low-tension glaucoma
Introduction
Introduction to low intraocular glaucoma The concept of glaucomatous optic atrophy, papillary depression, and glaucomatous visual field defects often attributed to elevated intraocular pressure has cast doubt. These changes have occurred in some patients without high intraocular pressure. This situation was first described by vonGraefe (1857) and has since attracted the attention of ophthalmologists and has been naming variously. Although some doctors have carotid calcification, some lesions such as alcoholism, pituitary tumors, etc. may cause similar changes, but after long-term observation, many patients with these changes can not find the above reasons. For such cases, the exact cause is that the intraocular pressure is within the normal range, and the glaucoma optic nerve head atrophy depression and visual field damage are classified into low-tension glaucoma (LTG). Many kinds of normal intraocular glaucoma in modern literature. The incidence of LTG in the population is about 0.15%, accounting for 18-20% of all open-angle glaucoma. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific people Mode of infection: non-infectious Complications: arachnoiditis
Cause
Causes of low intraocular pressure glaucoma
The etiology of LTG is very complicated. So far, its exact pathogenesis is not clear, and various pathogenic factors have been proposed. The vascular factors are more supported, followed by local anatomical factors.
Vascular factors (40%):
Many scholars have observed that the incidence of blood flow crisis in LTG patients is relatively high, and there are many patients with cardiovascular and cerebrovascular diseases and hypotension, often accompanied by abnormalities in blood rheology, such as increased viscosity of whole blood. At the same time, the incidence of optic disc hemorrhage is higher in these patients, the autoregulation of optic disc small vessels and the fundus fluorescein angiography show optic disc fluorescence filling defects. The above phenomena seem to indicate that the occurrence of LTG is closely related to optic nerve papillary ischemia. Related, as for the cause of optic disc ischemia may be as follows:
1 due to systemic or local small vessel disease obstruction of some small blood vessels supplying the optic disc, causing the segment along the optic disc to awake, resulting in damage to the visual field of nerve fiber atrophy, increased number of obstruction or obstruction of small vessel obstruction, further aggravation of nerve fibers Development has expanded the horizons.
2 due to hemorrhage, severe myocardial infarction and arrhythmia, shock and other blood flow crisis caused by blood pressure drop or long-term hypotension, leading to decreased intraocular pressure, opioid hypoperfusion and ischemia.
3 abnormalities in blood rheology, such as increased blood viscosity, increased platelet adhesion rate, fibrinolysis system disorders, etc., increase blood flow resistance and easy thrombosis, are related to ischemia.
Some scholars have suggested that although both LTG and ischemic optic neuropathy are ischemic diseases, the affected blood vessels may be different, and the former is the result of multiple factors interacting with chronic chronic blood supply to the optic disc.
Topical anatomical factors (30%):
Scholars who hold this view believe that the occurrence of optic nerve head atrophy in LTG patients is due to some defects in the anatomy of the optic papilla, such as the cross-continuous fibers of the sieve plate are less than normal, and the connected tissue is thinner than normal. The pore size of the sieve hole is large, especially on the sieve plate, and the pore diameter below is larger, so that the sieve plate tissue is extremely fragile, the resistance to intraocular pressure is low, and the intraocular pressure can not be resisted even under normal intraocular pressure. However, after the sieve plate collapses, the sieve hole is twisted and deformed to damage the nerve fiber or the nerve fiber is compressed, the axoplasmic transport is blocked, and the nerve fiber is dystrophic and atrophied, and the capillaries here are also distorted and indirectly cause blood supply obstacles. Further, the nerve fibers are atrophied. It has also been found that LTG patients have longer axial and vitreous cavities and relatively large C/D, which may be related to the pathogenesis of LTG.
In short, the pathogenesis of this disease has not been fully elucidated, and the pathogenic factors are complex. From the current data, the occurrence of LTG may be due to the difference in anatomical structure of the ocular structure, especially the nipple sieve plate, resulting in intraocular pressure. Or abnormally sensitive to poor blood perfusion, the difference in these organizational structures may be congenital or acquired.
