Primary acute angle-closure glaucoma

Introduction to primary acute angle-closure glaucoma Primary acute angle-closure glaucoma (APACG) refers to a type of glaucoma that causes an acute increase in intraocular pressure due to the closure of the angle of the eye. Because of the onset of anterior hyperemia, it has been called "congestive glaucoma". ". Pupil block is the main mechanism of this type of glaucoma, which means that most patients with acute angle-closure glaucoma are pupil-blocking, but a few patients are non-pupil-blocking. The basic cause of primary acute angle-closure glaucoma is related to the anatomy of the anterior segment of the eye, especially to the angle of the anterior chamber. In addition, emotional excitement, long-term work in the dark environment and close reading, climate change, seasonal changes may lead to acute attacks. basic knowledge The proportion of illness: 0.001% Susceptible people: no special people Mode of infection: non-infectious Complications: Central retinal vein occlusion Cataract

The cause of primary acute angle-closure glaucoma

(1) Causes of the disease

The basic etiology and anatomy of the anterior segment of the eye are particularly related to the state of the anterior chamber. In addition, emotional excitement, long-term work in the dark environment and close reading, climate change, and seasonal changes may lead to its acute onset.

(two) pathogenesis

1. Pupil block: Under normal circumstances, there is a certain resistance when the aqueous humor flows from the posterior chamber through the pupil to the anterior chamber. This is a physiological pupil block, which does not affect the pressure balance of the anterior and posterior chambers. Large (such as at night) or lens advancement (such as prone), the pupillary block force rises, it can change the refractive state of the eye to a certain extent, to adapt to certain physiological needs, with the gradual increase of the lens with age And close to the iris, the physiological pupillary block force is increased, if accompanied by congenital small eyeball, small cornea, hyperopia or shallow anterior chamber and other risk factors, the gap between the iris and the lens becomes narrower, when the pupil resistance The elevation is sufficient to prevent the flow of the aqueous humor, so that the pressure in the posterior chamber is higher than that in the anterior chamber, and the surrounding iris bulges forward and attaches to the trabecular meshwork to cause obstruction of the angle of the anterior chamber. This is a pathological pupil block, if the angle of the anterior chamber is closed Complete, it triggers an acute onset of glaucoma.

Pupil block is a common phenomenon in the shallow anterior chamber population (including angle-closure glaucoma and normal shallow anterior chamber). The same anterior segment anatomical features cause the same amount of pupillary block force, but the same amount of pupillary block force is different. Individuals do not necessarily cause the same effect, that is, they do not necessarily cause the angle of the anterior chamber to close. Although the physiological pupillary block can only be converted into pathological pupillary block in patients with narrow angle, but not all shallow anterior chamber, narrow angle People will have a corner closure, indicating that the corner is closed, in addition to the known factors, there are other incentives and unknown factors at work.

Common factors that affect pupillary block forces include:

(1) Anatomical factors:

1 Lens enlargement: With the increase of age, the lens volume increases, and the distance between the iris and the iris is shortened. According to some statistics, after 50 years old, the thickness of the lens increases by 0.75-1.1 mm, and the forward displacement is 0.4-0.6 mm. Ultrasound measurement of primary closure In patients with angular glaucoma, the lens is 0.6mm thicker than normal. The ratio of lens thickness to axial length increases with age. Glaucoma patients are more obvious. The enlarged lens also moves the peripheral iris forward and narrows the angle. .

2 lens suspensory ligament relaxation: age and adjustment can increase the convexity of the anterior surface of the lens, enlarge the contact surface with the iris, increase the pupillary block force, block the angle of the occlusion (such as high pleat iris), or keep the iris away from small when contracting The beam net widens the angle of the corner. The eye with this structure can see the lens protruding into or even beyond the pupil edge when the pupil is dilated. At this time, the iris and the lens can be easily seen under the slit lamp microscope. Phenomenon, contraction of the ciliary muscle caused by miotic drugs relaxes the suspensory ligament, and the anterior surface of the lens moves forward, becomes agglomerated, thickens, and also increases the pupillary block force.

