What Are the Most Common Causes of Bad Eyesight?

eye

Visually impaired

Eye functions include shape, color, and light. Visual acuity is a function that accurately expresses shape perception. It can be divided into central visual acuity and peripheral visual acuity. Central visual acuity is obtained through the center of the macula. Peripheral visual acuity refers to retinal functions outside the macula. Therefore, vision is one of the specific manifestations of visual function. Visual disturbances, although minor, also indicate impaired visual function.

Visual impairment

eye

Visual impairment

Cardiovascular Medicine, Neurology, Ophthalmology, Traditional Chinese Medicine, Oncology, Department of Physiology

Causes of visual impairment

First of all, you should understand the path from the retina to receive visual information to the formation of the entire nerve impulse transmission in the visual cortex of the brain, the visual path. Nerve fibers from retinal ganglion cells pass through the scleral sieve and are assembled into the optic nerve. In the optic nerve segment, the fibers from the retinal nose and the temporal side travel together, and the nerve fibers to the retinal nasal side of the optic cross intersect to the opposite side, and the nerve fibers of the temporal retinal site of the retinal non-crossed optic nerve form the optic bundle. Extend to the lateral geniculate body after exchanging neurons

Visually impaired

Enter human visual radiation, and then through the internal capsule into the visual cortex of the cerebral occipital lobe. When light strikes the refraction of the eye's refractive system (cornea, crystal, vitreous) in the eye, it focuses on the retina, passes through the ganglion cell layer and the bipolar cell layer, and reaches the photoreceptor cell layer. The photoreceptor cells are rich in vitamin A and protein. The combination of light-sensitive substances is called light-sensitive pigments (rhodopsin and rhodopsin). The light-sensitive pigments produce a series of photochemical changes under the action of light-discoloration and decomposition, and generate display energy, which converts light energy into electrical energy. Potentials occur, which in turn cause visual impulses, which reach the cortical visual center of the talus sulcus posterior to the occipital lobe through visual pathways, producing vision. Therefore, some causes, such as inflammation, trauma, tumor vascular disease, etc., cause lesions from the cornea to any part of the occipital visual center, which can cause visual impairment.

The location of the lesions that cause visual impairment is extensive, and the causes of visual impairment are also varied.

1. Inflammation is the most common cause of visual impairment

(1) Infectivity: keratitis, corneal ulcer, iris ciliary inflammation choroiditis, endophthalmitis, pancreatitis orbital cellulitis caused by bacterial viruses, chlamydia, fungal parasites, etc.

(2) Non-infectious: keratitis keratitis, uveitis (including iridocyclitis, choroiditis) sympathetic ophthalmia, Harada disease, Behcet disease, etc.

2. Hypermetropia, astigmatism, presbyopia

3 Strabismus and amblyopia.

4 Traumatic eye injury Perforation of eyeballs: blunt contusion, explosion injury. Chemical burns and radiation injuries.

5. glaucoma

6. Corneal scar caused by various eye diseases, pupillary membrane closure, pupillary closure, vitreous opacity

7. Disorders of systemic circulation and metabolism, and various eye diseases caused by genetic diseases Hypertensive retinopathy Diabetic retinopathy, Nephritis retinopathy, Pregnancy hypertension syndrome retinopathy Hematologic retinopathy, Retinitis pigmentosa, Macula Degeneration and ischemic optic neuropathy, Leber disease and other fundus diseases, diabetic cataract

8. Retinal vascular disease and retinal detachment retinal artery occlusion retinal vein occlusion, mesocardial serous choroidal retinopathy, retinal vasculitis and retinal detachment.

9. Senile and degenerative lesions Senile cataract corneal degeneration, senile macular degeneration.

10 Tumor Intraocular tumor Orbital tumor or eyelid tumor invading the eyeball.

11. Other visual pathology is scam.

Diagnosis of visual impairment

Patients complaining of vision loss should first understand the exact vision, including distance vision and near vision, in order to exclude refractive errors and presbyopia, if far, near vision is not good, you should see whether there is redness or ciliary congestion. If ciliary

Visually impaired

Congestion should consider keratitis, iridocyclitis (including trauma), and angle-closure glaucoma. If there is no ciliary congestion, the refractive interstitial substance should be checked for turbidity, such as corneal epilepsy, degenerative cataract, and vitreous opacity. Or open-angle glaucoma fundus lesions. Fundus examination can confirm retinal choroid and optic neuropathy. If the above lesions are not obvious, visual field examination should be used to exclude visual pathological changes. If all are negative, amblyopia should be excluded, and of course a comprehensive analysis in combination with other symptoms in the main complaint. Therefore, it is very important to inquire about the medical history in detail and check carefully from front to back.