Prevention
Low intraocular pressure glaucoma prevention
1, to maintain a happy mood: angry and anxious and mentally irritated, it is easy to raise the pressure of the eye, causing glaucoma, so usually keep a happy mood, do not be angry and anxious, not to worry about the chores of household chores.
2, maintain a good sleep: sleep uneasy and insomnia, easy to cause elevated intraocular pressure, induced glaucoma, the elderly should wash their feet before going to bed, drink milk, help fall asleep, if necessary, take hypnotics, especially those with higher intraocular pressure It is better to sleep well.
3. Work or play less in a dark environment: People who work in the darkroom should go out of the darkroom every 1 to 2 hours or turn on the lights appropriately. People who are emotionally excited should watch movies less and watch TVs with small lights next to the TV.
4, to avoid overwork: whether it is physical labor or mental work, the body is prone to fluctuations in intraocular pressure after overwork, so pay attention to the law of life, work and rest, avoid overwork.
5, do not overeating: overeating and eating too much, will increase eye pressure, induce glaucoma. Older people should "eat eight full meals, no smoking, no drinking, no coffee, no strong tea, no spicy and irritating food."
6, eat more honey and other foods: honey is a hypertonic agent, after oral honey, the osmotic pressure in the blood will rise, so the excess water in the eye is absorbed into the blood, thereby reducing intraocular pressure. In addition, watermelon, melon, and red bean are also beneficial to the effect of water and blood pressure. It is good for the elderly to eat more properly.
7, often touch your own eye, look at the light: glaucoma is characterized by hard eyeballs, see the lights have a rainbow circle, found early and early treatment.
Complication
Low intraocular pressure glaucoma complications Complications arachnoiditis
Hereditary atrophy, keratitis, arachnoiditis, non-specific giant cell arteritis, pituitary tumors, carotid calcification plaque compression nerves, sputum lesions may be misdiagnosed as this disease, alcoholism may also produce optic papilla atrophy Need to pay attention to exclude one by one.
Symptom
Low intraocular pressure glaucoma symptoms common symptoms hypotension visual field defect green weak intraocular pressure increased fatigue iris segmental atrophy wind and tear
POAG-like papillary changes with acquired acquiredness, RNFLD and visual field damage, untreated natural intraocular pressure 2.79 kPa (Goldmann applanation tonometry), open angle, excluding the optic nerve nipple atrophy depression and visual field defect Diagnosis can be established after other diseases. Therefore, the diagnosis of LTG is based on the exclusion of other lesions, so differential diagnosis is especially important.
The onset is very concealed, often unknowingly ill, due to the lack of subjective symptoms, patients often go to the middle, late to come to the doctor if found or in the routine experience.
1, early symptoms
Most patients in the early stage did not have any self-conscious symptoms. Individual patients may have eye length, discomfort such as fatigue and discomfort. The main complaints of vision loss are related to refractive, cataract and macular degeneration. Patients with advanced vision may have central vision loss.
2, intraocular pressure
(1) Mean intraocular pressure: The intraocular pressure of patients with LTG is within the normal range of statistics, but many scholars have observed that the intraocular pressure of patients is fluctuating within the upper limit of normal, the base pressure is high, and the average intraocular pressure seems to be high. The average intraocular pressure in normal people.
(2) 24-hour intraocular pressure: normal people may be affected by physiological factors, 24-hour intraocular pressure may fluctuate, but generally 0.67kPa, some scholars also noticed that some patients have 24-hour intraocular pressure fluctuations, the difference is greater than 0.67 kPa or 1.06 kPa.
(3) The effect of body position on intraocular pressure: The intraocular pressure measured by the normal person in the supine position is higher than the sitting eye pressure, but the difference is less than or equal to 0.79 kPa. In some patients with LTG, the difference in intraocular pressure between the two positions is large, according to some authors. Reported separately from 1.14 to 1.33 kPa.
(4) Long-term changes in intraocular pressure: Some scholars have noticed in the long-term observation of intraocular pressure in patients with LTG that the intraocular pressure of individual patients has an increasing trend, and the result is a rise from a low value in the normal range to a high value, such as from 1.33. The kPa rises to 2.66 kPa or changes beyond the normal range to open-angle glaucoma, but not all patients with LTG have the above characteristics, and some patients have lower intraocular pressure and are more stable.
