primary open angle glaucoma

• Introduction
• Cause
• Prevention
• Complication
• Symptom
• Examine
• Diagnosis

Introduction

Introduction to primary open angle glaucoma Primary open angle glaucoma (primary openangleglaucoma) is also known as chronic simple glaucoma, commonly known as slow single. It is due to the increase in intraocular pressure as a basic feature, which in turn causes optic nerve damage and visual field defects, and finally leads to blind progressive chronic eye disease. Open angle glaucoma is mostly wide angle, a few are narrow angles, and primary open angle glaucoma may be It is a disease of more than one type, accompanied by common damage to retinal ganglion cells and optic nerve. The disease is concealed and often has no symptoms. It is often found during routine eye examinations or health screenings. basic knowledge The proportion of illness: 0.001% Susceptible population: The patient is slightly more male, and the age is between 20 and 60 years old. Mode of infection: non-infectious Complications: ocular hypertension

Cause

Primary open angle glaucoma cause

In the etiology study, although the exact cause is still unclear, some factors are known to be closely related to the onset of primary open angle glaucoma, and they are called risk factors for primary open angle glaucoma. The risk factors are as follows:

Genetic factors (20%):

Primary open angle glaucoma has a genetic predisposition, but its exact genetic pattern has not been determined. It is generally considered to be polygenic. Therefore, the family history of primary open angle glaucoma is the most dangerous factor. Sexual open angle glaucoma has a higher incidence of positive family history, and the incidence of relatives of patients with primary open angle glaucoma is higher than that of normal people. The genetic law of open corneal glaucoma: modern genetics, especially pharmacology - Hormone Boost Gene and Immunogenetics HLA System There are two schools of genetics for open-angle glaucoma. Most believe that open-angle glaucoma is a multi-factor genetic disease. The occurrence of multi-factor genetic disease is determined by genetics and environment. The three measurement parameters of glaucoma: one intraocular pressure, C value, C/D ratio are quantitative traits, quantitative traits are usually determined by multiple pairs of genes, therefore, open angle glaucoma is a multifactorial genetic disease.

Myopia (14%):

The incidence of primary open angle glaucoma in myopia, especially in high myopia patients, is also higher than that in the normal population. The reason may be that the axial length of the patients with high myopia changes the structure of the sclera and optic nerve, resulting in its tolerance to intraocular pressure. It is related to reduced resistance.

Corticosteroid sensitivity (15%):

Primary open angle glaucoma is highly sensitive to corticosteroids and has a high sensitivity response rate of 4% to 6% in patients with primary open angle glaucoma compared with 4% to 6% in the normal population for corticosteroid tests. Elevation, up to 100%, the relationship between corticosteroids and the pathogenesis of primary open-angle glaucoma is not fully understood, but corticosteroids are known to affect the function of trabecular cells and the metabolism of extracellular matrices.

Pathogenesis

In the study of the pathogenesis of primary open angle glaucoma, the cause of elevated intraocular pressure is the increase of outflow resistance of aqueous humor, but the exact location and mechanism of obstruction of aqueous outflow are not completely clear. The study of Neo-Confucianism and the observation that the outflow of aqueous humor is caused by the pathological changes of the irradiance channel of the iris cornea. These pathological changes include trabecular meshwork collagen fibers and elastic fiber degeneration, trabecular meshwork endothelial cells proliferating edema, and endothelial cell reduction. Extracellular plaque and collagen accumulation in trabecular meshwork, thickening of trabecular meshwork, narrowing or disappearance of trabecular space, reduction of swallowing large bubbles in Schlemm's endothelial cells, collapse of Schlemm's tube, stenosis, closure, collection tube degeneration, Stenosis of the lumen, etc., but the above results are obtained by histopathological study of the trabecular tissue section, influenced by the material and the production technology, and some scholars believe that the above-mentioned pathological changes can also be seen in the normal age of non-glaucoma. Humans, therefore, the results of the above histopathological studies have not fully explained the cause of elevated intraocular pressure in glaucoma.