History of visual impairment

Ask in detail about the occurrence and development of visual impairment. Is the visual impairment monocular or binocular? Simultaneously or successively? Is it happening quickly or gradually? Is it far vision, poor near vision, or poor near and far vision? Congestion, shame, tears, and pain to exclude keratitis, iris, and ciliary body inflammation. Headache, swollen eyes, and rainbow are regarded as excluded glaucoma. Monocular diplopia considers subluxation of opaque crystals in the cornea, crystals, and midline of the vitreous. Symptoms such as dark spots, scotopic amblyopia, night blindness, deformed visual field defects, fluttering shadows in front of the eyes, and flash sensation should be considered. And note the history of trauma.

Physical examination for visual impairment

Visual impairment can be caused by systemic diseases, so a comprehensive physical examination is very important. In particular, attention should be paid to the inspection of the nervous, cardiovascular, and endocrine systems: the inspection must be performed systematically and comprehensively from the outside to the inside of the eye. Huitanyu turned right and left to prevent missing important signs.

(A) vision

Visual acuity includes distance and near vision examinations and a preliminary impression of visual impairment. Poor far vision, good near vision may be myopia, astigmatism, and so on. Poor near vision and good far vision may be hyperopia. Those over 40 years of age are considered to have presbyopia and near vision, which can be farsightedness or astigmatism or refractive interstitial opacity, fundus or optic neuropathy, and intracranial lesions. If there is ciliary congestion, keratitis and iris eyelashes should be considered. Stylitis, sudden visual impairment of glaucoma, may be central retinal artery occlusion, ischemic optic neuropathy, vision loss rapidly within a few days, may be central retinal vein occlusion, retinal detachment vitreous hemorrhage, eye and craniocerebral trauma, poisoning intracranial acute disease Wait. The lack of light perception may be caused by optic nerve atrophy, eyeball atrophy, eyeball density, absolute glaucoma, cortical blindness, etc. After you have a preliminary impression of the above vision, you should follow a certain step and check in depth from front to back

(Two) external eye examination

1. Eyelid eyelid lesions rarely cause vision impairment. Only when eyelid lesions cause irritation, vision impairment occurs. Such as eversion of the eyelids, trichiasis, conjunctival lithiasis, blepharoplasty, etc.

2. Are the orbits and eyeballs protruding or depressed? Is the eyeball position different

Visually impaired

Whether the orbital perimeter can touch the mass and whether the eye movement is restricted.

3 The size of the cornea is with or without blood vessels, infiltration, ulcer scars, degeneration, and foreign body deformities.

4 The depth of the anterior chamber is turbid, with or without pus. Hemorrhagic exudate.

5. Color and texture of iris, with or without defects (congenital, surgery), nodule atrophy, adhesion before and after, neovascularization (note the contrast of the eyes).

6. Pupil shape size, edge, light response (direct and indirect, radial). Exudate pigments in the pupil area.

7. Whether the crystal exists in position and transparency.

(Three) vitreous and fundus examination

Use a direct or indirect ophthalmoscope to check the vitreous body for opacity, hemorrhage, liquefaction, foreign body, parasites, etc. in the dark room. When inspecting the fundus, pay attention to the entire picture of the optic disc, retinal blood vessels, macula, and fundus. Deformity, etc.

(IV) Special inspections

1. Slit-lamp microscopy can further observe the subtle changes of various tissues in the eye. Pay attention to the microscopic lesions of the cornea, aqueous humor, crystals, and anterior vitreous combined with corneal staining (2% fluorescein solution staining ) to identify fresh corneal lesions. Anterior chamber angle was used to observe changes in anterior chamber angle.

2. The visual field includes the central visual field and the peripheral visual field to understand the functional changes of the optic nerve, retina, and visual pathway.

