Retinal pigmentary abiotrophy: causes, diagnosis and treatment. Hereditary diseases of the retina and optic nerve - description, diagnosis Retinal pigmentary dystrophy ICD code 10

Angioid stripes of the macula

Drusen (degenerative) macula

Retinal degeneration:

• lattice
• microcystic
• palisade
• reticular

Dystrophy:

• taperetinal
• vitreoretinal

Central serous chorioretinopathy

Detachment of the retinal pigment epithelium

In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

With changes and additions from WHO.

Processing and translation of changes © mkb-10.com

Retinopathy of prematurity (ROP) - description, causes, symptoms (signs), treatment.

Short description

Retinopathy of prematurity (ROP) is a lesion of immature retinal vessels in newborns with a small body weight (less than 1500 g), caused by exposure to damaging factors (mainly excess amount of O2 in the inhaled air when caring for a newborn). Incidence Approximately 30% of all newborns weighing less than 1500 g at birth have signs of ROP. 66% of newborns weighing less than 1250 g at birth and 82% of newborns weighing less than 1000 g have ROP. 2.2% of newborns born weighing 1000– 1500 g, have retrolental fibroplasia, 0.5% of them become blind.

Code according to the international classification of diseases ICD-10:

• H35.1 Preretinopathy

Causes

Etiopathogenesis Increased intensity of oxidative processes, caused by high O2 content, has a damaging effect and is perceived by the vascular system as a factor of aggression, requiring the inclusion of compensatory mechanisms (obliteration of blood vessels with subsequent abnormal proliferation). Cells of the nonvascularized retina most likely secrete a still unidentified angiogenic factor. In addition to the increased O2 content in the inhaled air, sepsis, hypo- and hypercapnia, vitamin E deficiency, bright light, etc. can play an etiological role. Quite often, ROP occurs in children who have not been exposed to exposure to high concentrations of O2.

Pathomorphological phases Narrowing of retinal capillaries and their obliteration Formation of new capillaries with growth into the vitreous body, edema and hemorrhages in the retina, its detachment Development of a fibrotic process at the site of newly formed vessels and hemorrhages. At this stage, the process becomes irreversible and is clinically characterized by the formation of fibrous films and strands in the vitreous body, the development of atrophic processes in the eyeball, leading to blindness. At this stage of the development of the process, the term retrolental fibroplasia is used.

Symptoms (signs)

Classification and clinical picture of acute ROP.

Localization Zone I - the posterior part of the retina, visible within 60°, centered on the optic nerve Zone II - from the edge of zone I to the anterior edge of the nasal region of the retina Zone III - the residual crescent zone of the anterior retina (temporal region).

Prevalence is determined by the clock face.

Stages of abnormal vascular reaction Stage 1 - formation of a line of demarcation between the vascularized and nonvascularized retina Stage 2 - presence of a demarcation line in the form of a ridge forming a groove in the vitreous Stage 3 - formation of a ridge is combined with extraretinal fibrovascular proliferation with penetration of blood vessels into the vitreous Stage 4 - penetration newly formed vessels into the vitreous leads to fibrosis, scarring and subtotal retinal detachment Stage 5 - complete retinal detachment.

A plus when designating a stage (for example, 3+) means the presence of dilatation and tortuosity of the vessels behind the formed ridge.

Special studies. Ophthalmoscopy is indicated for all newborns with a birth weight of less than 6, as well as premature infants receiving O2; The first examination is recommended at the age of 4–6 weeks, and then every 2–3 weeks until the retina matures.

Differential diagnosis Retinoblastoma Congenital cataract Norrie disease Familial exudative vitreoretinopathy Toxocariasis with eye damage Coats disease Retinoschisis.

Treatment

Mode. Treatment is usually carried out in the neonatal intensive care unit; in adulthood, outpatient or inpatient.

Management tactics Peripheral multicentric cryopexy is indicated for the threshold stage of ROP. The effect of cryotherapy is based on the destruction of cells that release angiogenic factor; The treatment results are very good. Note. The threshold stage of ROP is defined as stage 3 with a prevalence of more than five contiguous or eight disparate hours on the dial, associated with dilation and tortuosity of newly formed vessels (3+). This is a reversible stage of ROP, in which further development of the disease will lead to irreversible consequences. It is recommended to reduce the intensity of light entering the retina (the resulting beneficial effect is not theoretically fully substantiated) If retinal detachment occurs, it is necessary to consider the advisability of vitrectomy, lens removal, or scleral filling surgery. In infants, born with very low body weight and receiving prophylactic treatment with fetal calf lung surfactant extract, the incidence of ROP was significantly reduced.

Observation Repeated examinations must be performed every 2 weeks until complete vascularization of the retina or regression of ROP occurs; every week if there is a prethreshold stage of ROP. Note. Characteristics of the prethreshold stage: Zone I, any stage Zone II, stage 2+ Zone II, stage 3 Subsequent examinations of children should be performed every 1–2 years with complete regression of ROP (without residual changes in the retina and vitreous) and every 6–12 months in the presence of scars.

Complications Retinal detachment Vitreous hemorrhage Angle-closure glaucoma Amblyopia Strabismus Myopia.

Course and prognosis Spontaneous regression occurs after several weeks or months in 85% of cases at stages 1 and 2. At stage 3+ (threshold stage), spontaneous regression occurs only in 50% of cases. In some cases, ROP progresses. Then there is a gradual transition of the active form of ROP to retrolental fibroplasia. Cryotherapy can reduce the risk of complications by 45%. Retinal detachment due to vitreoretinal stretching can occur in adolescence, so long-term observation is indicated.

Concomitant pathology. Neonatal respiratory distress syndrome.

Prevention Pregnant women should avoid risk factors for prematurity or intrauterine malnutrition (smoking, drinking alcohol, drugs, poor nutrition, development of any diseases during pregnancy) Monitoring oxygenation when caring for premature babies Prescribing vitamin E.

Reduction. ROP - retinopathy of prematurity

Notes Normal vascularization of the fetal retina begins approximately from the middle of pregnancy and ends at 36 weeks in the medial (nasal) parts of the retina and at 40 weeks in the lateral (temporal) Cryopexy - the formation of chorioretinal adhesions when exposed through the sclera to low temperatures Toxocariasis - helminthiasis in dogs and cats; There are isolated cases of disease in humans caused by the larvae of Toxocara canis or T. mystax.

H35.0 background retinopathy and retinal vascular changes

ICD-10 diagnosis tree

• h00-h59 class vii diseases of the eye and its adnexa
• h30-h36 diseases of the choroid and retina
• h35 other retinal diseases
• H35.0 background retinopathy and retinal vascular changes(Selected ICD-10 diagnosis)
• h35.3 macular and posterior pole degeneration
• h35.5 hereditary retinal dystrophies
• h35.6 retinal hemorrhage
• h35.8 other specified retinal disorders
• h35.9 retinal disease, unspecified
• h35.2 other proliferative retinopathy

Diseases and syndromes related to ICD diagnosis

Titles

Description

Retinopathy of prematurity is a serious eye disease that develops mainly in very premature infants, accompanied by changes in the retina and vitreous body.

Symptoms

There are 3 periods in the development of retinopathy of prematurity.

1, Active (up to 6 months of age), including changes in the vessels of the retina (changes in the arteries, dilation of veins, tortuosity of blood vessels, opacification of the vitreous body, hemorrhages in the vitreous body, the formation of retinal tears and tears with retinal detachment.

2, Period of reverse development (from 6 months of age to 1 year). Possible in the early stages of the active period before changes in the vitreous body.

3, Scar period (after 1 year of life). Accompanied by the formation of moderate and high myopia, retinal tears and detachments, the development of lens opacities, increased intraocular pressure, and reduction of eyeballs (subatrophy).

Causes

The main risk factors for developing retinopathy of prematurity are the following:

* short gestational age (that is, the degree of fetal maturity).

* low birth weight.

* intensity and duration of mechanical ventilation and oxygen therapy (stay in the incubator).

* concomitant pathology of the fetus.

* the mother has chronic inflammatory gynecological diseases during pregnancy, bleeding during childbirth.

Retinopathy of prematurity occurs as a result of premature birth with subsequent nursing of newborns in oxygen incubators. Oxygen has an adverse effect on eye tissue, causing active growth of retinal vessels, which subsequently leads to a significant decrease in vision.

Treatment

1, Conservative - instillation of drops prescribed by an ophthalmologist. Most often these are vitamin and hormonal preparations.