3 lens-iris compartment advancement: usually the position of the lens is relatively fixed, the lens is dislocated, when the swelling, the front surface moves forward, the anterior chamber becomes shallow, and the prone can make the whole lens-iris compartment move forward, the back of the eye Bleeding, tumors, increased content in the posterior part of the eyeball, and a decrease in the relative volume of the eyeball after scleral cerclage can push the lens-iris compartment forward, and the angle of the room becomes narrower.

4 small eyeballs, small cornea, narrow anterior segment of the eye, relatively large lens: some people have statistics, the average axial length of patients with primary angle-closure glaucoma is 1mm shorter than normal, and the distance between the anterior surface of the lens and the corneal endothelium is reduced by 1mm. Acute angle-closure glaucoma occurs in hyperopia and small eyeballs.

5 Iris factors: iris texture and thickness have a certain effect on glaucoma, soft iris is more likely to swell than tough iris, Asian and black dark brown iris is thicker and tough, prone to slow closure, bile sphincter contraction produces two Force, one force is parallel to the plane of the iris, and the other force is pressed backward toward the lens. These two forces also directly affect the pupillary block force. In the early stage of pupil dilation, the pupils and pigment epithelium of the pupil move faster than the iris matrix. The sphincter that drags the edge of the pupil presses the lens backward, and the pupillary force increases. In addition, when the pupil is scattered, the surrounding iris accumulates in the corner of the room, and the shattered iris also increases its thickness, plus the existing angle. Stenosis and iris bulging, it is very likely that the angle of the corner is closed. The relationship between the iris and the angle of the corner is very complicated. When the iris root is short and the angle of the corner is narrow, the iris will clog the angle of the corner (such as the high pleat iris), and some irises are When contracted away from the trabecular meshwork, the angle of the angle is widened, and the size of the scorpion and its relationship with the iris seem to determine the pupil block and the high pleat iris. Proportion, when the pupil is dilated, these parameters directly affect the angle of the iris-corneal angle. The elasticity of the iris determines the degree of iris bulging when the pupil is blocked. The worse the elasticity, the degree of bulging may be affected by the posterior pressure. The heavier, the pupil contraction increases the tension of the iris, flattening the peripheral part, and alleviating the congestion of the corner. However, if the pupillary block is not relieved, the iris bulging still exists.

(2) Inducing factors:

1 Dilated: refers to drug or physiological dilated pupils, the pupil is most likely to produce a closed angle when the pupil is 3.5 ~ 6mm, because the pupil block is not released at this time, while the iris is loose, close to the trabecular mesh, the aqueous discharge rate is reduced The use of adequate dilatation for the treatment of acute angle-closure glaucoma is dangerous, but there are also successful cases, but for the already narrow neck, although there is no pupillary block, the loose iris accumulates in the corner and still hinders the aqueous humor. Excretion from the trabecular meshwork causes an increase in intraocular pressure, so it is usually not used.

2 : : : : : : : : : : : : : : : : : : : : : : : : : : : : And cause iris ciliary body congestion, ciliary muscle contraction, suspensory ligament relaxation, lens advancement, etc., can also induce acute angle-closure glaucoma, therefore, the miotic agent can improve the angle of the corner closure, but also make it worse, When the pupil is maximally contracted, the force of the sphincter to press the lens backward is minimal. As the pupil opens, the force of the sphincter points to the rear, so the pupillary block is especially prone to occur when the sphincter and the open muscle play the most important role. This theory was also used in the glaucoma challenge test, the pilocarpine-phenylephrine test.