3 Examining refraction for retinoscopy.

4 Measurement of intraocular pressure and eyeball protrusion is necessary for glaucoma, but for those who are difficult to determine the diagnosis, further 24 h circadian IOP curve, aqueous effluent ease C value measurement and intraocular pressure challenge test

Visual impairment laboratory test

In order to clearly diagnose or investigate the etiology of blood pressure, blood, urinary routine red blood cell sedimentation rate, blood glucose, tuberculin test thyroid function, pathological examination, etc. have important reference values.

Visually impaired equipment check

1. Fundus fluorescein angiography can further understand the microstructure dynamics and functional changes of fundus blood circulation (up to the level of capillaries), and provide more and more detailed diagnostic evidence for fundus disease

2. Visual electrophysiological examination includes electroretinogram (ERG), electrooculogram (EOG), visual evoked potential (VEP), etc. to understand the retina and visual pathway function

3 Imaging examinations include chest orbital X-rays, ultrasound ultrasound (A-mode ultrasound, B-mode ultrasound Doppler), CT scans, magnetic resonance imaging (MRI), etc. can show eye structure and pathological changes. Opaque tissue can achieve the purpose of direct inspection.

Differential diagnosis of visual impairment

For visually impaired diseases with red-eye symptoms, see the "red-eye" section of visual impairment caused by trauma based on a history of trauma. Generally, no identification is required. The following highlights the visual disorders without red-eyed eyes.

Visual Impairment, Refractive Error, and Dysregulation

Most of this visual impairment is gradually difficult to tell the date of onset, no abnormalities were found in the eyes.

1. Nearsightedness Farsightedness is normal. Axial myopia of moderate or above may appear vitreous liquefaction, turbid subjective perception, and dark shadows in front of eyes. The fundus is leopard-shaped, and there are curved spots on the side of the papillary neck. If the posterior plate sclera expands backwards, the BrUch membrane degenerates, resulting in lacquer-like cracks that cause new blood vessels under the retina and cause macular hemorrhage. It can also cause choroidal atrophy or sclera erythema after formation. At this time, myopia is also affected. It is said that pathological myopia is identified by observing the fundus signs and the scope used. Definite diagnosis by retinoscopy.

2. Farsightedness Mild hyperopia can be adjusted and compensated, so adolescents with mild hyperopia, farsightedness and nearsightedness can remain normal. Only high-degree farsightedness can show vision loss, and nearsightedness is earlier and more pronounced than farsightedness. Patients often have symptoms such as eye swelling and headache due to fatigue adjustment. Fundus examination and optometry can make a clear diagnosis.

3 Astigmatism is unclear at near and far visions, with ghosting, eye pain, headache, and even nausea and vomiting. Fundus examination sometimes shows that the optic disc has a vertical elliptical edge blur, and the fundus cannot be clearly seen with ophthalmoscope. Can be diagnosed clearly by optometry

4 Presbyopia is over 40 years of age. Farsightedness is normal and nearsightedness decreases. The older the age, the nearsightedness becomes more pronounced, especially when working at close range. The vision is unclear. To see clearly, unconsciously move the object away and tilt your head back. There may even be adjustment fatigue, such as bulging headaches and orbital pain. You can wear a positive lens to correct.

Visually impaired refractive interstitial lesions

(A) corneal scars or degeneration

The cornea is a transparent tissue with no vascular structure. Transparency is the biggest feature of corneal tissue and is the basic element responsible for its physiological functions. Once the loss of transparency due to trauma or harmful factors causes turbidity, it can cause visual impairment. Corneal opacity can usually be seen by inspection, the light one is slightly foggy like a curtain, and the heavy one is magnetic white. Very slight turbidity still needs special inspection to find that corneal opacity can be all or limited. As long as turbidity is found, you should learn more about its properties.

(B) Cataract

Cataract is one of the common eye diseases and the main cause of blindness. It can be classified by etiology, age, location and shape of clouding of the lens, but no matter what type of cataract can be diagnosed with the help of vision and clouding of the lens. If the opacity of the crystal is relatively light, a slit-lamp microscope examination is required to confirm the diagnosis. If the opacity is obvious, the pupil area can be observed with a flashlight to be gray-white opacity.