The choice of surgical intervention method depends on the stage of the process. As a rule, laser or cryosurgical (liquid nitrogen) coagulation of the retina or vitrectomy (removal of the vitreous body) is performed by experienced ophthalmological surgeons in specialized medical institutions. In half of the patients there is a tragic discrepancy between a successful surgical solution to the problem (that is, a technically successful operation) and the lack of vision of the operated patient. Many reasons and factors lead to such unsatisfactory results. These include underdevelopment of retinal photoreceptors and their damage as in the process of retinopathy itself. So during surgical treatment, the presence of severe concomitant pathology of the central nervous system, congenital damage to the visual pathways and subcortical centers.

Retinopathy of prematurity

Third level - ophthalmology hospital

1. Reverse ophthalmoscopy of the child’s eye

2. Echography (B-method)

Characteristics of treatment measures:

Stage II - may be reversible, but treatment may be required.

In stages III - IV of retinopathy of prematurity - laser coagulation, cryotherapy, lensvitreectomy in combination with scleroplastic operations for retinal detachment.

Surgery of the vitreous body and retinal detachment in stage V is inappropriate from the point of view of visual rehabilitation.

The final expected result is preservation of functions.

Treatment quality criteria:

Retinal fixation, retinal attachment, visual functions

Possible side effects and complications:

Retinal fibrosis, vitreous hemorrhage.

Dietary requirements and restrictions:

Requirements for the regime of work, rest and rehabilitation:

Retinopathy of prematurity

An achievement of modern medicine is undoubtedly the possibility of saving and nursing newborn babies even with catastrophically low birth weight in the early stages of pregnancy. However, premature babies have a high risk of developing various types of pathologies due to their lack of readiness for life outside the womb. One of these risks is the immaturity of the baby’s retina. This in turn can lead to retinopathy. Let's look at what it is.

Retinopathy of prematurity is negative changes in the retina due to the unprepared structure of the eye of a child born before the expected date of birth. Its code according to ICD 10 is N 35.1. This pathology is characterized by impaired vasculogenesis and clouding of the vitreous body. This in turn can lead to the development of strabismus, glaucoma and retinal loss.

The diagnosis is made after examining the premature baby by an ophthalmologist and conducting the necessary examinations, such as ultrasound of the eyes, electrotinography.

Causes

The formation and development of the retina, otherwise vasculogenesis (vascular growth), begins inside the mother's womb in the second trimester, from about the 15th week of pregnancy, and continues until childbirth. That is why children whose gestational age of birth is less than the prescribed 40 weeks are susceptible to retinopathy.

For example, early birth within a week, in 40-50% of cases guarantees the child some degree of retinopathy. The lower the gestational age, the more immature zones there are on the retina.

The paradox is that now doctors are able to deliver a very premature baby, however, almost all newborns weighing less than 800 grams will have a similar pathology. In developed countries, retinopathy of prematurity is the leading cause of childhood blindness.

The process of vascularization of the retinal vessels can be influenced by many negative factors. One of the most important is that glucose is involved in the processes occurring in the retina, the breakdown of which must occur without the participation of oxygen. While on a ventilator, a premature baby receives oxygen therapy due to the immaturity and underdevelopment of the lungs due to early birth. That is why the risk of developing retinopathy is closely related to the gestational age at birth.

In addition, there are additional factors, namely:

• hypoxia;
• infections;
• birth injuries;
• lack of iron in a newborn;
• low body weight;
• bleeding during childbirth;
• multiple pregnancy;
• gestosis in the mother during pregnancy;
• sexually transmitted diseases in women in labor.

An important problem in nursing premature babies is illumination, which also has a negative effect on the eyes, since normal angiogenesis should take place in the absence of exposure to light, as nature intended, namely in utero.

Negative factors can affect not only the formation of new retinal vessels and their growth, but also previously formed vascular tracts, they begin to form the vitreous body. All this subsequently leads to tension, new formations of glial tissue and, ultimately, to retinal detachment and, accordingly, blindness.

Development of retinopathy

The medical history begins from the moment the baby is born. From birth to six months of age, the premature baby goes through an active period of retinopathy. During this period, the retinal vessels become tortuous, the arteries and veins change, the formation and clouding of the vitreous body occurs, and retinal detachment is possible.

Then comes the regressive period. Basically, it occurs when the child is between six months and one year old.

After a year, the scarring period passes.

This phase is characterized by the appearance of problems with visual function. Pressure may increase, the eyeballs become smaller, the lens becomes cloudy, and the retina ruptures or detaches.

Symptoms of retinopathy of prematurity

Premature babies are at risk for developing retinopathy, but it is very difficult for a young mother to notice its symptoms.

Parents should pay attention to how the child’s eyes react to objects and their movements.

If you have the following symptoms, you should consult a doctor to examine the retina and fundus of the eye:

• twitching of eyelids;
• mild squint;
• the child does not pay attention to what is happening away from him;
• alternately closes eyes;
• brings toys close to eyes or sees objects and people only at close range.

Only diagnostic data are objective manifestations of retinopathy of premature infants, especially in the active phase of the disease, which means they can be symptoms of the appearance or development of pathology.

Types of retinopathy of prematurity

There are two phases of retinopathy: active and regressive (scarring).

The development of the disease begins precisely with the active phase, which, in turn, is divided into 4 stages, in accordance with the severity of the disease. Photos by stages.

The appearance of a whitish dividing line between the normally developed retina and the affected areas. In grade 1, weekly examinations by a pediatric ophthalmologist are indicated to identify the dynamics of the disease.

The appearance of a tubercle at the site of the dividing line. In this case, the vessels grow into the shaft and form small avascular areas on the retina. At the second stage, spontaneous recovery occurs in the majority of newborns, namely 70-80%. However, minor changes may remain in the fundus of the eye, requiring periodic examinations by a specialist.

In the shaft formed on the retina, the formation of fibrous tissue begins to occur, and the vitreous body above it begins to thicken. Tissue and vessels grow over the surface of the retina and penetrate the vitreous body. As a result, the retina is stretched and there is a high risk of detachment. If the disease progresses at this stage, it is almost impossible to reverse the effects of retinopathy, which is why it is called threshold.

It is divided into two substages: IVa - without involvement of the central region and IVb - with detachment in the central region. It is called terminal because the prognosis for the child’s health becomes negative, and vision deteriorates sharply.

A complete funnel-shaped detachment of the retina of the child’s eye occurs.

The duration of the active phase varies greatly, but generally occurs in the period from 3 months to six months. It can end either in spontaneous regression or in a scar formation phase with inevitable residual changes in the retina.

There is a separate type of retinopathy – “plus disease” or fulminant retinopathy. It is characterized by the absence of stages; changes in the retina occur much faster. As a result, retinal detachment occurs much earlier and we can talk about the terminal stage of retinopathy.

Localization of retinopathy of prematurity

An important point in making the correct diagnosis, and, accordingly, the necessary treatment, is determining the localization zone of the affected areas of the retina.

Depending on the localization of the process (that is, along the border between the zone of the healthy and the affected retina), 3 zones are distinguished:

Zone 1 – circle.

Zone 2 is a ring that runs along the periphery of the 1st zone.

Zone 3 – crescent, outward from zone 2.

The earlier the birth occurred, the closer to the posterior pole of the eye the damaged (avascular) areas of the child’s retina are located; accordingly, the localization of the process corresponds to the degree of retinal immaturity at birth.

Regressive phase

It is a relatively stable condition in which 5 degrees can be distinguished:

• 1st degree. It is characterized by minimal changes in blood vessels on the periphery of the fundus. These changes, as a rule, do not affect the baby's visual function.
• 2nd degree. Significant changes in the periphery of the fundus with ectopia or deformation of the macula and disorders in the retinal vessels themselves.
• 3rd degree. Gross changes associated with the presence of fibrovascular tissue outside the retina of the newborn.
• 4th degree. Characterized by serious impairment of visual function.
• 5th degree. Total retinal detachment and vision loss.

Diagnosis of the disease

It is very important to identify the symptoms of the disease as early as possible. To identify retinopathy at an early stage, episodic examinations of children at risk, namely those born before 35 weeks, are necessary.

Preventive examinations of the retina should be carried out from 3-4 weeks of life of a small patient.

Instrumental examinations

To clarify the diagnosis at stages 3-5, it is necessary to do an ultrasound, which will reveal the manifestations of retinopathy. Carrying out ultrasound in the first stages does not make sense, since they practically do not give ultrasound symptoms; they can only be detected by an ophthalmological examination.

Modern medicine has the ability to study the peripheral space of the fundus through the use of pediatric RetCam cameras. The results of the examination will not only help make the correct diagnosis, but also provide the opportunity for remote consultation in difficult situations.

However, you should not overuse examinations and interventions during the active phase of the disease. The diagnosis is made based on identifying characteristic signs over time.

First of all, during examinations, special attention should be concentrated on the periphery of the fundus, since it is in this area that clinical manifestations and the first stage of the process are noticeable. The use of binocular ophthalmoscopy and gentle movements of the eyeball is allowed. The use of scleral depressors is contraindicated when examining premature infants.