3, the general situation
The incidence of hypotension in patients with LTG is high. 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. There are many migraine patients. In terms of hemorheology, the whole blood viscosity of LTG patients is high, and there are more abnormal blood coagulation and fibrinolysis systems.
4. Progressive and non-progressive LTG
Some scholars have observed that some patients with LTG have no progress in optic nerve atrophy depression and visual field deficiency, and some of them are progressive. Therefore, according to this performance, the disease is classified into two types, progressive and non-progressive. The causes of the disease may vary, Drance (1985) suggests that most of the visual field and papillary lesions in patients who have had a hemodynamic crisis before LTG diagnosis do not progress, and no hemodynamic risk has occurred. In the case of patients, most of the vision is progressing. The former may be due to hemodynamic crisis or vascular lesions, such as opticil hair and segmental infarction. If the infarction no longer occurs, the damage will not develop. LTG, Chandler (1979) proposed that the intraocular pressure of these patients is mostly at the upper limit of normal and the fluency coefficient of aqueous humor is at the normal lower limit. The structure of the nipple sieve plate is extremely fragile and is extremely sensitive to the damage of intraocular pressure. This type of patient has a lower intraocular pressure to prevent progression of the optic papilla and visual field damage.
5. LTG with anterior segment lesions and no anterior segment lesions
Some scholars have proposed other conditions and limitations for the diagnosis of this disease, such as requiring multiple stimulation tests to be normal, the aqueous flow fluency coefficient and the patency ratio are normal, intraocular pressure fluctuations 0.67 kPa, etc., while other scholars believe that diagnosis LTG should have the above abnormalities. Levene (1982) believes that it is inappropriate and subjective to attach these conditions to diagnose or exclude the disease, and to classify it in order to truly and objectively understand LTG. Therefore, he advocates the disease. Divided into: 1 with glaucoma atrial hydrodynamic abnormalities (refer to C value, po / c and abnormal intraocular pressure fluctuations, positive test positive, etc.) LTG, 2 without glaucoma (aqueous hydrodynamic abnormalities) LTG, he believes that at least one-third of LTG patients are associated with atrial dynamics abnormalities.
6. Classification of Klaver
Klaver (1985) further classified LTG patients into focal ischaemic subgroup (FILTG), senile sclerotic subgroup (SSLTG) and not belonging to FILTG or SSLTG based on medical history, age and changes in papillary head. The miscellaneous subgroup (LTGmisc), the visual nipple change of FILTG is characterized by: the disc of the optic disc is partially sunken along the tissue, and the vertical diameter of the cup is enlarged upward or downward, accompanied by local atrophy around the optic papilla, and SSLTG is considered The nipples are pale, with discs along the worm-like and oblique depressions, with extensive choroidal sclerosis and atrophy around the optic papilla.
Examine
Examination of low intraocular pressure glaucoma
POAG-like papillary changes with acquired acquiredness, RNFLD and visual field damage, untreated natural intraocular pressure 2.79 kPa (Goldmann applanation tonometry), open angle, excluding the optic nerve nipple atrophy depression and visual field defect A diagnosis can be established after other diseases.
1, intraocular pressure tracing
The fluency coefficient of LTG patients is at the lower limit of normal value, some patients are lower, and there is an abnormality of squeezing ratio. However, some patients have no special changes in tonometry. Some scholars will have abnormalities in the fluency coefficient of aqueous humor. The basis for distinguishing between true and false LTG or the basis of classification, but the role of intraocular pressure in the diagnosis and prognosis of LTG remains to be further affirmed.
2. Excitation test
The results of the trials on LTG patients are very inconsistent. Some scholars have reported that corticosteroids in the majority of patients have a high incidence of elevated eye reactions, but there are reports that there is no difference between normal and normal people. The drinking water test has the same situation, in short, its value. It is still difficult to be sure.
3, refractive and eye living structure
The incidence of myopia in LTG patients is higher than that in normal people. The vitreous cavity and axial length of the patients are longer than normal, and the radius of curvature of the vertical cornea is larger than that of normal people, and tends to have a C/D value of the trap.