1. Senile cataract is the most common type of cataract after the age of 50, and the incidence increases with age. Most of the lateral eyes can be onset. Progressive vision loss may occur, or there may be diplopia or multiple vision and secondary vision. Cortical cataracts, nuclear cataracts, and subcapsular cataracts are classified into three types of cortical according to the location and morphology of crystal opacity. Initial opacity appears at the periphery of the lens, and the tip is wedge-shaped, so pupils are often not easily found. Following the hardening of the nucleus of the crystal, the increase in refractive power produces crystalline myopia, which improves myopia, that is, the opacity of the second vision gradually develops to complete opacity. The visual acuity can only be exponential, manual, or photo-induced nuclear cataract. Crystal opacity starts from the crystal. In the nucleus, vision is reduced due to pupil shrinkage under strong light, the progress is slow and often the disease progresses to a considerable degree, and still maintains good near vision, until the nucleus of the crystal becomes dark brown cortex and opacity occurs, the near vision is significantly reduced. Subcapsular cataract is a discoid turbidity that initially appears in the superficial layer of the posterior pole of the lens, with golden yellow or white particles or small vacuoles. Because the turbidity is located in the optic axis area, it affects vision and nuclear and cortex early. Sexual cataracts coexist.

2. Some congenital cataracts have systemic and ocular abnormalities in addition to opaque crystals. The opacity of the crystal is mostly binocular, with an anterior and posterior pole, a corolla, nucleus or complete opacity.

3 Complicated cataract refers to cataract caused by intraocular disease. Common eye diseases include glaucoma, uveitis, retinal detachment, retinal pigment degeneration, and retinal vascular disease. Crystal opacity is often located in the posterior capsule in brown chrysanthemum type.

4 The most common cataract caused by systemic disease is diabetic cataract, which is older in age. The signs are similar to senile cataract, except that the age of onset develops faster. Typical juvenile diabetic cataracts develop rapidly in both eyes. Spot-like or snow-like turbidity appears under the anterior and posterior capsules of the early crystals, and the crystals can be completely opaque within weeks or months

5. Hypocalcic cataract or tetanic cataract may have hypoparathyroidism, infantile osteochondrosis, pregnant women or lactating calcium deficiency crystal turbidity is located in the anterior and posterior cortex, showing most white spots or red, green and blue particulate crystals, turbid area There is a transparent boundary with the crystal capsule, and in severe cases, it can be quickly and completely turbid

(Three) crystal dislocation

When the lens is dislocated, the lens is absent during the total dislocation and incomplete dislocation. It shows deepened iris tremor in the anterior chamber, and the fundus shows high hyperopic changes. The convex lens can improve the visual dislocation. There may be single-eye diplopia, and spectacles show double breasts. Avatar. After light pupil dilation, observation with a slit lamp microscope can reveal that the obvious eye can see the crystal edge in the pupil, and there is a crescent-shaped light and dark contrast. May be associated with iris tremor or vitreous

(4) Opaque vitreous

Vitreous opacity is not an independent disease but a manifestation of some eye diseases. Many cases of intraocular inflammation, hemorrhagic degeneration, foreign bodies, parasites, etc. may cause dark shadows in front of the eyes, and vision may not be affected. In severe cases, the eyes are dim or even light-conscious. With ophthalmoscope, it can be seen that there is no red light reflection in the vitreous with heavy turbidity, and it is difficult to see the fundus.

(E) Open-angle glaucoma

Open-angle glaucoma is also called chronic simple glaucoma. Its main feature is that under high intraocular pressure, the anterior chamber angle is wide and open. It is fundamentally different from closed-angle glaucoma when the angle of the chamber is closed. Most patients have no symptoms in the early stage. When the patient's intraocular pressure is high, he feels dizziness, headache, bloating or blindness. Sometimes there are no obvious signs at this stage, often being missed or the IOP is unstable. Only 24h IOP measurement is helpful for diagnosis. With the development of the disease, the intraocular pressure gradually increases, the optic nipple cup-disk ratio increases, and the diagnosis of retinal nerve fiber layer defect and visual field defect can be established. Sometimes when typical symptoms appear, the visual field has been exhausted to an irreversible degree. Therefore, early diagnosis of this disease is essential. Those who have the following conditions should be excluded from glaucoma examination. Those with a family history of open-angle glaucoma. Reading difficulties in the morning. The elderly frequently change their presbyopia glasses Progressive high myopia. suffering from retinal vein occlusion. One eye is sick and the other eye should be checked in time. Despise the nipple cup-to-disk ratio C / D> 0.6 stone. In particular, when the intraocular pressure is high and the suspicious optic disc changes, a comprehensive examination should be done in order to confirm the diagnosis early.

