What Is Low Eye Pressure?

Low intraocular pressure is a medical term that refers to intraocular pressure with a natural intraocular pressure of 2.79kPa.

Low intraocular pressure

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Low intraocular pressure is medicine

Acquired acquired POAG-like optic papillary changes, RNLLD, and visual field damage, untreated natural intraocular pressure 2.79 kPa (Goldmann flattened intraocular pressure), and the angle of the chamber is open, which excludes optic nerve papillary atrophy and visual field defects The diagnosis can be established after other diseases. Therefore, the establishment of LTG diagnosis is to exclude other lesions, so differential diagnosis is particularly important.

Because the etiology of this disease is unknown and the causative factors are complex, there is no effective treatment so far. Some scholars use various measures such as drugs, lasers, and filtering surgery to lower the intraocular pressure to try to prevent the progress of visual field damage, but the general effect is not exact. Abedin (1982) believes that it may be effective to reduce the intraocular pressure to at least 1.59 kPa, while Bloomfield (1953) believes that surgery to prevent further deterioration of the visual function of the disease is not helpful. The effect of using animals that improve blood circulation is also satisfactory. Localized 1% L-adrenaline has the effect of increasing ocular arterial pressure and reducing ocular pressure. Intravenous injection of strophanthin can eliminate the blood pressure difference between the orbital blood pressure and the upper arm blood pressure. Treatment should also include other abnormalities in the patient, such as gastrointestinal disease, anemia, congestive heart failure, orthostatic hypotension, transient ischemic attack, arrhythmia, and cardiovascular disease, to improve blood in the optic nipples supply.

In short, there is no effective treatment to prevent the progress of visual nipples and visual field damage in patients with LTG. Early detection and timely treatment can effectively reduce intraocular pressure and improve visual papillary blood perfusion, which may delay the development of the disease. The course of most LTG patients progresses slowly, and visual function is maintained for a long period of time. The final outcome is similar to that of POAG. Recently Shirai (1988) reported the use of calcium antagonist Yoshihiko Shiose (1988) reported that mythlcolamin has been used to treat hypotensive glaucoma, and it is worthy of further research.

The etiology of LTG is very complicated, so far its exact pathogenesis is not clear, and various pathogenic factors have been proposed. The more supported are vascular factors, followed by local anatomic factors, which are described separately below:

1. Vascular factors Many authors have observed that the incidence of hemodynamic crisis is higher in patients with LTG, and there are more patients with cardiovascular and cerebrovascular diseases and hypotension, often accompanied by abnormalities in hemorheology, such as Increased blood viscosity, etc. At the same time, the incidence of disc bleeds in these patients is higher, the autoregulation of small blood vessels in the optic disc is dysfunctional, and fundus fluorescence angiography shows optic disc fluorescence filling defects. The above phenomena seem to indicate that the occurrence of LTG and the optic nerve Nipple ischemia is closely related. As for the causes of optic disc ischemia, there may be several aspects: due to systemic or local small vessel disease, some small blood vessels supplying optic disc are blocked, causing the segments along the optic disc to awaken to death, and nerve fiber atrophy and visual field damage occur. Aggravation of the small blood vessels or an increase in the number of obstructions, further development of nerve fiber atrophy, and the field of vision continues to expand. Due to the drop of blood pressure or long-term hypotension due to the occurrence of hemodynamic crisis such as large blood, severe myocardial infarction, arrhythmia, and shock, etc., the ophthalmic artery pressure is reduced, and the ischemia occurs due to poor perfusion of nipple blood; Academic abnormalities, such as increased blood viscosity, increased platelet adhesion rate, and fibrinolytic system disorders, increase blood flow resistance and are prone to thrombosis, all related to ischemia.

Some scholars have suggested that although LTG and ischemic optic neuropathy are both ischemic diseases, the affected blood vessels may be different. At the same time, the former is the result of long-term chronic insufficient blood supply to the optic disc due to the interaction of multiple factors.

2. Local anatomical factors Scholars holding this view believe that the occurrence of optic nerve papillary atrophy in LTG patients is due to certain defects in the anatomical structure of the papillary sieve plate, such as fewer continuous continuous fibers in the sieve plate and normal tissues. Normal people are thin, and the pores of the sieve are larger, especially the pores on the sieve plate and below, which make the sieve plate abnormally fragile and have low resistance to intraocular pressure. Hold the effect of intraocular pressure, the sieve plate collapses and sags, the sieve holes are twisted and deformed to damage or compress the nerve fibers, and the axonal pulp transportation is blocked, the nerve fibers are dystrophic and atrophy, and the capillaries there are also distorted Indirectly causes blood supply disorders, further leading to nerve fiber atrophy. It has also been found that the eye axis and vitreous cavity of LTG patients are relatively long, and the C / D is relatively large, which may be somewhat related to the pathogenesis of LTG.

