Since von Graefe discovered that the atrophy and depression of optic disc in glaucoma patients were caused by the increase of intraocular pressure in the clinical observation in the middle of19th century, it has been continuously confirmed in clinical work that the vast majority of glaucoma patients have the same characteristics of the increase of intraocular pressure. Therefore, a traditional concept has been formed: glaucoma is a comprehensive eye sign or a group of eye diseases characterized by the depression and atrophy of the optic disc and the corresponding visual field defect caused by high intraocular pressure, and the damage of its visual function until complete loss is the final result of high intraocular pressure.
For many years, although it has been emphasized that the diagnosis of glaucoma must have three elements: high intraocular pressure, concave atrophy of optic disc and characteristic visual field defect, there is still a habitual misunderstanding: all high intraocular pressure is glaucoma, and high intraocular pressure will inevitably lead to optic nerve atrophy and visual field damage of glaucoma, so we should actively treat it to avoid irreparable visual function damage.
According to the data of population survey, the average intraocular pressure (M) of normal people is 15 ~ 16 mmHg, and the standard deviation (SD) is 2.5 ~ 3.0 mmHg, that is, the applanation intraocular pressure value of Goldmann is 15.4 mmHg 2.5 mmHg, Schi? Tz indentation IOP is 16. 1mmhg 2.8mmhg. Based on this, the IOP range of normal people is 10 ~ 2 1mmHg(95% confidence limit, with an average of 2 standard deviations), and if it exceeds the upper limit of normal value, it is considered as suspected.
Clinically, based on the measurement of intraocular pressure, some patients with high intraocular pressure but lack of other glaucoma support are actively diagnosed as glaucoma, given anti-glaucoma drugs and even surgery. However, as early as the early 1950s, it was also observed in clinical work that some patients with ocular hypertension did not have optic nerve and visual function damage for several years, which also attracted the attention of ophthalmology. Later, it was found that normal individuals with intraocular pressure exceeding the statistically normal range accounted for a certain proportion (5% ~ 10%). Therefore, Hollows and Graham suggested using "high intraocular pressure" to define those special manifestations with high intraocular pressure but unchanged optic disc and visual field, so as to distinguish them from open-angle glaucoma with elevated intraocular pressure, depressed atrophy of optic disc and corresponding visual field damage. Subsequently, a series of clinical studies on ocular hypertension not only enriched the differential diagnosis of primary open angle glaucoma, but also observed that some patients with ocular hypertension would eventually develop glaucoma.
The consistent understanding of high intraocular pressure refers to the state that after repeated intraocular pressure measurement (Goldmann applanation tonometer), the intraocular pressure of both eyes exceeds the upper limit of normal statistical intraocular pressure, the angle of the chamber is normal, and no morphological changes and/or visual field damage are found during long-term follow-up.
Although ocular hypertension develops slowly and rarely causes optic disc depression and visual field damage, it has the same important pathophysiological background as open angle glaucoma-elevated intraocular pressure. In fact, some people with high intraocular pressure eventually turn to open angle glaucoma. At present, there is no clear boundary to distinguish between high intraocular pressure and open angle glaucoma. In order to study the internal relationship between high intraocular pressure and open-angle glaucoma, ophthalmologists are trying to explore the predictive index of the transformation from high intraocular pressure to open-angle glaucoma. High intraocular pressure is actually suspected glaucoma.
Only the intraocular pressure increased, and no damage to optic disc and visual field was found during follow-up. The development of ocular hypertension is a slow and benign process. Through long-term observation, the intraocular pressure of most patients with high intraocular pressure is stable or even decreased, which is in stark contrast to the slow progress and aggravation of open-angle glaucoma. Disc hemorrhage is considered as a sign of transition to open angle glaucoma, which is mostly located in the upper and lower poles of the disc, and the lower pole is more common. People with high intraocular pressure should be closely followed up.
Hypertensive intraocular pressure is only increased to varying degrees, and there is no optic disc damage and visual field defect, which is different from other types of glaucoma.
Due to the potential side effects and economic burden of drugs, there are still differences on whether to treat ocular hypertension. It is generally believed that patients with high intraocular pressure with risk factors can be treated selectively, such as intraocular pressure exceeding 30mmHg, family history of positive glaucoma, high myopia, cardiovascular disease or diabetes. Although most ocular hypertension will not develop into glaucoma, ocular hypertension is a risk factor for glaucoma after all. Therefore, patients with treated or untreated ocular hypertension should be followed up regularly to prevent the transformation to open angle glaucoma.
Name of disease: ocular hypertension
3 English name for ocular hypertension
4. Alias high intraocular pressure; High intraocular pressure; Intraocular hypertension
5 Classification Ophthalmology > Glaucoma > Primary Glaucoma
6 ICD number H40.8
Epidemiological consensus is that ocular hypertension is far more common than open angle glaucoma. The former is 10 ~ 15 times of the latter. Overall, the incidence of ocular hypertension is about 6%, while the incidence of open angle glaucoma is about 0.5%. In the general population, the incidence of ocular hypertension is about 2%, while it is as high as 4% ~ 10% in people over 40 years old. Women are more common than men. Although we haven't seen the investigation reports of large groups in China, it is not uncommon to leave an impression on people in clinic.