Examinations include: The detailed examination of the fundus mainly observes the C / D ratio and the defect of the retinal nerve fiber layer. Detailed inspection of the visual field mainly includes dark spots outside the center and step-like dark spots on the nasal side, arched dark spots, circular dark spots or concentric contraction, and a tubular visual field in late stages. Anterior gonadoscopy Tonometry C value. 24h intraocular pressure fluctuation. If necessary, do an intraocular pressure challenge test. The disease should be distinguished from chronic angle-closure glaucoma. The latter may also have no congestion in the outer eye, and the subjective symptoms are not obvious but there may be a typical history of small episodes. Even with mild eye distension, headache and blurred vision, but often rainbow vision. Open-angle glaucoma is mostly without symptoms. In chronic angle-closure glaucoma, the depression of the optic nipple is shallower than that of the open-angle glaucoma, the anterior chamber angle is narrow, and there is adhesion. The anterior chamber angle of open-angle glaucoma is wide and the narrow angle is the individual. The main method of identification of the two is to check the room angle under high intraocular pressure. If the room angle is wide and open, it is open-angle glaucoma.

(6) Fundus Lesions

Most of the external eye examinations have no changes, and the symptoms are mainly vision loss, deformed vision, diminished vision, and dark spots.

1. Retinal vascular occlusion

(1) Retinal artery occlusion: This disease is an ophthalmic emergency that can cause instant blindness. If not rescued in time, it will cause permanent visual impairment. Monocular disease is more common in the left eye. According to the obstruction site, it can be divided into central retinal artery occlusion and branch retinal artery occlusion. The fundus is mainly characterized by ischemia. The diameter of the arterial tube is narrow, and the posterior pole retina is milky white with edema and cherry red spots in the center. Fundus of the eye rarely bleeds, and secondary optic nerve atrophy such as occlusion is limited to the arterial branch in the late stage, and the lesion is limited to the retinal region where the branch supplies blood. Central retinal artery occlusion can manifest a reduced field of view or a tube, sometimes leaving only a small island-like field of view on the temporal side. Electrophysiological examination showed a typical negative phase wave. Fundus fluorescein angiography manifests as arterial filling delay, arteriovenous arteriovenous vascular fluorescein flow becomes thin or beaded, dendrite-like, capillary occlusion is occasionally dye leakage or hemangioma-like changes.

(2) Retinal vein occlusion: vision declines rapidly within a few days and is not as sudden as arterial occlusion. According to the obstruction site, the visual acuity decreases significantly when the macular area is divided into the central retinal vein, hemilateral retinal vein and branch retinal vein occlusion. The fundus appears as normal optic papillae or edema, and blurred borders can be masked by bleeding. The retinal arteries are thin and reflective, and venous fibrillation is dilated, like a sausage. Flammable hemorrhage of the retina can be seen along the venous trunk and sometimes cotton-like spots appear. Lesions can spread to the macula and have macular edema. Depending on the site of the obstruction, the scope of the lesions is not consistent, but the fundus changes are basically the same. Fundus fluorescein angiography may have extended venous return time, dilated capillaries in the optic papilla, and dye leaking into the vein wall. Leakage of fluorescein was also seen. Retinal capillaries dilate, microaneurysms form, and late dye leaks. Macular area may appear spot or petal-like dye leakage, the formation of macular cystoid edema or even cystoid degeneration, macular holes. The formation of large unperfused areas of the retina can induce new blood vessels, leading to vitreous hemorrhage and proliferative traction retinal detachment. Neovascular glaucoma can also occur.