In recent years, through the in vitro culture of trabecular cells, applied biology, biochemistry, pharmacology, molecular biology and molecular immunology, the structure and function of trabecular cells, the metabolism of trabecular cells, drugs against trabecular cells The effects of function, trabecular extracellular matrix, cell contraction skeleton, cell membrane receptor, and metabolism of corticosteroids have been extensively studied, which has enabled us to have a deeper understanding of the pathogenesis of primary open angle glaucoma. It is understood that the current primary open angle glaucoma is the abnormal shape and function of trabecular cells, which leads to obstruction of aqueous humor and increased intraocular pressure. The mechanism is: 1 extracellular matrix components of trabecular cells and Changes in content (mucopolysaccharide, collagen, non-collagen glycoprotein, elastin, biotin, etc.), stenosis and collapse of the trabecular meshwork; 2 abnormality of cell shrinkage skeleton content and composition in trabecular cells (microwire, Microtubules and medium fibers, in which the actin filaments of the microfilaments are significantly reduced), the contractility of the trabecular cells is reduced, and the mesh between the trabecular cells becomes smaller or stiffer, thereby The outflow of aqueous humor is blocked and the intraocular pressure is elevated. Other factors such as tissue fibrinolysis system, prostaglandins, and abnormal metabolism of corticosteroids may also affect the function of the aqueous outflow system. It is believed that with the continuous improvement and deepening of research methods and research methods. The etiology and pathogenesis of primary open angle glaucoma will be gradually recognized and mastered.

Chronic simple glaucoma, when the intraocular pressure is increased, the angle of the occlusion is still open, although the aqueous humor and trabecular surface can be fully contacted, but the aqueous humor can not be discharged, and the intraocular pressure is increased, the cause of increased intraocular pressure may be due to The following situations:

1. Variation of trabecular tissue: trabecular tissue hardening, degeneration, mesh shrinkage, trabecular lamellar layer becomes irregular or even destroyed, endothelial cells enlarge, collagen fiber degeneration, elastic fiber degeneration, trabecular mesh structure gap Narrowed.

2. The drainage function of the Schlemm's tube and its output tube or external collection tube is reduced.

3, increased venous pressure: vascular artery nerve instability, periodic sympathetic nervous, capillary venous pressure rise, upper scleral venous pressure increased, resulting in difficulty in aqueous humor discharge.

Prevention

Primary open angle glaucoma prevention

Open-angle glaucoma progresses slowly, and has no obvious symptoms. It is difficult to find early. Many patients have a tubular vision in both eyes. Even when they are blind, they come to seek medical treatment. However, they still do not know when they are sick. Some patients are unintentional. When I checked the fundus, I found it accidentally, even when I was blind, I came to seek medical treatment, but I still dont know when I got sick. Some patients accidentally found it when they accidentally examined the fundus. Therefore, be alert to this patient, otherwise the risk will be even more dangerous. Large, the patient is slightly more male, the age is between 20 and 60 years old, and the incidence rate increases with age. According to the relevant data, 24.7% under 40 years old, 75.3% over 40 years old, open angle Glaucoma includes: chronic simple glaucoma, low intraocular pressure glaucoma and hypersecretory glaucoma.

Early treatment, especially those with a family history of glaucoma, should be regularly followed by an eye exam, paying attention to rest and sleep, avoiding overwork and emotional agitation, reading or engaging close-up workers, and having sufficient light.

Complication

Primary open angle glaucoma complications Complications, high ocular hypertension

Major concurrent visual impairment and other visual dysfunction, severe blindness, optic disc damage and retinal nerve fiber atrophy are the most serious consequences of this disease, and directly related to its prognosis.

Symptom

Primary open angle glaucoma symptoms Common symptoms Increased intraocular pressure, fundus changes, intraocular pressure, sudden increase in eye pressure, high intraocular pressure, visual field defect, rainbow vision, eye swelling

Clinical manifestations:

(a) Conscious symptoms

There are almost no symptoms in the early stage. When the lesion progresses to a certain extent, there are visual fatigue, mild eye swelling and headache. When the intraocular pressure fluctuates greatly or the intraocular pressure level is high, rainbow vision and fog vision also appear. The reduction, but the central vision is not affected, often caused by night blindness and inconvenient movements, and finally the vision is completely lost.

(two) signs

1. Fundus changes: The early fundus can be normal. As the lesion develops, the physiological depression gradually enlarges and deepens, and the blood vessels move toward the nasal side. The posterior nipple is pale, the depression is straight to the edge of the nipple, and the retinal blood vessels are bent over the edge of the nipple. Or climbing the slope, the above three characteristics are typical of the blue light cup, it is important to identify the changes in the optic papilla of the early glaucoma in order to make an early diagnosis.