The main requirement during periodic inspections is the absence of trauma. Since pressure on the eye can lead to complications from the lungs and heart (apnea, arrhythmia, tachycardia). For premature babies, eyelid dilators and eyelid lifters, special hooks for turning the eyeball are used. Depending on the child’s health condition, examinations should be carried out in the presence of a neonatologist, resuscitator and nurse.

Premature babies are characterized by pupil rigidity, which requires repeated instillation of the medicine (3 times every 15 minutes until the doctor arrives).

Differential diagnosis

This type of diagnosis is resorted to if:

• there is a rapid development of pathology;
• there are changes in the posterior pole of the eye;
• swelling of the cornea is observed.

When carrying out such a diagnosis, one should take into account the presence or absence of deep prematurity, clinical manifestations and the phase of the disease.

For retinoblastoma, it is necessary to conduct a diaphonoscopic examination and ultrasound.

Difficulties in making a diagnosis can be caused by the lack of data on the active phase of the disease; this occurs when the diagnosis is detected late.

Treatment

Only treatment carried out in the first year of a child’s life can be effective. The goal of treatment is to prevent deterioration of health, avoid progression of the process and, if possible, minimize the negative consequences of regressive retinopathy.

All treatment methods can be divided into:

• Conservative. Experts consider this method ineffective. It involves the use of medications, which are dropped into the eyes.
• Surgical. In most cases, surgical intervention of various kinds is performed, as a rule, after the disease has progressed to the threshold stage 3. This may be laser or cryosurgical treatment. If there is a serious threat of retinal detachment or this process has already begun, a major operation to remove the vitreous is required. Only high-level professionals in specialized clinics can do it.

In some cases, hospitalization of the child is required:

• administration of anesthesia during planned surgery;
• to conduct a more detailed and in-depth examination under anesthesia;
• for treatment with drugs of complex stages of the disease, less often the scar period.

Non-drug treatment

Despite the fact that oxygen is a negative factor influencing the risk of developing retinopathy, in practice it is also used as a treatment. Dosed oxygen therapy is used in a number of cases and only in the active period of the disease, subject to its progression.

During the regressive phase, procedures aimed at developing vision are indicated: physiotherapy (electrophoresis, infrasound) and stimulating procedures (electrical stimulation of the optic nerve).

Surgery

Goals of surgery:

• to avoid the transition of retinopathy to the thermal stage;
• to preserve the organ of vision;
• rehabilitation in severe cases.

Coagulation of the damaged area of ​​the retina

Used for preventive purposes to preserve vision. Usually performed when retinopathy approaches a threshold stage. In this case, coagulation should cover the entire area of ​​the avascular retina.

Assessment of the performed retinal coagulation should be carried out in the second postoperative week. Treatment will be effective when retinal vascularization occurs or stabilizes.

The doctor decides which treatment method to choose based on the dynamic picture of the disease and the technical capabilities of the medical institution. It is possible to use a combined technique.

The effectiveness of coagulation for preventive purposes is quite high, ranging from 55 to 95%, despite the dependence of success on many factors.

For a long time, specialists have no doubt about the need to use coagulation, since spontaneous regression is observed only in 1/3 of cases.

Additional consultations

Unfortunately, quite often, retinopathy is accompanied by disorders of the central nervous system, so you may need to consult a professional neurologist.

Observation of children after retinopathy

In the case of surgical intervention, a premature baby requires special care and mandatory observation by an ophthalmologist for a month.

Premature babies who have suffered retinopathy should come for examination at intervals prescribed by the doctor. The observation period is usually 15 to 20 years, and in some cases lifelong.

For parents of patients

Premature babies born before the 35th week of gestation and gaining less than 2 kg during intrauterine development must be examined by an ophthalmologist. Moreover, it is better if this specialist works in a neonatal center or hospital department and has extensive experience working with premature babies. The first examination should be carried out when the baby is 1-2 months old; the frequency of observations is determined by the doctor.

Children born before the established date should be observed by an ophthalmologist, even in the absence of such a serious disease as retinopathy, since such patients often develop myopia and other anomalies. It is advisable to visit a specialist at six months, one year of age and at 1.5 years.

Forecast

In the vast majority of children, retinopathy of prematurity does not progress further than stage 2, regression occurs, eye function is restored and vision is preserved. However, by the age of 5-10 years, problems may arise, such as astigmatism, farsightedness, myopia, and strabismus. With retinopathy of the last two stages, the prognosis is unfavorable.

The rehabilitation prognosis directly depends on the stage of the disease and the presence or absence of disorders in the baby’s nervous system.

Even in the developed countries of the European Union, the USA and Japan, where they have learned to care for very premature babies weighing over 500 grams, retinopathy is a serious illness.

Prevention of retinopathy

The most effective prevention of retinopathy is the effective preservation of a complicated pregnancy, its maximum extension, at least up to 35 weeks. In addition, in the case of premature birth, proper nursing of the premature baby, under the constant supervision of neonatologists and an ophthalmologist.

In cases where the first signs of the disease appear, frequent examinations by an ophthalmologist are necessary, namely every week. When a diagnosis of fulminant retinopathy is made, the child's condition should be monitored every 2-3 days. Observations are required until regression begins or surgical intervention is required. When the disease recedes, the baby must be examined every 2 weeks to identify positive dynamics.

Retinopathy of prematurity consists of several stages, closely related to each other, and smoothly flowing into one another, including in the opposite direction during spontaneous regression.

The result of the disease may be the formation of a scar on the retina of a premature baby or complete regression, in which all manifestations of the disease go away on their own. However, after a few years, retinopathy may make itself felt as a consequence of the disease, in the form of myopia, farsightedness or astigmatism.

Retinopathy of prematurity

Retinopathy of premature babies is the most common. This is due to the underdevelopment of the visual organ in the womb. However, there are a number of other reasons and factors for the occurrence of this pathology. If we talk about statistics, then approximately every fifth baby has this disease. And 8% of them are in severe form. Retinopathy is characterized by pathological processes in the light-sensitive organ, that is, the retina. Retinopathy of prematurity code according to ICD10 (international classification of diseases) is H 35.1.

The main causes and factors for the development of retinopathy in premature infants

As is known, premature babies are placed in special pressure chambers (incubators) equipped with oxygen and normal air temperature to maintain the baby’s health. Back in the 50s of the last century, a relationship was discovered between high oxygen concentrations and the development of blood vessels. The fact is that metabolic processes in the retina of the eye occur not with the help of oxygen respiration, but with glycolysis. That is, when glucose is broken down, metabolic processes accelerate. If the baby’s body is exposed to an increased concentration of oxygen, then glucose begins to be suppressed, and the retina, in turn, begins to die. Connective tissue or scar tissue forms in place of the retina. A newborn premature baby is always placed in an incubator where the oxygen concentration is too high. It is at this moment that retinopathy begins to develop. This is what doctors believed until recently, until additional causes and factors for the occurrence of the disease were discovered. These include the following:

1. Infection of mother and fetus.
2. Chronic inflammatory diseases of a pregnant woman.
3. Complicated pregnancy and childbirth, including bleeding and hypoxia.
4. Hereditary predisposition.
5. Pathological abnormalities in fetal development.
6. Infant exposure to excessively bright light.
7. Too early birth - 32 weeks (the retina is finally formed only by the 36th week at least).
8. Insufficient weight - less than one and a half kg.

Classification features

Retinopathy is classified by severity:

1. Retinopathy of prematurity stage 1. Characterized by minimal pathological deviations. On examination, a white line is noted between the retina and spaces without blood vessels.
2. Retinopathy of the 2nd degree in premature infants is characterized by the formation of a certain elevation on the white line. This stage is characterized by spontaneous recovery.
3. Degree 3. In this case, on the raised elevation, vessels begin to actively grow, going deeper inside, that is, into the vitreous body. The visual organs undergo irreversible processes, so a decision is made on surgical intervention.
4. At grade 4, the retina exfoliates, the tissues become scarred, and the lens degenerates. There is a possibility of developing blindness.
5. Grade 5 is characterized by complete retinal detachment and loss of vision.

As a rule, retinopathy in premature babies has a typical form, but an atypical one can also be found. It occurs in approximately 25 percent of all cases. The first type is “pre-plus” disease, in which there is increased vascular activity. Then she outgrows the “plus” disease. In this situation, pathological processes are accelerated and complicated. This is followed by the most dangerous phase - the aggressive posterior phase, which does not have a favorable prognosis.

Symptoms of retinopathy

ATTENTION! Only an experienced ophthalmologist can make an accurate diagnosis. But parents are also obliged to monitor the child’s behavior, considering the symptoms of possible pathology. You need to know that babies' visual organs develop gradually, so it is quite possible that you will find signs of strabismus or farsightedness. No need to panic! It is better to consult a doctor.