2. Periretinal retinal vein inflammation is also known as Eales disease or recurrent retinal vitreous hemorrhage in young men and women. The eyes develop successively, and there is a tendency of recurrence in peripheral retinal veins. It can only be found during mydriasis of the fundus. When the lesions spread to the main vein, the veins are tortuous, with white sheaths, and there may be a large amount of bleeding and exudation in the fundus with retinal edema, macular stare exudation or cystic edema. Can be complicated by venous occlusion, if a large amount of retinal hemorrhage flows into the vitreous, vision will suddenly decrease. Peripheral capillaries are occluded to form a large non-perfusion area, resulting in the formation of new blood vessels can also cause bleeding into the vitreous, resulting in proliferative vitreoretinopathy and traction retinal detachment. Involved fluorescein angiography has fluorescein dripping and tube wall staining, capillary dilation, and microaneurysm formation. There is a large unperfused area around the retina, which can be surrounded by microaneurysms, arteriovenous short circuits, and neovascularization The macula may also show spotted or petaloid leaks.

3 Central serous choroidal retinopathy is a common fundus disease characterized by macular edema that can develop in one or both eyes, and often relapses. It is more common in men whose age is 20-45 years. The condition can be self-limited. About 70% of patients with conscious vision loss are between 0.5 and 1.0, rarely less than 0.1. The main complaint was that the vision was unclear with central dark spots, shape, color vision, or small vision fundus examination, localized swelling and bulging in the macular area, and halo foveal reflections disappeared. After a few weeks, there were most yellow and white dots, or fundus fluorescein angiography with pigmentation disorder. One or more high-fluorescence spots were seen in the venous phase, and there were central dark spots in the visual field examination of diffusing or ejecting dye leakage. Application Amsher checklist check, can detect visual deformation

4 Retinal detachment refers to the separation of the neuroepithelial layer and pigment epithelial layer of the retina itself into retinal detachment and non-perforated retinal detachment. The latter includes exudative, traction, and mass-induced retinal detachment, which is commonly referred to as retinal retinal detachment. Initially, the retina is stimulated to produce a flashing sensation and an increase in black shadows in front of the eyes. Then, fixed black shadows appear in the visual field, deformed vision and obvious visual impairment. The retina at the fundus examination showed a gray-white water wave-like bulge in the detached area, and blood vessels crawled on it. In patients with proliferative vitreoretinopathy, proliferative lines and stellate folds can be seen in the fundus. The intraocular pressure of the retinal hiatus with a red background is often found below or near the zone of separation. When localized detachment occurs, the visual field of the corresponding area is reduced and the red and blue visual fields are crossed.

5. Primary progressive retinal pigment degeneration. A chronic progressive retinal pigment epithelium and photoreceptor degenerative disease with a genetic predisposition. Night blindness and progressive narrowing of the field of vision to the heart are the main characteristics of the disease. Fundus examination showed that the nipples were waxy and gradually pale and atrophied, and the state was clear. Retinal blood vessels are significantly thinner. There are osteocyte-like pigments in the equatorial retina in the early stage, covering some blood vessels. The lesion gradually expanded to the posterior pole and even affected the macula. The retina was blue-gray. Fundus fluorescein angiography has a mottled background fluorescence in the early stage, prolonged arterial and venous filling time, and late stage may have choroidal vascular unperfusion zone and fluorescein leakage caused by macular edema. The electroretinogram (ERG) of the visual electrophysiological examination is extinguished, and the eye movement electrophoresis (EOG) is a flat wave.

It is not difficult to make a diagnosis based on the history of the visual field and the fundus. Early case can refer to visual electrophysiological examination

6. Fundus lesions of systemic diseases Some systemic diseases can cause fundus lesions and cause visual impairment. In addition to the clinical manifestations of systemic diseases, fundus manifestations have their own characteristics.

(1) Hypertensive retinopathy: Any increase in blood pressure can cause changes in the fundus, including retinopathy, choroidal vascular changes, and optic papillary edema, and hypertension, the former and the secondary, often occur in the elderly. More common in chronic progressive. The latter is more common in aggressive types and is also called malignant hypertension. More common under 40. Common in kidney disease pregnancy hypertension syndrome, pheochromocytoma and so on. The degree of visual impairment is mostly related to the degree of fundus changes in both eyes. Fundus examination, partial or general narrowing of the retinal arterioles is irregular. Blood pressure continued to increase for a long time, the blood vessel wall thickened, the lumen narrowed, the blood vessel reflective band widened, and the loss of transparency and the copper wire-like arteries became heavier and the silver wire-like arteries were accompanied by arteriovenous cross-compression. A sharp increase in blood pressure can also cause retinal edema, bleeding and exudate. Optic nerve papillary edema can also occur if hypertension enters a severe stage.