Etiology Although ocular hypertension develops slowly and rarely damages the optic disc and visual field, it has the same important pathological factor as open angle glaucoma, that is, elevated intraocular pressure. So what factors affect high intraocular pressure? Which of these factors are the risk factors for the development of glaucoma from ocular hypertension?
8. 1 The data of related factors of ocular hypertension showed that female patients with ocular hypertension, elevated blood pressure and winter were related to ocular hypertension. There are more women with high intraocular pressure, and most of them are over 40 years old, suggesting that it may be related to the endocrine changes of women, especially the dysfunction of autonomic nervous system before menopause. It explains the accompanying phenomenon of elevated blood pressure and intraocular pressure, and is also related to the dysfunction of vascular autonomic nerve. The relationship between intraocular pressure and seasonal and daytime changes (often higher in the morning) is mostly considered to be related to the periodic changes of adrenocortical hormones in the body. In addition, the systemic factors related to high intraocular pressure are race (black is more common), height, weight, pulse rate, diabetes, smoking and so on. The main factors related to high intraocular pressure are dark iris (that is, thick iris pigment), corneal thickness and myopia. As for the age factor, westerners report that intraocular pressure increases with age, but epidemiological data in Japan and China show that intraocular pressure decreases with age.
8.2 Risk factors of ocular hypertension Previous research data suggest that age, abnormal optic disc shape, degree of ocular hypertension, family history of glaucoma, cardiovascular disease and central retinal vein occlusion are risk factors for optic nerve damage and visual field damage in patients with ocular hypertension. In 2002, Gordon and others reported the latest multicenter randomized study of OHTS group, and followed up 1636 patients with ocular hypertension for an average of 72 months. Factors that may predict the development of primary open-angle glaucoma include age, race, sex, the ratio of vertical diameter to horizontal diameter of cups and plates, intraocular pressure, family history of glaucoma, Humphrey index, myopia, heart disease, hypertension, hypotension, oral calcium channel blockers or β -adrenergic receptor antagonists, cerebrovascular accident, diabetes, migraine and central corneal thickness. The results show that, among the above baseline factors of high intraocular pressure, older age, larger cup-to-disc ratio (including vertical diameter and horizontal diameter), higher intraocular pressure and larger visual field mode deviation (PSD) are the most powerful predictors of primary open-angle glaucoma, and thinner central corneal thickness is the most powerful predictor of glaucoma.
Although the pathogenesis of ocular hypertension develops slowly and rarely causes optic disc depression and visual field damage, it has the same important pathophysiological background as open angle glaucoma-elevated intraocular pressure. In fact, some people with high intraocular pressure eventually turn to open angle glaucoma. At present, there is no clear boundary to distinguish between high intraocular pressure and open angle glaucoma. In order to study the internal relationship between high intraocular pressure and open-angle glaucoma, ophthalmologists are trying to explore the predictive index of the transformation from high intraocular pressure to open-angle glaucoma. High intraocular pressure is actually suspected glaucoma.
The clinical manifestation of 10 ocular hypertension is only elevated intraocular pressure, and no damage to optic disc and visual field was found during follow-up. The development of ocular hypertension is a slow and benign process. Through long-term observation, the intraocular pressure of most patients with high intraocular pressure is stable or even decreased, which is in stark contrast to the slow progress and aggravation of open-angle glaucoma. Disc hemorrhage is considered as a sign of transition to open angle glaucoma, which is mostly located in the upper and lower poles of the disc, and the lower pole is more common. People with high intraocular pressure should be closely followed up.
1 1 auxiliary examination 1 1. 1 optic disc cup/disc ratio (C/D) has long been the most commonly used index to describe glaucoma optic neuropathy. The C/D value of normal fundus is mostly less than 0.4. If it is greater than 0.6, or the C/D difference between eyes is greater than 0.2, you should pay attention. Regular follow-up shows that the progressive deepening and enlargement of optic disc depression is more diagnostic for glaucoma. However, before the optic disc depression changes obviously, careful examination will find the related signs of glaucoma damage. In addition, the physiological ratio of optic disc in normal people is 5% ~ 10%, so the C/D value is no longer an effective specific marker for early diagnosis of glaucoma.