Progressive deterioration of vision over time can lead to dire consequences - from the development of local pathologies up to complete blindness. People, taught by bitter experience, use a proven remedy that was previously unknown and popular to restore their vision. Read more"

Symptoms of retinopathy of prematurity include:

1. The infant brings the rattles too close for inspection.
2. The child does not see objects located a meter from his eyes.
3. The baby quickly and unexpectedly develops strabismus (all babies have it from birth, but disappears over time).
4. The child looks at toys with only one eye.
5. Blinking too often.
6. You can easily cover one eye, but when you start doing the same with the other, the baby begins to protest.

Treatment methods for retinopathy

Treatment of any disease is prescribed in accordance with the severity, course and characteristics of the disease:

1. Retinopathy of prematurity grade 1, as well as grade 2, is practically not treated because it is considered not dangerous. There is a possibility of spontaneous recovery. Consequently, doctors adopt a wait-and-see approach. Definitely, the child is under the supervision of a doctor and parents.
2. For grade 3 severity, surgical intervention is urgently prescribed. This can be laser coagulation or cryocoagulation. The operation allows you to suppress the proliferation of connective tissue and stop the progression. Cryocoagulation is carried out under general anesthesia, and laser - without anesthesia at all.
3. It happens that the methods described above do not bring a positive result, or the disease is already at stages 4 and 5. In this situation, circular filling of the sclera and transciliary vitrectomy are prescribed. Filling allows you to eliminate detachment. During the operation, a silicone filling is installed in the sclera. Vitrectomy is based on the removal of the vitreous humor and scars from the retina.

Forecast, observation, prevention

After any surgical intervention, the baby should be observed by an ophthalmologist for many years (until adulthood). This is necessary to prevent relapse and prevent complications and consequences. The prognosis depends on the severity:

1. Retinopathy of prematurity grade 1 has a favorable prognosis. As a rule, the visual apparatus recovers on its own.
2. Grade 2 retinopathy in premature babies also has a very favorable prognosis. However, there is a risk of retinal detachment in the future.
3. With grades 3 and 4 retinopathy, the prognosis is unfavorable, but if surgery is performed in a timely manner, it will end successfully.
4. At grade 5, more complex surgery is required. However, modern technologies make it possible to solve this problem. The most important thing is to take action in a timely manner!

1. First of all, during pregnancy you need to follow all doctor’s instructions and lead a healthy active lifestyle. This will eliminate the risk of premature birth.
2. If a child has already been diagnosed with stage 1 and 2 retinopathy, treatment is not carried out. But preventive therapy is needed. It consists of the use of corticosteroid hormonal drugs and antioxidants.

Other retinal diseases

Background retinopathy and retinal vascular changes

Changes in the retinal vascular pattern

Retinal:

• microaneurysms
• neovascularization
• perivasculitis
• varicose veins
• vascular sheaths
• vasculitis

Preretinopathy

Other proliferative retinopathy

Excludes: proliferative vitreoretinopathy with retinal detachment (H33.4)

Macular and posterior pole degeneration

Angioid stripes of the macula

Drusen (degenerative) macula

Age-related macular degeneration (atrophic) (exudative)

If it is necessary to identify the drug that caused the lesion, use an additional external cause code (class XX).

Peripheral retinal degenerations

Retinal degeneration:

• lattice
• microcystic
• palisade
• resembling a cobblestone street in appearance
• reticular

Excludes: with retinal tear (H33.3)

Hereditary retinal dystrophies

Dystrophy:

• retinal (albipunctate) (pigmented) (yolk-like)
• taperetinal
• vitreoretinal

Retinal diseases - classification according to ICD-10 (codes)

According to the ICD, there are several categories of retinal diseases.

Chorioretinal inflammation (H30)

Chorioretinal inflammation includes the following specific nosologies:

• Focal chorioretinal inflammation (H30.0);
• Disseminated chorioretinal inflammation (H30.1);
• Posterior cyclitis (H30.2);
• Chorioretinal inflammation of other etiology (H30.8);
• Unspecified type of chorioretinal inflammation (H30.9).

Diseases of the choroid of the eyeball, not included in other sections (H31)

This section of the ICD includes:

• Chorioretinal scars (H31.0);
• Degenerative changes in the choroid (H31.1);
• Dystrophic processes in the choroid of a hereditary nature (H31.2);
• Ruptures of the choroid, hemorrhages in this area of ​​the eye (H31.3);
• Choroidal detachment (H31.4);
• Other pathologies of the choroid (H31.8);
• Unspecified diseases of the choroid (H31.9).

Secondary chorioretinal changes (H32)

Such pathologies include:

This pathology combines:

• Retinal detachment accompanied by a rupture (H33.0);
• Retinal cysts, retinoschisis (H33.1);
• Serous retinal detachment (H33.2);
• Retinal tear not accompanied by detachment (H33.3);
• Ordinary retinal detachment (H33.4);
• Other forms of retinal detachment (H33.5).

Retinal vascular occlusion (H34)

Occlusion of retinal vessels can be of the following types:

• Transient occlusion of the retinal arteries (H34.0);
• Central retinal artery occlusion (H34.1);
• Occlusion of other retinal arteries (H34.2);
• Other types of retinal vascular occlusions (H34.8);
• Unspecified type of retinal vascular occlusion (H34.9).

Other retinal pathologies (H35)

Other retinal diseases include:

• Background retinopathy or retinal vascular pathologies (H35.0);
• Preretinopathy (H35.1);
• The remaining pretinopathy is of the proliferative type (H35.2);
• Degenerative changes in the macula or posterior pole (H35.3);
• Degeneration of the peripheral retina (H35.4);
• Hereditary retinal dystrophy (H35.5);
• Hemorrhage into the retinal substance (H35.6);
• Splitting of cell layers in the retina (H35.7);
• Other specified disorders of the retina (H35.8);
• Unspecified diseases of the retina (H35.9).

Secondary retinal lesions (H36)

Retinal diseases can occur with other pathologies:

• Diabetic retinopathy (H36.0);
• Other disorders in the retina (H36.8).

Delayed detection of retinopathy of prematurity can lead to blindness of the baby!

Retinopathy is an inflammatory ophthalmological process that is often observed in premature infants.

This disease is detected during the very first ophthalmological examination of the baby.

What it is?

This disease, also known as vasoproliferative retinopathy, occurs mainly in very premature babies.

Already at the first examination, it is clear that the vascular network of such a child is not fully developed. This condition is called retinal vascularization.

In ophthalmology, such cases began to be recorded relatively recently - the first case of retinopathy in a premature baby was described in 1942.

This does not mean that the problem did not exist before: it was just at that time that diagnostic methods appeared that made it possible to conduct thorough studies of the eyeball.

Despite the fact that scientists have made great progress in the study of this pathology, they have not yet been able to fully establish the causes of the disease.

Disease code according to ICD 10 - N 35.1.

Causes

The obvious reason for the development of retinopathy in premature infants is not fully formed visual organs.

They cannot yet supply themselves with blood due to the underdevelopment of the retinal circulatory system.

The disease does not manifest itself in all premature babies, but there are certain risk factors due to which the disease can be diagnosed:

• infection of the fetus at the stage of intrauterine development;
• ischemic disease;
• hemorrhages of various types;
• complications during pregnancy;
• problematic childbirth.

Sometimes retinopathy can develop in the first days of a child's life.

This occurs due to excessive exposure to light on the fragile retina, since before birth the child is in complete darkness, and when entering this world, he finds himself under the bright light of medical lamps.

Research shows that the fetal retina is formed by the fourth month of human life.

At the moment, experts cannot say for sure, but they suggest that the development of the disease in premature infants can also be facilitated by head and eye injuries at the stage of intrauterine development, the accumulation of blood clots and the use of donor blood transfused to the mother.

Photos by stage

Classification of the disease

Retinopathy in prematurity occurs in several stages, each of which is characterized by certain symptoms.

1st degree

During the first ophthalmological examination of a newborn, the doctor may notice a white line that runs along the border between the avascular areas and the vascular tissue.

This is grade 1 retinopathy, which requires regular additional examinations to diagnose either remission (then the disease may not develop) or progression leading to the second stage.

Stage 2

As a result, after remission, only small traces of transformations may remain in the fundus of the eye, which do not affect the quality of vision.

Stage 3

If the shaft does not disappear, but becomes overgrown with fibrous tissue, the area of ​​the vitreous body above it becomes denser.

The retinal vessels are drawn into this body, and the retina itself begins to undergo tension, which in turn is fraught with detachments.

If no measures are taken at this stage, the disease may develop into an irreversible form in the future.