(2) Chronic nephritis retinopathy: The fundus manifestations and hypertensive retinopathy are very similar, especially when the renal function is impaired in advanced hypertension. Comprehensive analysis must be combined with clinical manifestations and laboratory tests. In general, the fundus of chronic nephritis retinopathy is anemia gray-yellow tone, obvious edema, flocculent exudation and more macular areas, star-shaped exudation spots are more common. Fundamentally different from rosy clear hypertension.

(3) Pregnancy-induced hypertension retinopathy: It occurs in the third trimester of pregnancy with hypertension, edema, and proteinuria, and convulsions. Ocular fundus examination, early retinal arteriolar spasm contraction, uneven thickness of the tube diameter, enhanced wall light reflex, near the spastic blood vessel and the retinal surface corresponding to the choroid infarcted vascular branch supply area or below the retinal surface with severe gray edema Retinal detachment and papillary edema of the optic nerve. Serious visual impairment can occur. Fundus fluorescein angiography shows limited choroidal circulation disorders with compensatory choroidal capillary dilatation and leakage around it, and leakage through the pigment epithelium damage area to the subepithelium leads to retinal detachment. In the same fashion, different degrees of dye leakage in retinal capillaries can be seen to generally restore vision after termination of pregnancy. If the lesion damages the macula, or if the optic nerve atrophy is caused by optic papillary edema, permanent visual impairment will also remain.

(4) Diabetic retinopathy: It is one of the serious complications of diabetes and one of the serious blinding diseases. The fundus showed venous fibrillation, extreme bleeding points after filling, microaneurysm formation, and yellow-white hard exudate or gray-white soft exudate and bleeding spots. In severe cases, there are retinal neovascularization, which causes retinal vitreous hemorrhage to form proliferative vitreoretinopathy and traction retinal detachment. Fundus fluorescein angiography in the early posterior pole showed micro-aneurysm formation of two-point hyperfluorescence, and retinal capillaries dilatation. In the late stages, there were dye leakage waves and macular area with petal-like strong fluorescence. There may also be low-fluorescence areas formed without perfusion areas, or high-fluorescence electrophysiological examinations of neovascularization: a-wave b-wave amplitudes decrease, retinal oscillation potential amplitudes decrease, latency increases, and visual evoked potential amplitudes decrease, and latency increases.

7. Optic nerve and optic pathology

(1) Optic neuritis: vision loss decreases toward the heart or there is a central dark spot. When inflammation affected the optic nerve papilla, the fundus showed blurred congested edges of the optic papilla, slight swelling, and a small amount of bleeding from the disc surface and disc margin. The arteries are thin and the veins are slightly dilated. Fundus fluorescein angiography, the optic nerve papillary capillaries in the arterial phase are dilated, and the dye gradually leaks out. The late optic disc is strongly fluorescent. If inflammation affects the posterior segment of the optic nerve bulb, it is said that posterior optic nerve neuritis has no positive signs in the outer eye and fundus except for visual impairment and visual field changes. Visual electrophysiological examination is helpful for diagnosis. When visual acuity is severely impaired in the acute phase, VEP shows that the amplitude of the incubation period prolongs significantly and the response disappears completely. Optic papillitis should be distinguished from optic papillary edema and ischemic optic neuropathy

(2) Optic nerve papillary edema: Lesions often caused by increased intracranial pressure are bilateral. Transient hazy vision appeared in the early stage, fundus examination in the late stage of vision loss, the degree of visual papilla bulge was higher, and the unclear physiological depression disappeared. There was flaming bleeding or exudation on the disc surface and disc margin, and the retinal arteries were normal or thin veins opened. Peripheral vision blindness was enlarged. Fundus fluorescein angiography. There are dilated capillaries on the papillae. A large number of dilated radial capillaries and microaneurysms in the venous phase are clearly visible. The fluorescein leaks quickly on the disc surface, and the late optic disc is significantly fluorescent

