elevated intraocular pressure, some inflammatory cells in the local area of iridocyclitis, seen in the KP on the surface of the trabecular meshwork under the gonioscopic examination to change the angular structure of the anterior chamber; the acute inflammatory phase of the eye can also release chemical media such as the prostate Prostaglandins, cytokines and nitric oxide all cause blood-aqueous barrier destruction, increased vascular permeability, increased protein content in aqueous humor, and increased aqueous humor viscosity, resulting in more aqueous humor discharge. difficult.

(2) trabecular dysfunction after trabecular meshwork: during inflammatory process of trabecular meshwork, trabecular meshwork directly suffers from decreased water drainage, and trabecular meshwork occurs in mild anterior uveitis without ciliary body inflammation. Due to the dysfunction of the trabecular cells, the trabecular mesh area accumulates debris, and the diameter of the trabecular mesh pores shrinks, causing the drainage of the aqueous humor.

(3) changes in vascular permeability after inflammation: due to changes in tissue structure, such as the blood-water barrier of the ciliary epithelium, causing changes in vascular permeability, in the quiescent period of recurrent chronic inflammation over many years, can also show the splash of aqueous humor , indicating that the mechanism of normal operation of prostaglandins and their inflammatory substances from the eye has been destroyed.

2. Closed angle glaucoma

(1) The angle of the anterior iris caused by the adhesion of the anterior iris: Uveitis is often accompanied by a concealed and irreversible trabecular meshwork change, that is, the peripheral iris of the inflammatory phase is affixed to the trabecular meshwork, and the inflammatory exudate machine After the formation of permanent adhesions, called the peripheral iris pre-adhesion, sometimes the endothelial cell membrane or fibrovascular membrane can cover the surface of the trabecular meshwork, forming a permanent obstruction, the anterior adhesion has different morphology, breadth and height, caused by uveitis The peripheral anterior iris adhesion is different from the angle occlusion caused by the iris bulging of the primary angle-closure glaucoma. The former iris adhesion is mostly columnar, and the latter is the full layer of the iris, that is, the whole layer of the iris is pulled toward the anterior wall of the anterior chamber. .

(2) Angle occlusion caused by post-iris adhesion: acute, recurrent iridocyclitis, especially exudative iridocyclitis, not treated with ciliary muscle paralysis and dilating agent, iris inflammation Protein and cellulite exudate in the aqueous humor can cause post-irisal adhesion. Complete post-iris adhesion often causes pupillary membrane closure or pupillary atresia. The aqueous humor channel in the anterior and posterior rooms is blocked, and the adhesion occurs in the posterior margin. The aqueous humor can not flow into the anterior chamber through the pupil and hoards in the posterior chamber. The pressure in the posterior chamber rises and pushes the iris forward, causing the anterior iris to bulge, the angle of the anterior chamber to be closed, and the intraocular pressure to rise.

(3) forward rotation of ciliary body: ciliary body swelling and forward rotation, can cause angle-closure glaucoma without pupillary block, appear in ciliary body inflammation, ciliary body swelling and ring When the choroid is detached.

Inflammation-related glaucoma prevention

1. Maintain a good mood and avoid excessive emotional fluctuations. The most important predisposing factors for glaucoma are long-term bad mental stimulation, temper, depression, anxiety, and panic.

2, life, diet and living rules, work and rest, moderate physical exercise, do not participate in strenuous exercise, maintain sleep quality, diet light and nutritious, non-smoking wine, tea, coffee, appropriate control of water intake, can not exceed 1000-1200ml per day , disposable drinking water should not exceed 400ml.

3, pay attention to eye hygiene, protect the eyes, do not read under strong light, the dark room stay time can not be too long, the light must be soft enough, do not overuse the eye.

Inflammatory-related glaucoma complications Complications, middle uveitis

It includes complications caused by the primary disease and complications caused by elevated intraocular pressure.

Inflammation-related glaucoma symptoms Common symptoms Green as green, weak intraocular pressure, increased iris, infertility, uveal uvitis, abnormal iris pupil

Different clinical features depending on the primary disease:

1. Acute iridocyclitis typical acute iridocyclitis is characterized by anterior segmental hyperemia, cells in the anterior chamber and flashing, dilated pupils, sometimes KP and inflammatory cells in the anterior vitreous, although inflammation can lead to The drainage resistance of aqueous humor increased, and the formation of aqueous humor decreased. In most patients, the intraocular pressure remained normal or decreased. However, when clinical diagnosis of acute iridocyclitis with or without glaucoma, the most common error is with primary acute Closed-angle glaucoma and its sequelae are confused. Because of the acute angle-closure glaucoma, the intraocular pressure often decreases or remains normal. Similar to acute iridocyclitis, there is a concealed flash in the anterior segmental congestion and aqueous humor. Cell, one of the characteristics of the two identification is the history, acute angle-closure glaucoma after the onset of little fear of light and small or slightly smaller pupil, the most important is the slit lamp to check the iris corneal angle narrowing and the angle of the corner mirror Narrow or closed, acute iridocyclitis under the gonioscopic examination, the angle of the anterior chamber is open.