Stage 4

The stage is divided into two “sub-stages”: 4A and 4B. In the first case, there is a partial detachment of the retina, in the second, the detachment affects its central part. In this case, the prognosis is already unfavorable.

Stage 5

At the last, fifth stage, complete detachment of the retina occurs, the newborn’s vision drops sharply, surgical intervention is impossible, and retinopathy becomes irreversible.

How is diagnosis done?

Preemies are babies who weigh less than two kilograms and are born before 35 weeks.

If the first signs of retinopathy are present, the child undergoes a weekly examination.

It is necessary to wait for the natural outcome of events, which will either lead to self-healing or reach the stage of the need for surgical intervention.

If conditions are favorable and the disease regresses, examinations are carried out less frequently (once every 14 days).

During the examination, drops are used to dilate the pupil, as well as eyelid dilators: this measure is necessary, since the child does not understand the actions of the doctors and will not keep his eyes open.

The use of such a device is absolutely safe for the eye and puts even less pressure on the eyelids than if the ophthalmologist held the eyelids with his fingers.

An additional research tool is ultrasound of the eyeball.

Retinopathy may regress on its own, but may recur after a short time. This is a reason to undergo regular examinations during the first few years of a child’s life.

This approach allows you to promptly notice the moment when the development of retinopathy will require surgical intervention.

How to treat?

Unlike the treatment of adults, in which such methods, if performed in a timely manner, are effective, in newborns the pathology is so strong and the body is so weak that neither one nor the other method guarantees a complete cure.

Moreover, drug methods are ineffective on their own, and can only serve as an additional measure to consolidate the results of the surgeon’s work.

These are mainly vitamin drops and medications that can shorten the postoperative rehabilitation period.

Depending on the severity of the disease and the stage of development, one of three methods of surgical treatment is used:

1. In the first stages, it is enough to make gluing in places where retinal pathology develops.

This is done using liquid nitrogen or by exposing the affected areas to a laser beam.

Indications and contraindications for different types of surgical intervention are strictly individual and can be announced by the attending physician only after a thorough examination.

Treatment prognosis

If timely measures are taken, the prognosis is favorable, and by detecting the disease in time, ophthalmologists have a 90% chance of saving the child’s vision.

But even in such cases, the quality and acuity of vision can only be maintained for several years, after which degenerative phenomena are possible in the visual organs.

This is explained by the fact that the retina in this case is still defective and is susceptible to various ailments.

There is also always the possibility of secondary retinal detachment, secondary glaucoma and clouding of the cornea of ​​the operated eye.

Prevention

The only possible preventive measure for retinopathy in newborns is to identify the disease, closely monitor it and take the necessary treatment measures.

Useful video

In this video you will see how retinopathy of prematurity is treated:

Considering that it was not possible to fully establish all the causes of the disease, it is worth remembering that retinopathy in a child can be caused by the abuse of bad habits, poor diet and the use of certain medications during pregnancy.

The risk group for macular degeneration of the retina includes older people. With age, central vision is subject to great changes due to the fact that problems with the circulatory system progress.

H35.3 Macular and posterior pole degeneration

Doctors and scientists have not recorded the causes of macular degeneration as an absolute list. They were identified as a series of assumptions indicating possible factors that could serve as an impetus for the formation of dystrophic changes. Among them:

• Age-related changes.
• Heredity.
• Smoking.
• Exposure to ultraviolet radiation.
• Unbalanced diet.
• Having excess weight.
• Diseases of the cardiovascular system.

Macular degeneration occurs more often in women due to their longer life expectancy compared to men. Moreover, those who have crossed the threshold of 50 years are predisposed to this disease.

Macular degeneration rarely develops in children. It occurs in them if their parents had a predisposition to this disease. At the same time, vascular sclerosis develops at the genetic level, which becomes the impetus for dystrophic changes in the retina.

There are dry and wet forms of macular degeneration. Moreover, each of them has a certain set of characteristics and symptomatic manifestations.

Diagnosed in 90% of cases. It represents the first stage of macular degeneration in which new vessels have not had time to form. A characteristic manifestation of dry macular degeneration is thinning of the retinal tissue and the accumulation of yellow pigments (drusen) in its layers. In the dry form of the disease, 3 stages of development are observed:

1. The early stage does not manifest itself as visual impairment. It can be identified by the formation of drusen.
2. The intermediate stage is characterized by the fusion of small drusen into medium-sized spots or into one large one. As a visual defect, a blurry silhouette appears before the eyes.
3. The pronounced stage implies an increase in the silhouette and its blackening. This suggests that light-sensitive cells are dying.

The dry form of macular degeneration causes vision loss if not treated at an early stage.

The wet form of the disease damages vision more than the dry form. This is due to the formation of new vessels (neovascularization process). They are very fragile, so they are often damaged, causing hemorrhages. They, in turn, lead to the death of light-sensitive cells and the appearance of a blind spot in the field of vision.

There are latent and classic types of macular degeneration. In the latter case, dystrophic processes are more pronounced. At the same time, vascular neoplasms appear more often. This is accompanied by the development of scar tissue.

If we talk about dry macular degeneration, then in the initial stages it does not cause pain or symptomatic manifestations. It is necessary to take the appearance of such signs seriously in order to identify the disease on time.:

• It becomes difficult to navigate in the dark.
• Vision begins to decline.
• Visible text becomes harder to see.
• It is more difficult to recognize surrounding faces.
• The field of vision is clouded by a dark spot without pronounced contours.

The same symptoms are characteristic of wet macular degeneration. Added to these are distortion of the outlines of the visible image and visual bending of straight lines.

Diagnosis of the disease involves drawing up a clinical picture in accordance with the patient’s complaints and research results. The following methods are used to detect the disease::

• Examination of the eye using an alkaline lamp and an ophthalmoscope.
• Determination of visual acuity and field using various tests (including the Amsler test).
• Fluorescein angiography.
• CT scan.

As a result of the research, the stage of the disease and the location of the lesion are revealed. Treatment is prescribed according to the data obtained.

Dry macular degeneration can be treated with conservative methods. The purpose of the measures taken is to stop the formation of new vessels, thereby eliminating the further development of the disease. The risk of further vision loss is prevented by antioxidant and zinc supplements. In the dry form of the disease, the patient is prescribed medications that include vitamins A, C and E, copper and zinc. In addition, the ophthalmologist prescribes Lutein and Zeaxanthin. The same drugs are used to prevent macular degeneration.

The conservative method in the treatment of wet macular degeneration is ineffective. Therefore, preference is given to such procedures:

• Laser surgery. It is used if the newly formed vessels are located at a distance from the fossa of the macula. Those that are characterized by fragility and bleeding are removed. They are destroyed by laser radiation, but healthy tissue can also be accidentally damaged. Laser treatment does not always help. In many cases, even after a second procedure, vision continues to deteriorate.
• Photodynamic therapy is a safer method compared to laser surgery. It is an intravenous administration of Visudin. Medicinal substances are attached to the walls of painful vessels and irradiate them with light radiation for 1.5 minutes without affecting healthy tissue. The result is a slowdown in the rate of vision deterioration. For 5 days after the procedure, you need to protect your eyes from bright sunlight and room lighting. The effect of photodynamics is unstable. After some time, a repeat procedure may be necessary.
• Intraocular injections or anti-VEGF therapy. To begin with, local anesthesia is performed. After this, Avastin, Lucentis, Macugen and other modern medications are injected into the eye cavity. Their action is to block the growth factor of new non-viable vessels. The procedure is carried out monthly. Doses of the drug are calculated for each patient separately.

Doctors talk about the treatment of macular degeneration as follows:

Only intraocular injections can improve vision. Other treatment methods only stop the further development of dystrophic changes.

Since dystrophic changes can be caused by poor nutrition, treatment with folk remedies involves its correction. It is recommended to eat chickpeas and wheat germ. Eye drops made from tinctures of aloe and mumiyo juice help improve vision. It is worth remembering that folk remedies are auxiliary and are used along with the main treatment. You should talk to your doctor about their effectiveness before using them.

Here's what they say about disease prevention on the Internet:

Thus, to reduce the risk of macular degeneration, you need to follow these tips:

1. Protect your eyes from ultraviolet exposure. For these purposes, wear sunglasses before going outside.
2. Quit smoking and the risk of developing the disease will decrease by 5 times.
3. Eat more fish, fruits and vegetables.
4. Set limits on fatty foods.
5. Take vitamins as advised by your doctor.
6. Make it a habit to exercise daily.
7. Monitor your weight.
8. Monitor your blood pressure and blood cholesterol levels.

An annual visit to an ophthalmologist will help to detect the disease in a timely manner.

comments powered by HyperComments

What kind of disease is this?