1 1.2 visual field examination Traditional visual field examination, such as Goldmann visual field examination and arc visual field examination, is a qualitative examination of dynamic visual field, which has been difficult to be used for the diagnosis of early glaucoma. At present, the visual field examination of early glaucoma is mainly static visual field with threshold quantitative detection, that is, it can measure the actual sensitivity of each point in the visual field, monitor small changes and make statistical probability judgment. Visual field examination is a subjective examination, that is, psychophysical examination, which will be disturbed by many factors. Therefore, when analyzing the results, we should consider the cooperation degree of patients and the reliability parameters of visual field examination, exclude other artifacts, and make a comprehensive analysis and judgment according to intraocular pressure and fundus morphology. Visual field damage can also be seen in other eye diseases and diseases such as nervous system and vascular system. In addition, the existing clinical visual field examination methods can only be detected after the optic nerve fibers are damaged to a certain extent. Although its specificity in diagnosing glaucoma is higher than that of fundus morphological changes, its sensitivity is not as good as that of fundus morphological changes. Therefore, when it is difficult to judge whether there is visual field damage at the moment, you can follow up regularly and compare and analyze the changes of visual field. Don't rule out or confirm the diagnosis of early glaucoma just by one visual field test.
1 1.3 Other visual function tests In addition to visual field damage, there may be other visual function abnormalities in the early stage of glaucoma, including: ① decreased sensitivity of spatial/temporal contrast; (2) The ability of color discrimination decreased, especially the blue and yellow senses were affected earlier and more seriously; ③ In electrophysiology, the amplitude of pattern electroretinogram decreased and the latency of pattern VEP peak prolonged. In recent years, frequency doubling visual field (FDP), short wavelength visual field (SWAP) and multifocal electrophysiology (MERG) have shown initial advantages in the early visual function evaluation of glaucoma, and it is expected to find the visual function damage of characteristic glaucoma earlier.
It should be emphasized that both ocular hypertension and primary open angle glaucoma are bilateral, and the diagnosis of both eyes should be consistent, but the allowable degree is different. If one eye has definite optic disc and/or visual field damage of glaucoma, the other eye should be diagnosed as glaucoma instead of ocular hypertension, even if only the intraocular pressure increases without optic disc or visual field damage.
The diagnosis of 12 ocular hypertension only depends on a single intraocular pressure index, so we should pay full attention to the measurement error when measuring intraocular pressure. The measured intraocular pressure is influenced by many factors. There are considerable differences in CCT between normal people, and CCT is significantly related to the measured value of applanation intraocular pressure. The thicker CCT is, the higher the measured IOP is, because CCT corrects the IOP measurement and gets a more realistic IOP value.
Because the clinical situation of ocular hypertension is complicated, and some ocular hypertension will eventually develop into primary open angle glaucoma, in recent years, most scholars tend to take "protective" antihypertensive treatment for ocular hypertension, including ocular hypertension with the following risk factors, in addition to regular follow-up observation (regular review of intraocular pressure, optic disc, retinal nerve fiber layer and visual field).
1. IOP ≥4kPa(30mmHg).
2. Have a family history of positive glaucoma.
3. The contralateral eye is primary open angle glaucoma.
4. High myopia.
5. The optic disc is sunken.
6. It is accompanied by systemic hemodynamic and hemorheological abnormalities that can cause optic disc hypoperfusion, such as diabetes, hypertension, history of cerebrovascular stroke, peripheral vasospasm, hyperviscosity, etc. The "protective" treatment to reduce intraocular pressure adopts drug therapy, and the principle of drug selection is the same as that of primary open angle glaucoma.
For patients with mild ocular hypertension such as intraocular pressure < 4 kPa (30 mmHg), there are no risk factors that can cause visual field damage. At present, they tend to be followed up regularly without treatment.
The differential diagnosis of 13 ocular hypertension only has different degrees of intraocular pressure elevation, ignoring disc damage and visual field defect, which is different from other types of glaucoma.
Treatment of 14 ocular hypertension Due to the potential toxic and side effects and economic burden of drugs, there are still differences on whether to treat ocular hypertension. It is generally believed that patients with high intraocular pressure with risk factors can be treated selectively, such as intraocular pressure exceeding 30mmHg, family history of positive glaucoma, high myopia, cardiovascular disease or diabetes. Although most ocular hypertension will not develop into glaucoma, ocular hypertension is a risk factor for glaucoma after all. Therefore, patients with treated or untreated ocular hypertension should be followed up regularly.
The most important thing to deal with high intraocular pressure is close follow-up, mainly to monitor the changes of intraocular pressure, fundus optic disc morphology and visual field. If the intraocular pressure has been at a high level (such as ≥25mmHg) or the intraocular pressure continues to increase, the fundus optic disc morphology (preferably quantitative analysis) and threshold visual field 1 time should be detected every 6 months. If there are high-risk factors or obvious unfavorable factors in the follow-up process, drug treatment can be given as appropriate. However, laser or surgical treatment is generally not recommended, because the damage caused by the latter two will be irreversible. If drug treatment is given, we should weigh the advantages and disadvantages, choose appropriate drugs to reduce intraocular pressure as much as possible to the normal statistical range, or reduce the basic intraocular pressure by 30%.
15 prognosis Some patients with high intraocular pressure, especially those with fundus damage, need close follow-up and monitoring to prevent the transformation to open angle glaucoma.
16 related drug epinephrine
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Inner canthus