2, corner: the shape of the corner is not affected by intraocular pressure.

3. Intraocular pressure: The change of intraocular pressure is manifested in the increase of fluctuation amplitude and the increase of intraocular pressure level. The amplitude is mostly high in the morning, low in the afternoon, lowest in the middle of the night, unstable in the intraocular pressure, and the amplitude is greater than the increase in intraocular pressure. Earlier, changes in intraocular pressure are sometimes fast, sometimes slow, and sometimes relatively static.

4, visual field: continuous high intraocular pressure, direct oppression of optic nerve fibers and its blood supply system, so that the optic nerve head ischemia and atrophy, a change in visual field, through the state of vision changes can be estimated the severity of the lesion and treatment.

(1) Change of central visual field: Early detection of the dark spot in the side center of the Bjerrum area. As the disease progresses, the dark scorpion expands and bends toward the center to form a bow-shaped dark spot (Bijerrum dark spot), and finally reaches the central horizontal line of the nasal side. Terminates the formation of the nasal stepped shape (Ronne Ronne). If the step appears at the top and bottom, and the center of the nose is connected, a circular dark spot is formed, which can be gradually widened and the visual field defect of the nasal side is formed. Connected.

(2) Peripheral visual field change: At the same time or later, when the central visual field appears dark spots, the visual field of the nasal peripheral part is reduced, firstly above the nose and then under the nose, and finally at the temporal side, the nasal side is faster, and sometimes the nasal side has a quadrant. Defect or complete defect, and there is no obvious change in the temporal field. If the temporal field of view is also reduced, the last part is only 5 to 10o in the central part, which is a tubular field of view. At this time, the central vision of 1.0 can be retained from time to time.

Retinal nerve fiber bundle atrophy: strip atrophy occurs early under the large vascular arch of the iliac crest and under the armpit. The ophthalmoscope can be seen between white nerve fiber bundle stripes, black stripes widened, medium and late, white stripes completely Disappeared, neurotrophic quadrant atrophy and diffuse atrophy.

Examine

Examination of primary open angle glaucoma

Intraocular pressure measurement

Perform 24h intraocular pressure measurement, which is the daily curve of intraocular pressure. The intraocular pressure is a necessary condition for maintaining normal visual function. Normal intraocular pressure has a special effect on the optical characteristics of the eye, liquid circulation in the eye, and crystal metabolism. Under normal circumstances, the formation of water, discharge and eye contents are in the state of arterial balance. If this balance is blind, pathological intraocular pressure will occur.

2.Heidelberg Retinal Tomography

According to the principle of confocal laser scanning, layer-by-layer scanning and morphometric quantitative measurement of the optic disc are made to determine the boundary of the optic cup, and the measurement parameters of the disc edge are more objective, but the standardization of the optic disc boundary is determined, but the different discs cannot be ignored. Individual differences.

3. Optical coherence tomography

Using a 820nm diode laser to scan the retinal nerve fiber layer around the optic disc, a cross-sectional view of the nerve fiber layer surrounding the optic disc area is obtained, and information on the thickness of each quadrant nerve fiber layer is obtained, but the insufficiency is that the error caused by the measurement plane tilt cannot be corrected. Improvements are in progress.

4.GDx glaucoma diagnostic apparatus

780nm diode laser was used to quantitatively measure the optic disc and its surrounding retinal nerve fiber layer. Compared with the previous two instruments, the detection range was wide and more parameters were obtained. However, in clinical application, the results were greatly affected by corneal morphology.

5. Retinal thickness analyzer

Using a topographic map-like imager to quantify parameters such as local extent retinal thickness, changes in retinal parameters are more sensitive than changes in optic disc morphology.

6. Other psychophysical and visual electrophysiological examinations

Subjective visual function test for glaucoma visual function impairment evaluation, in addition to visual field, there are color vision resolution and contrast sensitivity. Many studies have shown that glaucoma can selectively damage blue-yellow vision in the early stage, and these changes can occur in visual field defects. In the past, color vision disorder was related to the degree of visual field defect. The contrast sensitivity of glaucoma patients also changed. The early performance showed that the spatial contrast sensitivity of the high frequency part decreased, partly the low frequency spatial contrast sensitivity decreased, the late stage was the full frequency decrease, and the time contrast sensitive. The degree of damage in the middle frequency band is obvious in the early stage of glaucoma, and the contrast sensitivity can also occur before the visual field defect, but the color vision and contrast sensitivity changes in the early glaucoma overlap with normal people, and the specificity is not high.