Macular degeneration

Dry form:

Wet form:

Main features:

• straight lines are refracted;

cytomegalovirus

Treatment

Video:

Related articles:

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  • ??????????? ??????? ?????? ? ??????????? ??????????:
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  • ?????? ????????????? ??? ?????? ?????? ??????? ??? ??????? (???????????);
  • ?????????????? (??? ????????? ?????? ????????? ?????? ????????? ????????????, ????????, ?????????? ?????????);
  • ????????????? ??????? ? ????????????? ???????????? ???? 60 ?/??? 90D, ? ????? ????? ????? ? ????????? ?? (????? ??????????, ????????? ? ??.), ????? ?????????? ?????? ????????????? ???????????? ????????????.

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  • ??????????, ???????? ???????????? ?????????? ??????????, ? ????????? ?????????? ???? ? ?????????? ?????????? ???????????????? (??? ?????? ??????? ?????? ?????????? ??????? ?????????? ?? ??????????, ? ??????????????? ??????? pa????? ? ??????? ???????);
  • ?????????????????????? ???????????? (?????????-???, ??????????? ???, ???????-???, ?????????? ???, ??????????????? ???).

  ??? ????????? ? ???????????????? ????????????? ????????? ? ?????? ????????? ????????? ??????.

  • ??????? ?????????????????????? ???????? ??? : ???????????? ? ????????? ????? ??????? ???????? ?????????? ????????? ?? ?????? ??????? ? ?????????? ?????????? ? ???????? ????, ?? ? ????????????? ?????????? ???????????, ??????????? ?? ???? ?? ?????.
  • ??? ? ????????????? ?????? ?????????????? ??????????????? ????? ??? ???? ???????????, ??? ??? ????????? ?????? ?????????? ??????????? ????????? ? ??????? ???????? ??????????????? ???????? (???. 31-52).

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    ?????? ?????????? ? ????.

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    ????? ???? - ?????????? ???????????????, ??????? ?????.

    ??? ???????? ????? ???????? ???????????????? ???????? ?????????? ??????????? ???????????. ???????? ???????????? ?????? ??????? ? ???, ??? ??? ????????? ?????????? ??? ???? ????? ?????????????? ?????????????? ???????. ??????????????, ??????? ??????? ? ????????????? ????? ???? ??????? ???? ??? ???????????????? ????????????????? ????????????. ? ????????? ????? ? ????? ?????? ??? ?????????????????? ????????????? ?????????? ?? ???? ??????, ????????? ?????????? (???????) ? ??????????? (????????) ??????? ? ???????????. ? ????????? ??????? ??? ????????? ??? ?????????? ??? ??????? ??????? ? ??????????? ??????????????????.

    ?????????? (???????) - ????????? ???-??????? ????????, ?????????? ??????? ????????? ? ?????????? ??????????????? ??????? ????? VEGF (vascular endothelial growth factor). ???????????? ??????? ??????? 165 ????? ??????? ?????, ?????????? ???????????? ????? ???????????????? ??????? ? ?????????? ????????????? ?????????? ?????? - ???? ??????? ?????????? ????????????? ????? ???. ??????? ???????????? ??? ???????????????? ???????. ?????????? ?????? ?? ?????????? ???????????? - ??????????, ??? ?????????, ???????????? ?????? ??????? ?????? ??? ??????? ?????????? ?????????? ???, ?? ????????? ? ?????????? ???????. ??? ?????????? ?????????? ???????????? ?????????? ??????? ??????????????? ? ????????? ????? (0.3; 1.0 ? 3.0 ??) ?????? 6??? ? ??????? 54???; ?????? ???????????? ??????? ?????? ?????????? ? ??????? ??????? ??????? ??? ??? ?????????? ?? ????????????? ???.

    ? ???? ?? ????? - ??? ????????????? ??????????? ? ?????????? ? ?????? ???????? - ??????????? (????????) . ?????????? ? ????????????? ??????????, ????????????? ??? ??????? ??????? ????? VEGF. ???????????????? ??????? ????????? ????????? 1 ??? ? 4 ???. ??? ?????????? ???????????????? ?????????? ???????????? (ANCHOR ? MARINA) ????????????? ??????? ??????????????? ? ???? 0.3? 0.5??. ? ?????????? ??????? ???? ??????? ?? ?????? ????????????, ?? ? ????????? ????????? ??????? ??????.

    ????? ????, ? ??????? ????????????? ?????????? ????????? ???????????? ????? ??????? ?????????, ???????????? ????????????, ? ???????????? (???????). ??? ??????? ? ????-VEGF ??????????? ??????? ????????? ?????????? ??? ??????? ??????????????? ????. ? ????????? ?????, ?????? ?????? ?? ????????? ??????? ????????? ??????????, ???????????????? ?? ??? ??????? ????????????????, ?????? ????????? ??????? ????????????? ????????????? ? ???????????? ???????????? ? ????????????.

    ?????????? ??????????? ? ??? ???? ??????????? ??????? ? ??????? ??????? ??????????? ? ???????????????? ???????? ??????????????? ????????????????. ? ????????? ????? ?????????? ??????? ?????? ????????? ??????? ????????????? (???????-40). ??????? ?? ?? ??? ?? ???? ???? ???? ??????? ????????? ??????????????? ?off-label? (?? ???? ??? ???????????? ??????????), ????? ??????? ??????? ??????? ???????????????. ??????? ?????? ???????????????, ???? ????? ? ???? 4 ??. ? ????? ?? ??????? ???????????? ???? ???????, ??? ?????????? ???????????????? ??????? ????? ??????????????? ??????? ? ?????????? ??????? ????? ?????????, ?? ?? ?????? ?? ?????????? ????????????? ??????? ??????.

    ??????? ?????? ???????? ??????? ??????? ???????????????? ???????: ???????????????? ??????? ? ????????? ? ???????????????? ????????? ?????????????. ?????? ????????????? ?????? ??????? ??? ????????? ? ????????????? ???????????????? ???????????? ??????????????.

    ??? ???????? ????????????? ?????????? ?????? ??????????? ???????? ????????, ? ?????? ???????, ??????????????????? (????? 40% ???????), ?????????. ????? ????, ???????????? ????????? ? ????????? ?????? ? ????????? ????????? ??????? ?????? ????? ? ????, ??? ??????? ? ???? ?????? ???????? ??????? ??????????? ???????????. ?? ?????????, ??? ?? ???????? ????? ??????????? ????? ????????????????? ?????????? ???????????????? ???????? ???????????????? ? ??????????? ???????????.

    ?????????? ? ???????????? ???????, ????????????? ? ????? ?????? ??? ???, ?????? ????? ??????? ??????? ?????????????? ??????? ??????????? ????????????.

    • ??? ?????? ????? ??? ????????? ????????? ??? ????????? ???????????? ??????????????, ?????? ??????? ?? ????????????? ??????? ?? ?????? ????, ??? ??? ?????? ??????????????? ?????????????? ??? ???????? ????????????????????? ??????? ???????? ??? ?????? ?????? ?????? ??? ????????. ??? ???? ????? ??? ????????? ????? ? ????????????? ???????.
    • ??? ???????? ????? ??? ??? ?????????? ???? ????? ???????????? ??????????????????? ???????? ???????????????? ? ???????????? ??????. ????? ??????? ????? ????????? ?? ?????????? ???????????????.
    • ????????????? ?????????????? ????? ????????????? ?????????? ? ?????? ?????????? ????????, ????????, ????????? ??????????????, ? ????????? ???????????? ???????? ???? ????? (????????????).

    ??????-???????? (???????? ?????? - 2 ??, ???????? ??????? ??????????????? ???? - 130 ??, ????????? ? - 100 ??, ??????? ? - 15 ??, ??????? A - 1100 ??, ?? ???-????? - 1.3 ??, ???? - 5 ??, ???? - 0.5 ??, ????? - 15 ??, ?? ???? - 50 ??).

    1 ???????? 1 ??? ? ???? (?? ???????? ????? ???? ????? ???? ????????? ?? 3 ???????? ? ????). ????????, ??? ???????? ???????? ?????-???????, ??? ?????? ????????? ???????????. ? ???????????????? ????? ??????????? ??????? ?? 2 ??? 2 ???? ? ???.

    ?????? ???? ????? (???????? ??????? ? ? 225 ??, ??????? ? - 36 ??, ?????-??????? ? 1,5 ??, ?????? ? 2,5??, ?????????? ? 0,5 ??, ???? (? ???? ???????? ????) - 1 ??, ???? (? ???? ?????? ?????) ? 5 ??) - ?? 1 ???????? 2 ???? ? ????. ???? ????????, ? ??????? ?? ??????, ??????????????? ? ????? ?????? ??? ??. ????????? ? ?????? ?????? ????????? ???????? ???????.