4, the nipple
The optic papilla changes in LTG patients are similar to those of POAG, but recently some scholars have observed that LTG's optic discs are narrower than POAGs, with the narrowest regions below or below the sac; the cups have different characteristics, LTG's optic cups Tilting to the lower jaw, while the POAG's cup wall is steeper, the narrowing of the disc is more consistent, and the strip-shaped mesh and vascular overhead are more common in open-angle glaucoma. Identification.
The incidence of optic disc flaky hemorrhage in LTG is significantly higher than that of POAG and normal eyes. The flaky hemorrhage is often flaming or linear, and occurs frequently in the disc along the incision or after 2 to 3 months after the appearance of hemorrhage. Traces can occur repeatedly, usually at 7 or 11 points in the right eye, 1 or 5 points in the left eye. Many scholars believe that optic disc hemorrhage is the result of vascular infarction in the nipple; others believe that it is due to the deformation of the sieve plate and the damaged blood vessel. As a result, the incidence of optic disc hemorrhage in LTG patients is high, which may be related to the fragile structure of the sieve plate, but regardless of the cause, optic disc hemorrhage is a sign of worsening disease progression.
5, retinal nerve fiber layer defect (RNFLD)
LTG's RNFLD is similar to DOAG, with localized and diffuse defects. In the early stage, the nerve fiber bundles in the supraorbital area are fissure-like, wedge-shaped dark bands, and can also be diffuse thinning. Like the combed hair-like appearance; the late stage is mostly atrophy, and the retina has a dark granular appearance. Some scholars have observed that RNF's RNFLD involves more nerve fiber bundles under the ankle than POAG.
6, vision
It is generally believed that the damage of the disease is similar to that of POAG, but some scholars have observed that the visual field defect is earlier than POAG, more close to the fixation point, the slope is steeper, the defect is deeper, and the visual field defect occurs above the lower More, this is related to the fact that the change of the disk edge occurs more under the sputum. The damage of the visual field of the LTG is different from that of the POAG suggesting that the two damage mechanisms may be different.
7, fluorescent fundus angiography
Fluorescein fundus angiography showed that most patients with LTG had filling defects in the optic disc, and most of them had segmental low fluorescence, suggesting papillary ischemia. Some scholars have observed that there will be a field of vision from a comparative filling defect to an absolute filling defect. Damage, new visual field defects are always accompanied by the emergence of new optic disc filling defects or the expansion of the original filling defect, and the optic disc filling defect appears before the visual field damage, which seems to indicate that the visual function damage of this open door is directly related to optic disc ischemia. However, Quigly (1986) believes that the optic disc filling defect does not provide a basis for primary blood supply deficiency, but may be the result of tissue atrophy and disappearance together with blood vessels.
8, ophthalmic artery pressure and perfusion pressure
Drance (1973) reported suspicious POAG patients with low intraocular arterial pressure in LTG patients. Goldberg (1981) believed that ocular diastolic blood pressure was lower than suspected POAG, but Spaeth (1975) suggested that LTG's ophthalmic arterial pressure is no different from POAG and normal people.
Regarding perfusion pressure, Goldberg (1981) reported that diastolic perfusion pressure in patients with LTG is similar or may be lower than suspected POAG, while Kramer (1987) believes that perfusion pressure in patients with LTG is not different from normal, and he believes that perfusion pressure is susceptible. The conclusion of blood pressure is unreliable, and the ciliary choroidal vascular network resistance measured by eye pulse amplitude and arterial blood flow can reflect the blood supply. He proposed that the ciliary choroidal vascular network resistance of LTG patients is higher than that of normal people. In addition, resistance increases and blood flow is reduced. Perkine (1981) also studied this aspect. In one of his reports, it was mentioned that LTG's eye pulse amplitude is lower than that of normal eyes, while in another report, it is considered It is no different from normal eyes, but the amplitude changes are larger than normal eyes.
In summary, the observations of ocular arterial pressure and perfusion pressure of LTG are not consistent, and may be lower than normal eyes and suspected POAG.