2. Recurrent and chronic iridocyclitis Some recurrent and chronic iridocyclitis have obvious features and special names, including glaucoma-ciliary body syndrome, iris heterochromia syndrome, intermediate uveitis, etc. Similarly, severe uveitis and secondary glaucoma sometimes have arthritis, especially in young cases of rheumatoid arthritis and in some cases of sympathetic ophthalmia, severe glaucoma, most recurrent or chronic iridotropes There are no special or obvious features in the case of scuritis, and the cause of the disease is usually unknown. There are no specific signs of chronic iridocyclitis, such as cells, glimmers and KP. Sometimes it is not sustainable and lasts for a long time. Incomplete treatment, glaucoma has become a serious problem in some of these cases due to chronic chronic disease and marked increase in intraocular pressure.

In other cases, due to long-term anterior segmental inflammation, the intraocular pressure is reduced due to the decrease of the rate of aqueous humor production, but when the inflammation subsides and the rate of aqueous humor returns to normal, the intraocular pressure can return to normal; but secondary to the trabecular meshwork Inflammatory changes caused by aqueous drainage disorders, intraocular pressure can be elevated, and in some cases, when inflammation is controlled, there may be an increase in intraocular pressure that cannot be controlled by any drug. At this time, we need to force us to reduce anti-inflammatory treatment and allow light Judgment and choice between the presence of degree of inflammation, or between the implementation of high-risk glaucoma surgery.

The treatment of residual glaucoma is the same as that of primary glaucoma. It can be treated with -blockers and carbonic anhydrase inhibitors. Although the effect of sputum reduction is less, when the inflammation is completely static, try to use a miotic agent. Glaucoma filtering surgery, preoperative, intraoperative and postoperative need to use systemic hormone or immunosuppressive drugs to avoid recurrence of active inflammation, can promote successful surgery.

Inflammation-related glaucoma examination

Laboratory examination of primary diseases such as uveal disease can be performed with glaucoma-related examinations such as visual field, fundus, intraocular pressure, and angle of the eye when the visual function is acceptable and the refractive interstitial is transparent.

Inflammation-related glaucoma diagnosis

diagnosis

The diagnosis of the primary disease, accompanied by an increase in intraocular pressure, can be diagnosed.

Identification

1. Primary open angle glaucoma Primary open angle glaucoma is easily misdiagnosed as NPG in the following cases. The intraocular pressure of day and night fluctuated greatly. No intraocular pressure peak was found because of 24 hours of intraocular pressure. Some patients had occasional elevated intraocular pressure, but single daily curve examination failed to measure; POAG patients with myopia had scleral hardness. Low and low intraocular pressure measured by Schi??tz tonometer; taking -blockers or cardiac glycosides to reduce intraocular pressure. Therefore, it should be emphasized that the intraocular pressure measurement and the daily curve examination should be repeated under the condition of stopping all local or systemic medication with suspicious intraocular pressure reduction, and the intraocular pressure should be measured with an applanation tonometer as much as possible to confirm that the intraocular pressure is indeed NPG can be diagnosed within the normal range.

2. Other types of glaucoma such as early stage of chronic angle-closure glaucoma, glaucoma ciliary inflammatory syndrome, hormonal glaucoma, pigment dissemination syndrome, ocular trauma and uveitis may have transient eyes Increased pressure, causing glaucomatous optic nerve and optic disc damage, and then the intraocular pressure returned to normal, easy to be misdiagnosed as NPG, detailed history, detailed eye examination, including angle examination to identify. For example, in the case of pigment dissemination syndrome, the pigmentary Krukenberg spindle and trabecular mesh dense pigment are seen in the corneal endothelium of a typical pigment disseminated syndrome in young patients, and the intraocular pressure is elevated, which is easily distinguished from NPG. However, some elderly patients with pigmented glaucoma stopped releasing pigment, trabecular meshwork function and intraocular pressure returned to normal, corneal and trabecular pigmentation decreased, but optic disc and visual field damage still exist, easily misdiagnosed as NPG. It needs to be identified by detailed medical history, careful examination and follow-up observation.

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