In short, the pathogenesis of this disease has not been fully elucidated, and the causative factors are complicated. From the current data, the occurrence of LTG may be due to the differences in the ocular tissue structure, especially the anatomical structure of the papillary sieve plate, which is related to the abnormal sensitivity of intraocular pressure or poor blood perfusion. May be acquired the day after tomorrow.

The onset is very hidden, often unknowingly, due to the lack of subjective symptoms, patients often come to the doctor in the middle and late stages, such as being noticed or found in routine experience.

1. The majority of patients in the early stage of medical history do not have any conscious symptoms, and individual patients may have discomfort such as eye length and fatigue. Complaints that vision loss is mostly related to refractive, cataract, and macular degeneration; patients with advanced vision may have central vision loss.

2. IOP

Mean intraocular pressure: The intraocular pressure of patients with LTG is within the statistically normal range. However, many scholars have observed that the patient's intraocular pressure fluctuates within the range of the normal upper limit, and the base pressure is high, and the average intraocular pressure seems to be higher than that of normal people;

24-hour intraocular pressure: normal people are affected by physiological factors, 24-hour intraocular pressure may fluctuate, but generally 0.67kPa. Some scholars have also noticed that the fluctuation of the 24-hour IOP in some patients is greater than 0.67kPa or 1.06kPa.

(3) The influence of body position on intraocular pressure: The IOP measured in the supine position in normal people is higher than that in the sitting position, but the difference is 0.79kPa. The IOP difference between the two positions of some LTG patients is larger, according to some authors. It is 1.14 1.33kPa;

Long-term changes in intraocular pressure: Some scholars have noticed in the long-term observation of intraocular pressure in LTG patients that the intraocular pressure of individual patients has an upward trend. As a result, the intraocular pressure has increased from a low value in the normal range to a high value, such as from 1.33kPa At 2.66 kPa or beyond the normal range, it turns into open-angle glaucoma. However, not all patients with LTG have the above characteristics, and some patients have lower and more stable IOP.

3. Tonometry: The humoral fluidity coefficient of patients with LTG is at the lower limit of normal value, and some patients are low, accompanied by abnormalities of the pressure ratio. However, there were some patients with no special changes in the tonography. Some scholars regard the abnormality of the aqueous humor coefficient as the basis or classification basis for distinguishing between true and false LTG. However, the role of tonography in the diagnosis and prognosis of LTG remains to be further confirmed.

4. Provocation test The results of the provocation test on LTG patients are very inconsistent. Some scholars report that most patients have corticosteroids with moderate and high eye-lifting response, but there are also reports of no difference from normal people; drinking water tests have the same situation. . In short, its value is hard to be sure.

5. Refractive and living eye structure LTG patients have a higher incidence of myopia than the normal population, their vitreous cavity and eye axis are longer than normal people, the vertical corneal radius of curvature is larger than normal people, and tend to have a trapped C / D value.

6. Papillary nipples in patients with LTG are similar to POAG. However, some scholars have recently observed that the disc disc edge of LTG is narrower than that of POAG. The narrowest area is below or below the temporal. The characteristics of the optic cups of the two are also different. Depending on the cup wall being steeper, the narrowing of the rim is more consistent. Banded sieves and vascular overhead are more common in open-angle glaucoma. These characteristics help distinguish between the two.

The incidence of disc bleeds in LTG is significantly higher than that in POAG and normal eyes. Sheet bleeds are often flame-like or line-shaped, and most often appear at disc-rim notches or discontinuous hemorrhage occurs 2 to 3 months after the disc-like hemorrhage. Traces can occur repeatedly, usually at 7 or 11 o'clock in the right eye and 1 or 5 o'clock in the left eye. Many scholars believe that optic disc hemorrhage is the result of vascular infarction in the nipples; others believe that it is caused by morphological damage caused by sieving and deformation of the retinal plate, and the high incidence of retinal hemorrhage in LTG patients may be related to the fragile structure of the retinal plate. Regardless of the cause, the occurrence of optic disc hemorrhage is a sign of disease progression.

7. Retinal neurofibrous layer defect (RNFLD) The RNLLD of LTG is similar to that of DOAG, and presents localized and diffuse defects. In the early stage, the nerve fiber bundles involving the subtemporal and supratemporal regions are often shown as fissured, wedge-shaped dark bands, and they can also appear as diffuse thinning and thinning, like a combed hair-like appearance. Dark granular appearance. Some scholars have observed that RTNLD in LTG involves more nerve fiber bundles in the temporal region than POAG.