Diagnosis
Diagnosis and identification of low intraocular pressure glaucoma
Differential diagnosis:
1. Primary open angle glaucoma (POAG)
Since no intraocular pressure was measured for 24 hours, no peak intraocular pressure was found, or the scleral hardness of myopia was low. The intraocular pressure was low with Schiotz intraocular pressure, or the patient used -blocker and cardiotonic drugs to reduce intraocular pressure. It is easy to be misdiagnosed as LTG. Therefore, it is necessary to stop using all kinds of intraocular pressure-lowering drugs to repeatedly measure intraocular pressure, including 24-hour intraocular pressure. For myopic eyes, use the applanation ophthalmometer to measure LTG when the intraocular pressure is within the normal range. Diagnosis.
2, other glaucoma
Corticosteroid glaucoma, blue eyelash syndrome, pigment dissemination syndrome, ocular trauma and uveitis secondary to glaucoma may have a transient increase in intraocular pressure, and then in a static state and misdiagnosed as LTG, can be detailed Ask about the medical history and examine the eye for detailed examination.
3, congenital or acquired acquired papillary abnormalities
Such as physiological papillary sag, optic papilla defect, congenital optic papilla cavity, nipple dysplasia, etc. may be confused with glaucoma papillary sag atrophy, but as long as the age of the disease is noted, carefully check the nipple, see Whether or not there are visual field defects and defects and whether they are progressing or not can be excluded.
4. Ischemic optic neuropathy
Ischemic optic neuropathy generally does not produce atrophy of the papillary sag, which is enlarged, but it has also been reported that some of the anterior ischemic optic neuropathy, especially arteritic anterior ischemic optic neuropathy, can cause glaucoma-like papillary complaints. Atrophy, and easy to be confused with LTG, but the disease has the following characteristics: 1 acute onset, acute or subacute, with a sudden decline in conscious vision, may be associated with headache, eye pain and other discomfort; and LTG patients often Lack of complaints, concealed onset, slow development of the disease; 2 ischemic optic neuropathy, the pale range of the optic papilla is larger than the depression, the disc edge is pale, and the glaucoma papillary atrophy depression is only the expansion of the cup, the residual disc The edge is still reddish; 3 visual field damage of ischemic optic neuropathy often involves the fixation point, and is horizontally semi-blind or quadrant blind but not bounded by the horizontal midline or vertical midline, protruding from the horizontal semi-blind or quadrant blind The arc defect is connected with the physiological blind spot, the degree of visual field defect is greater than the visual cup depression; 4 fundus fluorescein angiography: optic disc fluorescence of ischemic optic neuropathy, early table Abnormal fluorescence leakage for small blood vessel dilation, high fluorescence of blurred optic disc boundary, filling retardation and low fluorescence in the late stage; 5 general condition: often accompanied by massive cell arteritis, collagen disease, diabetes, syphilis Arteritis and hypertension arteriosclerosis.
5, myopia
Myopia, especially high myopia, sometimes presents shallow depressions similar to glaucoma's optic papilla depression, and can be misdiagnosed due to atrophy of the choroidal retina. At the same time, high myopia with glaucoma is also easily missed. The morphological size of the papillary sag and the presence or absence of retinal choroidal lesions caused by visual field defects are not carefully examined by the three-sided mirror with slit light. Meanwhile, fluorescence fundus angiography may also be helpful for differential diagnosis. The nipple depression of myopia does not produce LTG like LTG. Absolute filling defects like the nipple.
6, retinopathy
Schreiber (1906) has suggested that lesions such as retinal vascular occlusion can cause ascending optic atrophy after ganglion cell death and produce a glaucoma-like papillary atrophy depression, but many scholars have observed that such retinopathy can occasionally produce glaucoma-like The visual field is deficient, but there is no change in glaucomatous papillary changes.
7, other
Hereditary atrophy, keratitis, arachnoiditis, non-specific giant cell arteritis, pituitary tumors, carotid calcification plaque compression nerves, sputum lesions may be misdiagnosed as this disease, alcoholism may also produce optic papilla atrophy Need to pay attention to exclude one by one.