Visual electrophysiological examination is also applied to the detection of glaucoma visual function. Because glaucoma is a disease that damages retinal ganglion cells and optic nerve, it is mainly visual evoked potential examination, especially the pattern visual evoked potential, and its typical glaucomatous change is the incubation period. Prolonged and reduced amplitude, pattern visual evoked potential is very sensitive to optic nerve damage, and some patients with primary open angle glaucoma or ocular hypertension without visual field changes can detect abnormal pattern visual evoked potentials, but some have been obvious In patients with primary open-angle glaucoma with visual field defects, the pattern visual evoked potentials are still normal. The sensitivity of the large square, fast conversion rate and small stimulation field stimulation or sub-quadrant stimulation can improve the sensitivity, originating from retinal ganglion cells. The graphical electroretinogram is more sensitive than the graphical visual evoked potential.

Psychophysical examinations have entered clinical application. The status of these experiments in the diagnosis and treatment of glaucoma has not been determined. Combined with some histopathological studies, psychophysical examinations have significantly increased our understanding of how glaucoma affects visual function. Visual evoked potentials detect the degree and extent of optic nerve damage and its damage in glaucoma patients. Many studies have shown that this method is feasible and sensitive. The analysis of its waveform is based on objective data and can avoid the subjective judgment of the examiner. The error, but this method of detection is still in the exploration stage, and it cannot be used alone for the diagnosis of glaucoma.

7. Fluorescence angiography

The fluorescein angiography of the patients with primary open angle glaucoma shows that the optic disc is generally weakly fluorescent, and there is a finite local absolute filling defect at the upper and lower extreme edges of the optic disc, which is often consistent with the location and severity of the visual field defect. Patients with ocular hypertension have more filling and defect areas than normal people. Glaucoma patients have optic nerve perfusion reduction at the local level of the optic disc. The fluorescein angiography shows a relative fluorescence filling defect, and then develops into a localized absolute visual field defect, some normal. People also have filling defects, so it can not be used as a basis for differential diagnosis. In patients with ocular hypertension, the prognostic value of fluorescein angiography filling defects is not certain.

8. Excitation test

For patients with suspected glaucoma, when the intraocular pressure is not high, the test can be stimulated to increase, in order to confirm the diagnosis. The triggering test for glaucoma lies in the pathogenesis of different types of glaucoma, and the corresponding method is adopted for those suspected of certain types of glaucoma. Targeted measures stimulate their elevated intraocular pressure to facilitate early diagnosis.

9. Anterior chamber angle examination

According to the clock direction, the width, opening, closing, shortening and the width and height of the front anterior adhesion and the positive or reverse image are described in the clock direction, and the shape of the surrounding edge (convex or concave) is recorded, using the Soheie classification. Record the pigment grading, first observe the vein, distinguish the width of the angle of the anterior chamber without changing the angle of the angle of the anterior chamber, then observe the artery, determine the degree and extent of the opening and closing of the anterior chamber and the surrounding anterior adhesion, record the intraocular pressure and medication during the examination. Happening.

10. Genetics and genetic testing

Diagnosis

Diagnosis of primary open angle glaucoma

Differential diagnosis of open angle and closed angle glaucoma:

After determining primary glaucoma, it is necessary to clarify its type and to develop a correct treatment policy. Generally speaking, acute angle-closure glaucoma is not misdiagnosed as an open angle type.

Identification point

1. History: Comprehensive analysis based on the status and characteristics of the history of the episode.

2. General situation:

Age: Primary glaucoma under the age of 30 used to be called open-angle glaucoma. Now called congenital glaucoma, it is mostly closed angle around 50 years old.

Gender: There are more women in the angle-closure type than men; more men than women in the open-angle type, women with more than 40 years old have a closed angle, and men under the age of 30 are congenital glaucoma.

Refractive status: There are more angle-closure types in hyperopia; more open-angle types in myopia, more glaucoma in high-distance hyperopia, and open-angle glaucoma in high myopia.

3, the front of the performance: small cornea (less than 10.5mmm), shallow anterior chamber (less than 2.5mm), the iris is mostly bulging for the angle of closure, the anterior chamber is normal, the iris is flat open.