3 vascular nerve factors: primary acute angle-closure glaucoma is a multi-factor syndrome, pupillary block is not the only cause of angle closure, it is believed that the occurrence of angle closure is mainly due to the activity of parasympathetic nerves in the anterior segment of the eye. Moreover, sympathetic activity should be used as an auxiliary force. When the two are in the maximum active state, the angle of the anterior chamber is closed, the vascular nerve regulation center is dysfunctional, and the vasomotor function is disordered. The result is: A. Ciliary body congestion, exudation , edema, causing the ciliary process to rotate and press the root of the iris, close to the trabecular mesh; B. increase the secretion of aqueous humor, increase the pressure of the posterior chamber; C. open the pupil, causing pupillary block and surrounding iris accumulation, above Factors can cause the angle of the cervix to close, and thus the intraocular pressure rises. Therefore, in the case of systemic dysfunction and mental frustration, the onset of acute angle-closure glaucoma is significantly increased.

4 psychological quality: primary acute angle-closure glaucoma is a typical psychopathological disease, its seizures often accompanied by strong emotional changes.

5 Others: long-term close work, fatigue, systemic trauma, large amounts of infusion, drinking water, etc. are also common causes of this disease.

2. Shallow anterior chamber: The easiest way to observe the depth of the anterior chamber is to use the flashlight sidelight to roughly estimate the depth of the anterior chamber axis. It can be inferred that the angle of the anterior chamber is narrow, but sometimes it is misleading. It is clinically observed with a slit lamp microscope. The depth of the anterior chamber is more reasonable and reliable than the flashlight method. The depth of the most peripheral anterior chamber is measured in terms of corneal thickness (CT). The depth is more than 1CT and the width is wide; 1/3CT is narrow or even closed. Further gonioscopic examination should be performed. The accurate anterior chamber measurement can be attached to the Haag-Streit 900 slit lamp with the Haag-Streit anterior chamber depth gauge. It is mainly used for clinical statistics and observation during the treatment of angle-closure glaucoma. The change of the room.

The anterior chamber depth of normal people was 2.60mm±0.34mm, and the average angle-closure glaucoma patients were 1.78mm±0.32mm. There was a highly significant difference between the two (P<0.001), although the shallow anterior chamber and the narrow angle were not necessarily Closed angle glaucoma occurs, but the primary acute angle-closure glaucoma must be shallow anterior chamber, narrow angle, and the shallower the anterior chamber, the higher the risk, Alobirk's glaucoma survey of the Eskimo shows that all primary The angle of the anterior chamber of patients with angle-closure glaucoma is below 2.3mm, of which primary angle-closure glaucoma occurs in 1.3mm, nearly 40% of the depth is 1.4-1.7mm, and 2.3mm is only 1% of the onset, China's survey report shows that 88.8% of patients with primary angle-closure glaucoma have a anterior chamber depth of less than 2.10mm, while in the normal population, the anterior chamber is shallower than 2.10mm, males only account for 2.5%, and women account for 5%, and mainly in the 50s and older.

Observing the depth of the anterior chamber is ultimately to predict the state of the angle of the anterior chamber, so the most direct and ideal for all patients suspected or diagnosed with glaucoma is the gonioscopic examination, not only to understand the status quo, but also to guide the treatment.

Primary acute angle closure glaucoma prevention

The disease belongs to a type of glaucoma caused by the acute closure of the angle of the sensitive person due to certain physical and mental and environmental factors, which leads to an increase in intraocular pressure. Therefore, psychological adjustment is very important in prevention.

Primary acute angle closure glaucoma complications Complications, central retinal vein occlusion, cataract

When the intraocular pressure rises, especially in acute high intraocular pressure, pathological changes and functional damage can occur in various tissues of the eye, such as eyelids, conjunctival congestion and edema, corneal edema, iris atrophy, lens opacity, fundus hemorrhage, arteriovenous obstruction. Etc. If not treated promptly, the consequences are often severe and permanent. The main damages caused by acute high intraocular pressure include:

1. Vascular changes: acute high intraocular pressure can cause small blood vessel obstruction in the eye, common in the iris and ciliary body, a segment of the iris, ciliary body vascular obstruction, so that the area of the iris ciliary body is ischemic, atrophy, off Pigment, ciliary process, glassy changes, etc., iris atrophy can be extended to the surrounding angle, each acute attack can have a new atrophy area, the sphincter of this part or accompanied by loss of open muscle function, severe pupil permanent Large, fixed, oval, decompressive and mydriatic have no effect, severe pigment loss when the iris shrinks, thin matrix or even front and rear room traffic, the aqueous water can be directly from the back room into the anterior chamber. One or two iris atrophy, like iridotomy, can alleviate pupillary block. In addition, the angle corresponding to the iris atrophy area is widened accordingly, and there is no more iris congestion, which prevents the corner from further closing. Therefore, this The direct pathological significance of the change is to prevent recurrence of glaucoma. When the iris is atrophied, especially in the eye with only a small episode and currently in a state of relief, mild pupil deformation, thinning of the pupillary margin may also indicate Iris domain has been shrinking, should be carefully examined to avoid misdiagnosis.

Small ciliary vascular obstruction after acute attack, partial ciliary mutation, decreased aqueous humor secretion, and also reduced the state of high intraocular pressure to some extent.

When the acute intraocular pressure rises, if it is possible to observe the fundus, due to the compression of high intraocular pressure, the retinal artery pulsation can often be seen, the optic disc is congested, and after the remission is relieved, the retina near the optic disc can undergo extensive bleeding, and the intraocular pressure is too high. It can also cause central retinal vein occlusion or arterial occlusion, decreased vision, and even blindness, so it is important to prevent and control acute attacks.

2. Corneal decompensation: Increased acute intraocular pressure can reduce corneal sensitivity, endothelial cell pump dysfunction, early epithelial cell edema, initial air-like or misty, severe formation of large bubbles; followed by matrix edema The cornea can be increased to twice the normal thickness. The corneal thickening makes the anterior chamber shallower, closer to the iris, and more prone to peripheral anterior iris adhesion. When the intraocular pressure drops, the corneal edema often subsides from the peripheral part and can appear at the same time. Desemet membrane wrinkles will generally disappear quickly, but sustained high intraocular pressure, or the original corneal endothelial dysfunction, acute attacks can increase endothelial cell loss, and even functional decompensation, the amount of cell loss is related to the duration of seizures, It has been estimated that an acute glaucoma episode can cause a loss of 33% of the corneal endothelium, up to 91%. At this time, corneal thickness and transparency are difficult to recover, and epithelial vesicles will persist, even if the intraocular pressure is lowered again. , causing permanent visual impairment, in addition, sustained high intraocular pressure also causes corneal fibrosis and neovascular proliferation, loss of normal transparency, in the corneal splitting site Calcification and lipid deposition species are a common manifestation of advanced glaucoma corneal decompensation, called strip corneal degeneration.

3. Lens opacity: High intraocular pressure itself and changes in aqueous components during high intraocular pressure cause dysregulation of lens metabolism, leading to cataract formation or exacerbation of cataract, while cataract can cause lens expansion, close to the iris, and increase pupillary block.

A sudden change in intraocular pressure can form a flaky, mellow opaque plaque under the anterior lens of the lens - glaukomflecken, which is characteristic of acute high intraocular pressure. In tissue sections, these opacity spots appear to be Necrotic material of anterior epithelial cells or lens fibers. When the intraocular pressure drops, turbidity may be partially or completely absorbed, and a small amount may be permanently present. Over time, new lens fibers are covered and pushed deep into the eye. Therefore, according to the depth of the opacity, it is possible to estimate the time elapsed since the onset of the episode. This pathological change occurs almost in the pupil area, but does not occur in the posterior pole of the lens. It is worth mentioning that some cause acute intraocular pressure rise. Such high opacity may also occur in secondary secondary glaucoma.

