Toxic cataract

Introduction to toxic cataract Many substances have been recognized for the occurrence of cataract in experimental animals. In humans, local or systemic drugs and toxic substances induced cataracts, many clinical reports have been made and attracted people's attention. Many drugs and chemicals can cause cataracts. Toxic cataracts, which are directly related to ophthalmology, are mainly caused by some drugs. basic knowledge Sickness ratio: 0.0001% Susceptible people: no specific population Mode of infection: non-infectious Complications: glaucoma osteoporosis

Causes of toxic cataract

(1) Causes of the disease

It mainly includes some drugs and toxic substances:

1. Glucocorticoid: long-term systemic or topical application of large doses of glucocorticoids, which can produce posterior subcapsular opacity, similar in morphology to radiation cataracts, initially with fine spots or streaks turbid under the posterior capsule, slit lamp Under the inspection, the visible color of the color is reflected, and there is a vesicle-like change. If the drug is not stopped, the turbidity will be further enlarged and aggravated, eventually forming a typical pale brown disk-like opacity. Once the cataract is formed, it is reduced in most cases or The withdrawal of the drug can not cause it to subside. The occurrence of cataract is related to the dose and duration of the drug. The larger the dose, the longer the time, and the higher the incidence of cataract.

2. Collapse agents: long-term use of anti-cholinesterase-like miotic agents, especially long-acting mites such as iodine-based esters, can cause microvesicles under the anterior capsule, and can cause posterior subcapsular and Changes in the lens nucleus.

3. Chlorpromazine: Long-term administration of chlorpromazine can cause fine white opacity in the anterior capsule and superficial cortex, often forming a typical star turbid appearance in the pupil area.

4. Other preparations : drugs that inhibit mitosis, such as busulfan, nitro compounds such as dinitrophenol, dinitro-o-cresol and trinitrotoluene (trinitrotoluene, TNT); the latter plays an important role in occupational disease prevention. In addition, naphthalene, tetracaine, and thallium preparations can also induce cataract production.

(two) pathogenesis

The incidence is mainly related to the individual's sensitivity to drugs and poisons.

Corticosteroids inhibit the pumping mechanism of Na+-K+-ATPase

It has been reported that in the lens incubated with dexamethasone, the K+ in the lens decreases, Na+ and water increase, which is due to the inhibition of the pumping mechanism of Na+-K+-ATPase, the growth zone of the lens, the relative reduction of epithelial cells, and hormones. The induced lens opacity is very similar to the lens opacity formed by the excess of galactose, indicating that the action of the hormone is similar to that of galactose because the permeability of the galactitol accumulated in the lens cells is poor, so that excess water enters the lens cells to cause cataract.

Hormone binds to lens protein to form lysine-ketosteroid adduct

Hormone lens opacity is associated with the formation of covalent glucocorticoid-crystallin adducts. The reaction of glucocorticoids with proteins is non-enzymatic, through the formation of Schiff groups, in the amino group of proteins and the C-20 carbonyl group of ketosteroids. Occurs between and then involves the adjacent C-21 hydroxyl group causing Heyns rearrangement to form a stable product.

Oxidation of SH-based proteins in lysine-ketosteroid adducts leads to polymerization of lens proteins

Gel filtration analysis of the lens protein of human ocular hormonal cataract confirmed that in vivo, prednisolone protein adduct is present in high molecular sulfur compounds, glucocorticoid-induced cataract is through special into lens fiber and lens protein The amino acid gene reacts such that the lens protein is altered, causing the thio group to excite to form a disulfide bond, resulting in protein aggregation and a photorefractive complex.

Cataracts caused by various toxic substances have different causes. For example, dinitrophenol can increase the oxidation process of tissues, so that oxygen is used up, resulting in cataracts. Some people think that it interferes with creatine metabolism, affects the decomposition of sugar and thus causes cataracts. Liver poisoning, ergot poisoning may be due to vasoconstriction and vascular wall degradation, causing lens dystrophies, or may be due to direct poisoning of the lens capsule, causing lens metabolism disorder.

Toxic cataract prevention

Pay attention to the dosage and time of application of cataract drugs, and pay attention to labor protection to avoid contact with some poisons. Should be reviewed regularly to prevent recurrence, such as conscious symptoms of recurrence, should be diagnosed early.

Active exercise, enhance physical fitness, prevent colds, eat less irritating foods, pay attention to work and rest, maintain physical and mental health, and also have important significance in the prevention of toxic cataract.

Toxic cataract complications Complications glaucoma osteoporosis

Related to other systemic changes caused by drugs and toxic substances, such as hormonal glaucoma, osteoporosis, etc.

Toxic cataract symptoms Common symptoms Lens opacity lens enlargement Glaucoma plaque lens shrinkage Eye squint Vision disorder

Toxic cataracts are characterized by binocular involvement and occur for a longer period of time from poisoning to months to years. Once they occur, the progression is quite rapid.