    ????? ???????, ??? ?????????, ?????????? ?????-???????, ?????? ????????? ??????????? ??-?? ????????? ?????????? ???????? ???? ?????.

    ????????? ??? ????????? ???????????? ??????????????:

    • ?????????? ?? 5 ?? 3 ???? ? ???? ??????, ??????? ?? 2 ???;
    • ?????????????? ?? 100 ?? 3 ???? ? ???? ??????, ??????? ?? 1 -2 ???;
    • ?????? ????????????? ??????? ???????? ?? 1 ???????? 3 ???? ? ???? ??????, ??????? ?? 2 ???.

    ????????????? ?????????:

    • ????????? ? ?????????? ??????? (????????, ????????? ?????) ?? 1 ???????? 2 ???? ? ???? ??????, ??????? ?? 2-3 ???;
    • ??????? ????????? Spirulina platensis ?? 2 ?????????? 3???? ? ???? ??????, ??????? ?? 1 ???.

    ????????? ??? ?????????? ???? ????????:

    • ???????????? ?? 0.5 ?? ? ???? ??????????????????? ???????? (10 ????????);
    • ???????????? ?? 250 ?? 1 ??? ? ???? ????? ?? ??????? ?? ??? 3 ???, ????? ????? ??????????? ???????? ???? ????? ?????????.

    ????????? ????????????? ? ??????????? ???????? ???? ????? (?????????) ? ???? ??????????????????? ???????? (5 ?? 1 ??? ? ?????, ? ?????????? 0,5 ?? 0,5% ???????? ??? 0,9% ???????? ?????? ???????, ???? 10 ????????).

    ????????????? ??????????????? ????? ???????????????? ???????. ??? ? ????????????? ????? ??????????? (???????), ??????????? ??????????????.

    ??????? (???????????) - ???????????? ????????, ??????????? ? ?????????? ? ?????? ??? ??????? ????????? ? ????????????? ?????????????????? (???).

    ????????? ? ??????????. ?????????? ??????????? ?????? ? ????????? ? ??????????????? ???????????? ????????????? ??? ??? ????????????? ??? ??? ?????????????? ??????.

    ?????? ?????????? ? ????. ??? ? ????????? - 2-????????? ???????. ? ??????? 10 ??? ??????????? ?????? ???????. ????? 15 ??? ????? ?????? ???????? ??????? ?????????? ????????????? ??????? (689 ??) ? ??????? 83 ?.

    ???????? ????????? ???????? ?? ???, ??? ?? ???????? ??????????????? (?? ???? ???????????? ???????? ????????????) ????????, ??? ????????? ???????? ??????? ???????? ????????? ????? 680 ? 695 ??. ??????????? ? ????????????? ?????, ??? ???????????? ???????? ?? ?????? ????????? ? ????? ????????? ? ?????????? ????????????? ?????????? ???????????????? ??????? ?????????????? ????????. ????????? ????? ????????????????? ???????????? ??? ?????? ???????? ?????? ? ?????? ????? 689 ??, ??? ????????? ???????? ??????? ???????? ????????? ????? ?????, ??????? ? ????????? ?????. ????? ???????, ???????? ???????????? ?????????????? ?? ?????-??????, ?? ????????? ?????????? ????? ???????????????? ???????????. ??? ????????? ??????????? ????????? ????????? ??????????? ?????????? ????????? ????????, ???????????? ????????? ???????????????? ???????, ??? ???????? ? ???????? ? ??????????? ??????? ?????????????? ?????????????????. ????????? ?????????? ???????? ? ????????? ???? ????? ?????????? ???, ????? ??????? ????????? ??????? ? ????????????? ?????????????.

    5-6 ??????? ???????????????? ??????? (?????? ???????? ?? ??? ??????????? ? ??????? 1-?? ???? ????? ?????? ???????). ?????? ????????? ?????? ? ??????????? ??? ???????? ?????? ????? 3 ???. ???? ???????? ????????????, ????????? ????????? ?????????????. ???? ?? ??????????????????? ??????? ? ????????? ??? ???????? ????????, ???????????? ???????????, ?? ??????? ???????????? ???????????? ???????????, ???????? ????????? ?????? ??? ????? 3 ???.

    ?????????? ?????????? ???????????? ????????, ??? ????? ??????? ????? ???? ????????????? ? ????????? ???????:

    • ??? ????????????? ???????????? ?????????????? ?????????????? ????????, ??? ??????? ?????? 0,1 ? ???? (????? ???????? ?????????? ?? ????? 20% ???? ???????, ?????????? ???);
    • ??? ???????????????? ???????????? ??? ??? ???????? ????????????? ???;
    • ??? ??????????????? ?????????, ????????????? ???, ??? ??? ?????????? ??????????????? ??????????? ??? ?? ???????? ????? ?????????? ????????????? ????;
    • ??? ???????? ??? ??? ???????? ????? ????? 4 ???????? ??? ???????????????? ???????: ?????? ??? ????? ?????? ??????? ?????? (????? ????, ???? ??????? ????? ????????? 5400 ???, ???????? ??????? ??????????, ??? ???? ??????? - ???????????? ?????????? ???????);
    • ??? ????????? ??????? ???????????????? ????????? ??? ? ??? ???????, ????? ??????? ?????? ??? ??????? ?????? ????? ?????? ???? ????????? (?? ???? ??????????? ???????? ?????????? ??? ??????????? ??????).

    3% ????????? ????? ?????????? ? ??????? ?????? ?????????? ??????? ??????? ?????? (? ??????? ?? 4 ?????? ??????? ETDRS).

    2 ??? ???????? ??????????? ?????? ????????? ????? ? ?????? ?????, ?????? ?????? ????.

    ? ????????? ????? ???????????????? ??????? ???? ????????? ? ??? ???????, ??? ????????? ???????????????? ???????? ?????????? ???????????.

    ?????????? ???????????????? ???????????? ???? ?????????? ? ?????? 90-? ????? ??? ??????? ??????? ?????????. ????? ??????? ?? ???????????????, ??? ??????? ??????? ???? ???????????? ????? ??????? (810 ??) ???????????? ? ????? ?????? ????? ?????? ??? ?????? ???????? ??????. ???????? ????????? ?????????????? ? ???????? ????????? ??? ? ?????????. ?????? ???????? ?????????????? ??????????? ??? ??????? ??? ??????? ???????. ????????, ??????????? ??????????? ??????????? ?? ????????????? ????????.

    ????????? ??? ?????????? ???????????????? ???????????? ? ??????? ??? ??? ??????? ?????????????? ?????????????? ???????? ? ??????????? ???????????? ???????????. ????? ???????, ???????????????? ???????????? ????? ????????? ? ??? ???????, ????? ? ??????? ??????????? ?? ???????? ?????????????? ??????? ?? ???????????????? ???????. ????? ????? ? ?????????? ? ???????????? ???????.

    ?????? ??? ????????????? ???????????????? ???????????? ???????? ?????? ??????????, ????????? ? ?????? ??????? ? ?????????????? ???????? ??????? (? ????? ??????????? ?????? ???? ????????????): ??????? ???????? ? ?????????? ????, ???????? ??????? ????????, ??????? ???, ?????????????? ????????????? ? ???????????? ????? ? ?????????. ???????? ????? ?????????, ???????????? ?????? ???????. ????????, ?????? ??????? ????? ?? ??????? ???????? ???????????????.

    ???????? ????????? ?????????? ?? ????? ? ????? ?????????????:

    • ?????????????? ????????????? (?? ???????????? ?? ????? ??????????, ?????????? ????????????? ????????);
    • ?????????? ??????? ???????? ?? ? ?????????:
    • ???????????? ??????????? ?????????:
    • ???????????? ?????????????? ????????;
    • ????????????? ??? ?????????????? ?????????????? ?????????????????.

    ????? ????????????? ????????? ????????? ?????????????, ???????????? ????? ?????????? ????????????? ????????, ??? ????? ????????????? ?????????? ??? ???????????? ????????? ??????. ???????? ?????????? - ?????????? ????????? ??????? ?????? ? ?????????? ????????????? (? ??????????? ??????? ??? ?? ????????? 0.1 ????? ?????????????).

    ??????????? ???????? ???????? ????????? ?????????????? ????????????? ??????????? ?? ????????? ????? ???????????????? ?????????. ? ?????? ???????????????? ???????? ??????????? ?? ????? ????????????? ??????? ????????????? ?????????????? ???????? ????????? ????????????. ??? ????????????? ???????? ????????????? ?? ?????????? ???? ?????????????? ???????? ????????? ?????????? ???????????? ??????? ??????????? ? ????????? ???? (??????????????????? ??????????) ? ??????? ??. ? ????????????????? ??????? ??????? ????????? ??????????? ????????? ????? ????.