4. Iris ciliary body reaction: When the angle of glaucoma is acute, the first effect of sudden increase in intraocular pressure may be necrosis of the iris matrix. Due to the acute increase in intraocular pressure, the vascular permeability of the iris ciliary body changes, and congestion Exudation or even obstruction, causing tissue edema, degeneration, necrosis, and can lead to destruction of the iris matrix, protein decomposition, manifested as aseptic anterior uveitis, anterior chamber flash, floating matter, free pigment and even anterior chamber empyema These can promote post-pupil adhesion and anterior adhesion of the iris, further increase the pupillary block force, further reduce the drainage of aqueous humor, and lay a foundation for future recurrence and deterioration of the disease, but the anterior chamber reaction in the acute onset of glaucoma is generally Compared with the usual iridocyclitis, the pupil adhesion rate is slower. When the angle of the glaucoma is acute, if the intraocular pressure is higher than 60mmHg, the pupil is no longer sensitive to the miotic agent because when the intraocular pressure is higher than the diastolic pressure Iris ischemia around the pupil, pressure on the pupil sphincter, loss of contraction ability, if the intraocular pressure can drop as soon as possible, the pupil can restore the original size, aqueous humor The ring function will not be affected. If the intraocular pressure continues and even the pupil adhesion occurs, it will become permanent expansion. When the iris is resected, the aqueous humor is drained from the bypass to the anterior chamber, and the aqueous humor in the pupil area is reduced. After adhesion, iris adhesion can also occur in the angle of the anterior chamber, which is punctate or cone-shaped. Each episode causes new adhesions, and the drainage area of the aqueous humor gradually decreases. This is an important reason for the disease to enter the chronic phase. Loss is often deposited in the cornea, the angle of the horn and the surface of the lens, including posterior corneal pigmentation KP, iris segmental atrophy and lens glaucoma. The three are collectively referred to as "triple syndrome", which is a powerful episode of acute angle-closure glaucoma. evidence.

5. Corner angle change: Unlike open-angle glaucoma, the angle-closure glaucoma has no structural abnormalities before the corner of the room is closed. The trabecular meshwork and the Schlemm tube itself have no obstruction. At the beginning, the peripheral part of the iris It is almost juxtaposed with the surface of the trabecular meshwork, but does not affect the normal drainage of the aqueous humor. Any factor that causes the pupil to dilate or increase the pupillary block force may cause the iris root to adhere closely to the trabecular meshwork. Causes the closure of the angle of the anterior chamber. Timely medical treatment can reopen it without causing abnormalities in the structure and function of the trabecular tissue, such as recurrent or prolonged high intraocular pressure, plus the inflammatory response time of the iris ciliary body. More than 24 ~ 48h, will form a corner adhesion, iris matrix and trabecular mesh progressive fibrosis and degeneration, the occluded angle can not be opened again, Schlemm tube will also be blocked due to compression deformation, tissue specimens in the later stages of the disease It can be seen that there is pigmentation, fibrosis in the trabecular mesh space, Schlemm tube is narrow, the cavity is filled with red blood cells, and the closure can be partial or all, whether the intraocular pressure can return to normal or increase The degree of highness depends mainly on the extent of the adhesion of the angle of the corner and the function of the trabecular meshwork without adhesion. Repeated or severe attacks cause damage to the trabecular meshwork itself. Even if the angle of the anterior chamber is reopened, its aqueous drainage function It may also be significantly reduced, so clinically, there will be cases where the angle of adhesion of the corner is not large but the intraocular pressure continues to rise.

6. Optic nerve damage: After acute attack of angle-closure glaucoma, if the course of disease is short, the optic disc can be unaffected, no glaucoma cup, acute angle-closure glaucoma optic disc often shows fading and small depression, chronic angle-closure glaucoma is more common optic disc The color is accompanied by sag enlargement, long-term sustained high intraocular pressure, neurofibrillary degeneration of the retinal ganglion cells, atrophy, and the number is significantly reduced, which is manifested by partial or general physiological depression of the optic disc, and the optic disc is the weak part of the eyeball. It is easy to be affected by high intraocular pressure to produce posterior processes and form glaucoma depression. This kind of condition often occurs in the advanced and chronic phase of acute angle-closure glaucoma. At this time, the patient's fundus and visual field are not different from open-angle glaucoma.