(3) Ischemic optic neuropathy: Anterior and posterior ischemic optic neuropathy is an acute malnutrition disease caused by circulatory disorders of the nutritional vessels of the optic nerve. Both suffer from sudden visual impairment. Fundus examination of the former may have changes in the optic nerve papilla with mild edema, pale color, normal blood vessels or slightly fine arteries. The visual field examination is usually a horizontal semi-fertility or quadrant visual field defect connected to a physiological blind spot. Fundus fluorescein angiography is characterized by asymmetric fluorescence intensity in the obstructed and non-obstructed areas of the optic papilla. This point is significantly different from optic papillitis and optic papillary edema for identification. Posterior ischemic optic neuropathy is normal in the early fundus. Visual field examination has central or central blind spot dark spots, horizontal or vertical hemianopia, and quadrant defects or irregular peripheral defects in the late stage (after 4-6 weeks) can cause optic nerve atrophy.

(4) Pathological changes: The lesions in this area can cause visual impairment, but it is not easy to make a clear diagnosis by direct external inspection. Visual field examination is a more effective diagnostic method. Inflammation and trauma, foreign bodies, and toxic tumors can cause lesions in this area. According to the changes in the visual field, the location of the lesion can be determined initially. If the visual field is reduced with a dark spot in the center, consider the lesion in the optic nerve. Double-collar lateral visual field defect indicates that the lesion is at the optic cross. Ipsilateral visual field defect lesions in both eyes are in the contralateral visual bundle. The ipsilateral visual field defect in both eyes, but the absence of blinded pupil rigidity suggests that the lesion is radiating on the opposite side of the visual field defect. The eyes are dark, the pupils are normal, and the fundus is normal. The cortex is blind, suggesting that the lesions in the talus cortex need to be combined with full physical signs and imaging examinations.

8. Amblyopia: Anyone with no organic lesions on the outside and inside of the eyeball. If the corrected vision is lower than 0.9, it can be diagnosed as amblyopia.

9. If the blindness is not commensurate with vision and action, no disease can explain the cause of the visual impairment. The patient refuses to check, or the pupils on both sides of the uncooperative test respond well. Repeated tests of the visual field can give different results. Pay attention to whether the blindness is further passed He was diagnosed blindly. There are many ways to check for blindness. Frequently, if the distance for checking vision is shortened or moved away, the blindness is the same if the vision result is the same. For example, if the visual acuity is 0.2 at 5 meters and the visual acuity is shortened at 2.5 meters, the result is 0.2, which can be diagnosed as scam blindness or the visual field of healthy eyes, but it does not cover the blindness. A nasal visual field of more than 60 degrees may be suspected of fraud. Blindness should be distinguished from plague blindness or amblyopia. The latter has normal visual evoked potentials in the presence of mental factors, suggesting that the treatment is effective. Scam blindness and cortical blindness identify the latter as a result of central vision lesions, and foreign bodies suddenly appear without a blinking reflex in front of the eyes. Optokinetic nystagmus disappears and blindness is distinguished from posterior optic neuritis. The latter has pain in eyeball rotation, the pupils' photoreaction cannot be sustained, the field of vision has dumbbell-shaped dark spots, and abnormal visual evoked potentials.

Visual impairment

l Reasonable and balanced diet, persuade children to develop good eating habits, do not picky eaters.

2.Pay attention to guide children to eat more coarse grains (such as cornmeal, millet, etc.) to increase the necessary vitamin supply.

3.Eat more fresh fruits and vegetables, increase the intake of protein appropriately, and limit the intake of polysaccharides to promote the development of the retina and optic nerve.

4.Do not allow children to eat overcooked protein foods.

5.According to the nutritional status of the child, supplement some vitamins (such as vitamin B1, vitamin B12, vitamin C, cod liver oil, etc.) and minerals (such as zinc, iron, calcium, etc.) when necessary.

6. Parents need to know that the nutrients that the eye needs are divided into four categories: vitamins A and carotene, vitamins B, minerals such as calcium and zinc, vitamins C, vitamin E, and carotenoids. Can take these nutrients.

7, let your child eat more nuts, such as walnuts, almonds, melon seeds, pine seeds, hazelnuts.

8.You can also drink tea to improve vision, such as: green tea, wolfberry tea, chrysanthemum tea, cassia seed tea.