4, anterior chamber angle: open angle type of wide angle, no adhesion, when the intraocular pressure rises, the angle of the corner is still open, the angle of the angle of the angle is narrow, when the intraocular pressure rises, the angle of the angle is closed, intraocular pressure The decline can be reopened and the trabecular mesh is seen. If the chronic angle-closure type is present, most or all of the angles will stick.

5, intraocular pressure tracing: open angle glaucoma, the intraocular pressure fluency coefficient is generally small when the intraocular pressure is increased or decreased, the angle of closure angle is closed, the intraocular pressure is high, the C value is low, the angle of the room is open, the intraocular pressure is low, the C value high.

6, intraocular pressure and fundus: high intraocular pressure, often up to 7.98kPa (60mmHg), while the normal fundus nipple is closed angle, and open angle glaucoma to advanced blood pressure to reach a higher level, and more The nipple depression is enlarged, or the intraocular pressure level is not high, only about 3.99 kPa (30 mmHg), and the nipple depression is obvious, it may be an open angle type.

The differential diagnosis of chronic angle closure and chronic open angle (slow single) glaucoma is listed below (Table):

Identification of chronic angle-closure glaucoma and chronic simple glaucoma:

Differential diagnosis of chronic angle closure and chronic angle closure glaucoma:

Chronic angle closure glaucoma

1. Early rise in intraocular pressure is volatility and can be naturally relieved.

2, although in the state of high intraocular pressure, the angle of the corner will not be completely occluded, and even a considerable range of ciliary body bands can be seen.

3, the pupil is slightly enlarged, no obvious iris atrophy.

Acute angle closure glaucoma chronic phase

1. It is caused by the sudden closure of the patient without proper treatment. The patient has a history of acute attack.

2, the intraocular pressure can be maintained at 3.9 ~ 5.32kPa (30 ~ 40mmHg), can not be naturally relieved.

3, can have varying degrees of corner adhesions.

4. Most cases have acute signs of iris atrophy, glaucoma and vertical pupil dilation on the iris.

Differential diagnosis of glaucoma and ciliary body syndrome and axillary glaucoma:

Glaucoma ciliary body syndrome

1, the disease belongs to secondary open angle glaucoma: mostly middle-aged patients with monocular onset, and can be repeated in the same side of the eye, but there are also two eyes.

2, the onset of elevated intraocular pressure, each episode in 1 ~ 14 days or so, natural relief improved, the general symptoms are light, only blurred vision or rainbow disease.

3, the general intraocular pressure is as high as 5.32 ~ 7.8kPa (40 ~ 60mmHg), but also up to 10.64kPa (80mmHg), elevated intraocular pressure and the symptoms and visual acuity is not proportional, although the intraocular pressure is very high, but the eye is mildly discomfort There are no symptoms such as nausea, vomiting, severe headache and eye pain.

4, each episode presents mild ciliary congestion, small or medium large round gray-white sediment after the cornea, a small number, when the intraocular pressure is elevated, the angle of the anterior chamber is open, the C value is reduced, the intraocular pressure is normal C The value is normal.

5, the onset of the affected side of the pupil is large, although repeated episodes, but no post-iris adhesions.

6, visual field: generally normal, there is no abnormality in the fundus, if there is a change, it may be a slow single merger.

7. In the intermittent period, all kinds of excitation tests are negative.

Differential diagnosis between glaucoma caused by cataract and iridocyclitis :

In the acute attack of glaucoma, some iritis manifestations are often combined, while acute iritis is sometimes accompanied by a certain degree of elevated intraocular pressure. These two diseases have different principles in treatment. If the diagnosis is wrong, it will cause bad results.

Its identification point:

1. Glaucoma eye pressure and extreme increase, the eyeball is as hard as stone, and the eye pressure of the eyelash is normal or elevated, but to a lesser extent.

2, glaucoma pupil dilated and irregular, the pupil of the iris cyanitis is smaller.

3, glaucoma corneal deposition is pigment particles, while rainbow eyelash inflammation is inflammatory exudation, grayish white.

4, after the acute onset of glaucoma, there is often a typical glaucoma triad, but iridocyclitis is not.

5, in the treatment, acute angle closure glaucoma in the acute attack period to reduce the pupil to open the anterior chamber angle, as soon as possible to reduce the intraocular pressure to improve the condition, acute iritis should sooner or later expand the pupil to prevent post-irisal adhesions, which is principled in treatment the difference.