Primary acute angle-closure glaucoma symptoms common symptoms elevated intraocular pressure, high intraocular pressure, pain, eye pain, lens, glaucoma, plaque, visual field, defect, swelling, iris, segmental atrophy, ciliary congestion, blind spot

According to the clinical course and disease outcome of acute angle-closure glaucoma, it can be divided into preclinical, aura, acute, remission, chronic, and absolute.

Preclinical stage

Theoretically, preclinical refers to angle-closure glaucoma, which has not seen any pathological damage in the eye before the onset of acute angle-closure glaucoma, but it is difficult to distinguish such patients from the narrow-angle population in clinical practice. Therefore, clinically, acute angle-closure glaucoma occurs in one eye. The contralateral eye and the eye have the same anatomical features of angle-closure glaucoma. It is possible to have acute angle-closure glaucoma, but there is no case of angle-closure glaucoma. .

Precursor

About 1/3 of acute angle-closure glaucoma may have a history of intermittent small attacks before an acute attack. Patients may experience mild to moderate eyeball pain after working or working in a dark environment for a long time. Over-exposure to menstruation, self-remission after rest or sleep, the intraocular pressure increased moderately at each episode, and sometimes rainbow vision may appear. At the beginning, each episode has a long interval, such as several weeks to several months, and then gradually turns to frequent, and finally leads to an acute attack.

3. Acute attack

It is a critical stage of acute angle-closure glaucoma, and the patient feels severe eye pain and ipsilateral headache. Often combined with nausea and vomiting, sometimes accompanied by fever, chills, constipation and diarrhea.

4. Relief period

After treatment or natural remission of acute angle-closure glaucoma, intraocular pressure can be restored to the normal range. The eye is congested, the corneal edema subsides, the central vision returns to the pre-onset level, or the angle is slightly lowered. These patients have different degrees of adhesive closure in the corners of the room, and the trabecular meshwork leaves a large amount of pigment, especially at the corners of the square. At this time, a small number of patients had paralysis due to pupillary sphincter paralysis, or segmental atrophy of the iris, and perforation. In addition, most patients' stimulation test can still stimulate the increase of intraocular pressure. The acute angle-closure glaucoma remission period is temporary. If the peripheral iridotomy is performed in this period, the pupillary block can be relieved to prevent the re-acute. purpose.

5. Chronic phase

The acute attack period may be delayed into a chronic phase without timely and appropriate treatment, or due to extensive adhesion of the angle of the anterior chamber. The acute symptoms were not completely relieved, the intraocular pressure was moderately elevated, the cornea was basically restored to transparency, and the angle of the eye was found to be extensively closed. If the proper treatment is not obtained during this period, the fundus and visual field will cause similar damage to chronic angle-closure glaucoma.

Absolute period

Due to delays in treatment during acute attack or failure to receive appropriate treatment in other stages, the eye is referred to as the absolute period after blindness. The clinical symptoms in the absolute phase are mainly high intraocular pressure. In addition to the eye signs after acute attacks, the late absolute glaucoma can be combined with corneal calcification, iris and trabecular mesh fiber membrane formation and cataract.

Examination of primary acute angle-closure glaucoma

No special laboratory tests.

1. Excitation test: Because the pathogenesis of angle-closure glaucoma is mainly pupillary blockage and iris root blockage angle, the aqueous humor can not contact with the trabecular meshwork, so the use of these principles can be used to artificially cause the increase of intraocular pressure. Suspected glaucoma makes a diagnosis in advance, although this will cause the patient's temporary burden, but the glaucoma episode in the hospital can be controlled in time, and start treatment in time, much better than the out-of-hospital episode, delay diagnosis and treatment.

For a suspected glaucoma patient (if there is eye swelling, rainbow vision, transient vision loss and family history of glaucoma, etc.), those with shallow anterior chamber and normal intraocular pressure may be considered for the challenge test. It should be clear unless the challenge test is positive. Can be diagnosed with angle-closure glaucoma, but negative test results do not guarantee that glaucoma will not occur in the future.