The morphology of toxic cataract is close to endocrine cataract and complicated cataract. At the beginning, gray dust and spot turbidity appear under the anterior capsule, sometimes turbidity appears as streak or villi, turbidity can be dispersed or composed of flowers, and there may be Color crystallization, the cortex under the posterior capsule is sometimes ring-shaped turbid, turbid granules, metallic luster, visible color reflection by specular reflection method, irregular dark gray turbidity in the cortex, turbidity progresses quickly, first Invade the cortex, and then reach the nucleus, so that all the lens is milky white, and finally the pearl gray turbid, which is also common in the water to form a dark space, cataract can mature within a few days to several weeks, in the process of maturity, due to the lens It absorbs water quickly and is prone to secondary glaucoma. Characteristics of corticosteroid cataract:

Part 1: The opacity of the lens is located in the posterior cortex, just under the posterior capsule of the lens, sometimes invading the posterior capsule, or irregularly invading the anterior cortex.

2 Form: The boundary of turbidity is usually clear, and occasionally there is a light gray halo around it. This fine structure is composed of yellow-white small crystal turbidity, and is separated by vacuoles of the same size to form granular aggregates, occasional lines. Stripes or several large vacuoles.

Examination of toxic cataract

The cause of the poisoning can be identified and the necessary laboratory tests can be carried out.

1. Eye special examination

There are doubts or special requirements for the surgical results, and patients suspected of having other eye diseases should be examined.

(1) Corneal endothelial cell examination: observe the ratio of cell density (CD) and Hexagocyte (Hexagocyte). When the corneal endothelium is lower than 1000/mm2, the cataract surgery should be carefully considered to avoid postoperative cornea. Decompensation affects the surgical outcome and postoperative recovery.

(2) Retinal visual acuity test: a specific image or visual target is projected onto the retina, regardless of whether the refractive interstitial is turbid, directly check the visual acuity of the retina to understand the best visual acuity that can be achieved after the patient is operated, and is a preoperative evaluation of the macula. An important check method for function.

(3) Visual field examination: For patients with light opacity of the lens and a certain vision, other diseases with cataract can be found by visual field examination. For example, the central dark spot should be alert to the presence of macular degeneration, the expansion of physiological blind spots and the characteristic of visual field. Defects should be alert to the presence of glaucoma and other fundus lesions. Because cataracts can also cause changes in visual field, they should be identified by contacting the opaque area of the lens observed by the slit lamp.

(4) Retinal current map (ERG) examination: There are currently 3 kinds of ERG, such as flash, graphic and multi-focal, which can record the cone function of the retina, rod function and mixed function. The flash ERG reflects the function of the whole retina, graphic ERG mainly reflects the function of the macula. Multifocal ERG can simultaneously record ERG on more than 100 retinal sites in the central 30° field of view, which is conducive to the diagnosis and judgment of postoperative retinal function. The clinical application of flash ERG is as follows. Preoperative ERG was normal or slightly reduced, and postoperative visual acuity recovery was estimated to be good. If preoperative ERG was significantly reduced or not recorded, postoperative visual recovery was estimated to be unsatisfactory.

(5) Visual evoked potential examination (VEP): VEP includes flash VEP and graphic VEP for recording the function of the nerve pathway from the retina to the visual cortex. When the macular and optic nerves appear lesions, they can show amplitude reduction and latency. Prolonged, when the patient's preoperative visual acuity is less than 0.1, the flash VEP examination is generally used, and when the patient's visual acuity is good, the visual VEP examination can be used. Therefore, when the lens is obviously turbid, the VEP examination has a more accurate degree of recovery of postoperative visual function. Predictive.

2. Other related auxiliary examinations of the whole body : such as bone density determination.

Diagnosis and diagnosis of toxic cataract

diagnosis

The diagnosis is mainly based on clinical manifestations.

1. There is a history of exposure to drugs or poisons, mostly bilateral.

2. Due to turbidity, there are no more symptoms or slight visual impairment, and occasionally a sense of flash.

3. It first occurs under the posterior capsule of the lens, showing irregular localized turbidity, sometimes with color.

4. If the condition develops further, turbidity develops to the cortex and along the posterior capsule to the peripheral cortex, but more surgery is not required.

5. Stop using the medicine in time, and the turbidity may be dissipated.

Differential diagnosis

1. uveitis: high myopia, retinal detachment and retinitis pigmentosa and other ocular lesions can cause lens damage, this lens opacity caused by ocular inflammation can be seen in the posterior capsule lens swelling, high rainbow flash, lens opacity The halo is visible on the border, which is the difference from corticosteroid cataract.

2. Post-cortical senile cataract: There may be changes in the posterior capsule or posterior capsule of the lens, which is easily confused with lenticular lens opacity, but the former is often accompanied by lens changes in other parts, such as anterior or anterior capsule. Cavitation, wedge or punctate cortical opacity and nuclear sclerosis, this senile cataract significantly affects vision, hormonal lens opacity rarely affects vision.

3. Diabetic cataract: rapid progression, often with anterior cortical changes, the most important feature is the small turbidity of snowflake.

4. Atrophic myotonic cataract: It is a star-like opacity of the posterior cortex, and it is clear with the multi-color small turbidity of the posterior capsule.

5. Low-calcium cataract: located in the posterior cortex, separated from the posterior capsule by a transparent band.

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