8. Kameno generally believes that the god damage of this disease is similar to that of POAG. However, some scholars have observed that the visual field defect is earlier and more close to the fixation point than POAG, the slope is steeper, the defect is deeper, and the visual field defect occurs more than the lower part. . The visual field damage of LTG is different from that of POAG, suggesting that the two damage mechanisms may be different.

9. Fluorescence fundus angiography Fluorescence fundus angiography shows that most patients with LTG have filling defects of the optic disc, and most of them show segmental low fluorescence, suggesting ischemic optic nipples. Some scholars have observed that from comparative filling defect to absolute filling defect, visual field damage will occur. When there is a new visual field defect, there will always be a new video disc filling defect or the original filling defect will expand, and the video disc filling defect will appear in Before visual field damage, this seems to indicate that the visual impairment of the open door is directly related to optic disc ischemia. However, Quigly (1986) believes that the disc filling defect does not provide a basis for primary insufficient blood supply, but may be the result of tissue atrophy and disappearance along with blood vessels.

10. Ocular arterial pressure and perfusion pressure Drance (1973) reported that ocular arterial hypotension in patients with LTG was suspected of POAG: Goldberg (1981) believed that diastolic ocular arterial pressure was lower than suspected POAG; but Spaeth (1975) proposed ocular arterial pressure in LTG No different from POAG and normal people.

Regarding perfusion pressure, Goldberg (1981) reported that the diastolic perfusion pressure in LTG patients is similar or may be lower than that of suspected POAG, while Kramer (1987) believes that the perfusion pressure in LTG patients is no different from normal people. At the same time, he believes that the conclusion that perfusion pressure is susceptible to blood pressure is unreliable, and the ciliary choroidal vascular network resistance measured based on the eye pulse amplitude and arterial blood flow can better reflect the blood supply. He suggested that the resistance of the ciliary choroidal vascular network in patients with LTG is 2 to 3 times higher than that in normal people, and the increase in resistance results in decreased blood flow. Perkine (1981) also studied this aspect. In one report, he mentioned that the eye pulse amplitude of LTG is lower than that of the normal eye. The change is larger than that of the normal eye.

In conclusion, the observation results of ocular arterial pressure and perfusion pressure of LTG are not very consistent, and may be lower than those of normal eyes and suspected POAG.

11. Systemic conditions LTG patients have a high incidence of hypotension. Many authors believe that low tension is a risk factor for this disease. The incidence of hemodynamic crisis and cardiovascular and cerebrovascular diseases is also significantly higher than that of normal people. More migraines occur in patients with LTG. In terms of hemorheology, the whole blood viscosity of patients with LTG is high; there are more abnormal blood coagulation and fibrinolytic system.

12. Progressive and non-progressive LTG, some scholars have observed that in some patients with LTG, the atrophy of the optic nerve papillae and lack of visual field do not progress, and some of them progress. Therefore, the disease is classified into progressive and non-progressive based on this performance. The causes of these two types may be different. Drance (1985) proposed that in patients who had hemodynamic crisis before diagnosis of LTG, most of the visual field and visual nipple damage did not progress, and in patients who did not have hemodynamic crisis, most of the fields of vision were Progressively, the former may be due to hemodynamic crisis or vascular lesions that cause optica and segmental infarction. If the infarction no longer occurs, the damage will not develop. For progressive LTG, Chandler (1979) proposed that the IOP of these patients is mostly at the normal upper limit value and the aqueous humor coefficient is at the normal lower limit value. The papillary sieve structure is abnormally fragile and sensitive to the damage of intraocular pressure. It is necessary to lower the intraocular pressure of these patients to prevent the development of visual nipples and visual field damage.

13. Some scholars of LTG with anterior segment lesions and no anterior segment lesions have proposed other conditions and limitations for the diagnosis of this disease, such as requiring multiple challenge tests to be normal, the aqueous humor coefficient and pressure ratio to be normal, and intraocular pressure. Fluctuations 0.67kPa, etc .; while other scholars believe that the diagnosis of LTG must have the above-mentioned abnormalities. Levene (1982) believes that it is inappropriate and subjective to diagnose or exclude the disease with these conditions, and to classify it in order to truly and objectively understand LTG. Therefore, he advocates dividing the disease into: LTG with glaucoma-related abnormal hydroaqueous dynamics (referring to C value, po / c and daily intraocular pressure fluctuations, positive challenge test, etc.); without glaucoma (Aqueous hydrodynamic abnormalities) LTG. He believes that at least one-third of patients with LTG have abnormalities in aqueous humor.