The use of the challenge test should be based on the type of glaucoma. The principle of the challenge test should be first understood for rational use. For angle-closure glaucoma, the main mechanisms of the challenge test are two:

1 increase the pupil blocking force;

2 The root of the iris is blocked and blocked. At present, the excitation test for the angle-closure glaucoma mainly includes darkroom test, prone test, dilated test, etc. Results analysis: the intraocular pressure rise before and after the test is 8mmHg, or the intraocular pressure after test is 30mmHg Positive, the intraocular pressure increased <6mmHg before and after the experiment was negative, before and after the test with tonometry and gonioscopic examination, if the C value decreased by 25% to 30%, the angle of the anterior chamber was closed, even if the intraocular pressure was not high.

The challenge test is only a means of artificially inducing high intraocular pressure. Negative does not exclude the possibility of angle-closure glaucoma in the future. Positive does not spontaneously produce acute angle closure, but it does not deny the significance of the challenge test for diagnosis and treatment, but Comprehensive consideration should be given to clinical and other examinations.

2. UBM check.

3. Corner inspection.

4. B-ultrasound can measure the depth of the anterior chamber, the thickness of the lens and clear the position of the lens.

Diagnosis and diagnosis of primary acute angle-closure glaucoma

diagnosis

The patient had ocular anatomical features of primary angle-closure glaucoma; acute intraocular pressure was elevated, and the angle of the anterior chamber was closed; patients with monocular disease were examined by contralateral eye and found to have anatomical features of primary angle-closure glaucoma Eye examination can be seen with the signs of ocular damage caused by the above various acute high intraocular pressures.

The early anterior chamber angle of patients with APACG is variable. When the intraocular pressure is normal, the angle of the anterior chamber can be opened and the diagnosis is difficult to establish. Therefore, the sensitive population should be thoroughly examined, and if necessary, stimulated with the experiment, combined with the medical history, can improve Early diagnosis rate, early intervention of this type of glaucoma, not only may block the progress of the disease, and some may even prevent its onset.

Differential diagnosis

1. Digestive tract diseases: As acute angle-closure glaucoma can cause severe headache and gastrointestinal symptoms during acute exacerbation, it may be misdiagnosed as a medical or other medical condition and may be delayed in treatment. In order to avoid this, For non-ophthalmologists, it is important to master the basics of acute angle-closure glaucoma.

2. Secondary glaucoma: In addition to acute angle-closure glaucoma, blood-stained glaucoma, lens expansion, lens solubility, glaucoma caused by subluxation of the lens, neovascular glaucoma, secondary glaucoma caused by uveitis Can cause acute increase in intraocular pressure, and even left the signs of ocular damage caused by high intraocular pressure, in order to identify the above situation, the most important of which is to check the contralateral eye, for primary angle-closure glaucoma Both eyes often have the same anatomical features. If the contralateral eye is found to have the same characteristics, further examination should be performed to make a differential diagnosis.

3. Acute iridocyclitis and acute conjunctivitis: The differential diagnosis has been introduced in general textbooks, it is relatively easy, but it must be emphasized that there are contradictions in the treatment of these three diseases, therefore, the wrong diagnosis will lead to The condition worsened and even caused blindness.

4. Malignant glaucoma: Because the clinical manifestations and anatomical signs of primary malignant glaucoma and the disease have many similar aspects, it is easy to cause misdiagnosis. In addition, due to the different treatment principles of the two diseases, serious misdiagnosis can cause serious losses. Therefore, the differential diagnosis of the two is very important. Malignant glaucoma also has a narrow feature of the anterior segment of the eye, but it is often narrower than the anterior segment of the eye, the thickness of the lens is thicker, the axis of the eye is shorter, and the relative position of the lens is higher. The anterior chamber is shallower and the disease is different. The iris appears to be anteriorly consistent with the front of the lens. The most important thing is that the condition deteriorates after treatment with the miotic agent.

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