14. Klaver's classification: Klaver (1985) further classified LTG patients into the ischemic group (focalischaemicsubgroup, FILTG), the senile sclerosis group (senilescleroticsubgroup, SSLTG), and those who did not belong to FILTG. Belongs to the SSLTG mixed group (miscellaneoussubgroup, LTGmisc). FILTG's changes in the optic papilla are: the disc of the optic disc is locally sunken along the tissue, and the vertical diameter of the optic cup expands upward or downward, with corresponding local atrophy around the optic nipple; SSLTG treats the nipple as pale, and the disc edge is wormlike and Sloping depressions with extensive choroid sclerosis and atrophy around the optic nipple.

1. Primary open-angle glaucoma (POAG): Because no intraocular pressure is measured for 24 hours, no peak IOP is found, or those with low scleral stiffness in myopia have low intraocular pressure measured by Schiotz tonometer, or patients taking - Blockers and cardiac glycosides reduce intraocular pressure and are easily misdiagnosed as LTG. Therefore, it is necessary to stop the repeated measurement of intraocular pressure under all intraocular pressure-lowering drugs, including 24-hour intraocular pressure, use an applanation tonometer to measure myopia, and establish the diagnosis of LTG when it is clear that the intraocular pressure is within the normal range.

2. Other glaucoma: Corticosteroid glaucoma, glaucoma syndrome, pigment dissemination syndrome, ocular trauma and uveitis secondary glaucoma may all have a transient increase in intraocular pressure, and then be at rest and misdiagnosed as LTG. It can be ruled out by asking a detailed medical history and detailed examination of the eyes.

3. Congenital or acquired acquired papillary abnormalities

For example, the large depression of the optic papilla, the defect of the papilla, the congenital papillary holes, and the development of the papillae may be confused with the atrophy of the glaucomatous papilla. But as long as you notice the age of disease, carefully check the visual nipples to see if there are visual field defects and the characteristics of the defect and whether it is progressing, etc. can be ruled out.

4. Ischemic optic neuropathy

Ischemic optic neuropathy generally does not produce atrophic optic nipples, atrophy, and enlargement of visual acuity. However, it has also been reported that in some anterior ischemic optic neuropathy, especially arterial anterior ischemic optic neuropathy, glaucoma-like optic nipple atrophy can occur, and it is easy to be confused with LTG, but the disease has the following characteristics: More urgent, acute or subacute course, with the main complaint of sudden decrease in visual acuity, which may be accompanied by headaches, eye pain and other discomforts; while LTG patients often lack the main complaint, the onset of concealment, and the disease progresses slowly. The pale range of the optic papilla of ischemic optic neuropathy is larger than the depression, and the disc edge is pale, while the atrophy of the glaucomatous optic nipple is only the enlargement and deepening of the optic cup, and the remaining disc edge is still reddish; ischemic optic nerve The visual field damage of the lesion often involves the fixation point and is horizontally semi-blind or quadrant blind but not bounded by the horizontal midline or vertical midline. An arc defect extending from the horizontal semi-blind or quadrant blind is connected to the physiological blind spot. The degree is greater than the depression of the optic cup; fundus fluorescence angiography: optic disc fluorescence of ischemic optic neuropathy, early manifestations of abnormal vasodilation of small blood vessels, abnormal fluorescence leakage of the optic disc, blurring the optic disc with high fluorescence, late filling and low fluorescence Wait. Systemic condition: It is often accompanied by giant cell arteritis, collagenous disease, diabetes, syphilitic arteritis, and hypertension arteriosclerosis.

5. Myopia: Myopia, especially the highly myopic nipples, sometimes show a shallow depression, similar to the depression of the optic nipples in glaucoma, and can be misdiagnosed because of atrophy of the choroidal retina. At the same time, high myopia with glaucoma is also easily missed. The main point of identification is that the morphology and size of the optic nipple depression are not carefully checked with a trinocular mirror using slit light and whether there are retinal choroidal lesions that cause visual field defects. At the same time, fluorescein fundus angiography may also help differential diagnosis. Absolute filling defects like LTG vision nipples are created.

6. Retinopathy: Schreiber (1906) has proposed that retinal vascular occlusion and other diseases can cause ascending optic nerve atrophy after the death of ganglion cells and produce depressions similar to glaucomatous optic nipples. However, many scholars have observed that this type of retinopathy can occasionally produce glaucoma-like visual field defects, but there will be no change in glaucomatous optic nipples.

7. Others: Hereditary atrophy, neurofasciitis, arachnoiditis, non-specific giant cell arteritis, pituitary tumors, carotid calcified plaques compressing nerves, and sacral lesions may be misdiagnosed as occasional diseases. Alcoholism may also cause vision Nipple atrophy and depression should be eliminated one by one.