    ????? ????, ??????? ? ??????????? ????? ???? ??????? ??? ????????? ????????????????? ????????????? ? ??, ????????? ?????????? ??????? ?????????????? ??????????.

    ? ????????? ????? ???????? ????????????????? ???????????? ?? ????????? ?????? ???, ?? ??? ???? ?????????????? ???? ???????? ??????? ???????? ?????????????.

    ????????? ????? ????????????? ????????????? ?? ???????????? ?????? . ???????? ???? ?????? ????????????? ??????? ? ???, ????? ???????? ????????????? ?????????? ???? ????????, ????????????? ??? ????????????? ?????????????? ?????????, ???, ????? ? ????? ????????? ??? ??? ?????????? ???????????? ??? ? ???????????????? ????. ??? ????? ??????? ????????? ???????????? ???????????, ? ????? ????????? ??? ???????? ?????????? ????????. ???????? ????? ???? ????????? ? ??????????? ??????????? ?? ???? ?????????? (360?) ? ??????????? ????????? ??? ????????? ????????, ? ????? ???? ???????????? ??????? (?? ???? ??????????) ??????. ????? ???????? ??????????? ? ????? ????????? ??? ?????? ??????????, ? ?????????????? ???????? ????????? ??? ?????? ???????????????. ?????????? ??????????????????, ????? ???? ??????? ?????? ????????? ??????????? ????????? ? ??????? ?????. ??? ?????????????? ?? ???????????? ?????? ???????? ????? ??? ??????????: ??????????????? ????????????????? (???) (? 19% ???????), ???????? ???????? (? 12-23%), ???????????? ??????????? ????????? (9%), ? ????? ??????????, ????????????? ??? ?????????? ??????????? ?? ?????? ??????????. ??? ???? ????? ????????? ?????? ?? ?????? ????????????, ?? ? ??????????????? ??????. ? ????????? ????? ???????? ?????????? ??? ???????? ?? ?????.

    1,5; 3 ? 6 ??? ? ??????? ?????????????, ? ????? ? ?? ???? 1 ???? ? 6 ???.

    ??? ????????? ?????? ???? ??????????? ?????? ????????????? ???????? ????????? ????????? ???????????? ??? ?????? ??????? ??????? ? ?????????? ? ???????????? ??? ????????? ????? ????? ?????????, ??? ??? ???? ??? ???? ?????????????? ??????? ?????? ???????? ??????.

    ??? ??????? ??? ??????? ?????? ?????? ????????? ??????????????? ?????? ????????? ????????, ??? ??? ???? ??? ??????? ?? ????????? ???????? ??????????????? ????????. ??????? ?????? ????????, ??? ???? ??????? ???????????? ????????? ?????? ??????, ? ??? ????? ? ??????? ??????, ? ?? ????????? ??????. ???????? ????? ?????????: ????????? ?????, ? ???? ?????????? ?????????????? ??????.

    ??????? ???????????, ??? ?????? ???????? ? ?????????? ??????? ???????????? ?????? ?? ????? ?????? ????? ?????????????? ??????????? ?? ?????? ? ????? ???????????? ????????????, ???????? ??? ????????????? ??????????????? ???????, ? ? ??? ?? ??? ??? ??????????? ??????? ???????? ?????.

    ??????? ? ?????? ???????? ?????? ????? ????????????? ??? ?????????? ???????? ?????? ????????????. ??? ??????????, ?????????? ????????? ????????????? ??????????? ? ??????????? ???????????? ????????. ????? ????? ????????? ????? ???? ??????? ??????????? ????????????? ????, ???? ? ?????????? ?????? ?????????, ????????????? ??????? ? ????????? ????????, ????????? ???????? ?????? ? ????????? ??????????? ?? ?????. ???????? ?????? ???????????? ???????? ????? ??? ??????? ? ?????? ???????? ?????? ????? ????.

    23 - 46% (? ??????????? ?? ??????????? ????????), ???????????????? ??????? ? ????????????? ? ? ??????? ?? 40%, ????????????? ???????? ? ?? 19% (?????????? ??????, ??? ??????? ??????????? ????????? ? ?????????? ???????????????? ??????????????? ????????, ??????? ????????? ????? ???????).

    ?????? ?? ?????: ?????????????. ???????????? ??????????? | ???????? ?.?.

    At the center of the retina is the macula, the light-sensitive element. Macular degeneration is a disease of the retina that occurs due to vascular pathology and disruption of their nutrition. Due to these reasons, central vision is damaged.

    Macular degeneration is considered an age-related disease, which most often causes blindness in people after 50 years of age.

    The disease code according to ICD-10 is H35/3 – degeneration of the macula and posterior pole.

    There are dry and wet forms of the disease. The division is based on the presence or absence of newly formed vessels in the eye.

    Dry form:

    Diagnosed in 90% of cases. It occurs due to age-related changes, during which the tissue becomes thinner and pigment is deposited in it.

    The disease goes through three stages. During the first, the patient has several drusen (yellowish deposits) of small size; the symptoms of the disease are not felt.

    At the second stage, the small drusen increase in size, in some cases a single large one is detected. A spot appears in the center of the visual field of the eye, which prevents a person from seeing well; he constantly feels a lack of light.

    At the third stage, the spot increases, reading and fine work are significantly more difficult.

    Wet form:

    It is characterized by the appearance of newly formed vessels in which hemorrhages occur. This damages light-sensitive cells. They die off over time and as a result, a person sees spots in the center of the field of vision.

    Due to the fragility of the newly formed vessels, the patient thinks that the lines are curved, although in fact they are straight. Fragile vessels act on the visual cells, creating an optical effect - distortion of the shape of objects.

    Consequences of micro-hemorrhages: due to the resulting fluid, retinal detachment occurs and scar tissue appears in this place, which leads to loss of vision.

    Characteristic symptoms depend on the stage of the disease.

    Main features:

    • there is a feeling of lack of lighting;
    • almost complete lack of vision in the twilight;
    • straight lines are refracted;
    • spots appear before the eyes;
    • Fragments fall out of the field of view when looking directly.

    Symptoms may appear in one or both eyes.

    Scientists have not been able to identify why degenerative changes in the retina develop. Based on numerous studies, we can only talk about factors contributing to the appearance and development of the disease:

    1. Older people are primarily affected; the risk of the disease increases significantly after 70 years of age;
    2. Poor lifestyle – dietary errors, drinking strong alcoholic drinks, smoking, lack of exercise;
    3. Hereditary factor - if your parents were sick, the risk almost doubles;
    4. Health problems - diabetes, atherosclerosis, heart attack, stroke, myopia.

    The cause of macular degeneration may be cytomegalovirus– an infectious disease caused by the herpes virus. A healthy person does not notice its presence, but it is dangerous for people with immunodeficiency.

    If macular degeneration is diagnosed, you can seek help from specialized medical institutions. The clinic named after Academician S.N. is considered one of the best. Fedorov “Eye Microsurgery” - it is recognized throughout the world as one of the leading centers in the field of ophthalmology. For many years, treatment at the Fedorov Clinic has been carried out using the most modern equipment and the latest technologies.

    Depending on some factors - the patient’s age, duration and form of the disease - conservative therapy does not always bring visible relief. In this case, surgical treatment is resorted to.

    Treatment methods for macular degeneration:

    1. Drugs Avastin, Lucentis, Makujden. They are injected intravitreally (inside the eye) to stop the growth of blood vessels. This procedure is done in a hospital setting using a thin needle. Course – 3 injections with a break of one month. A large number of patients experience improved vision.
    2. The drug Verteporfin is administered intravenously. Its action is activated by laser surgery. Photodynamic therapy improves visual function, but after some time the effect of the drug weakens and a repeat procedure is required.
    3. Laser coagulation of the retina - the laser acts on newly formed vessels and on the retina. Used for progressive forms of the disease. After such an operation, vision improvement does not occur.
    4. Agents that strengthen the walls of blood vessels: Vitamins E, A, group B.
    5. Drugs to reduce edema.

    At the current level of medical development, macular degeneration of the retina incurable. All measures are aimed at slowing down the process and improving the quality of life.

    When a person is helpless, his quality of life decreases. To be active and independent, you need to take care of your health, especially your eyes. An active lifestyle, feasible physical exercise, and giving up bad habits will help delay vision loss for many years.

    Video:

    9-06-2012, 06:46

    Description

    SYNONYMS

    Age-related macular degeneration, sclerotic macular degeneration, involutional central chorioretinal dystrophy, AMD, age-related maculopathy, age-related macular degeneration, age-related macular degeneration, etc.

    DEFINITION

    AMD- a progressive disease characterized by damage to the macular zone (the central zone of the retina and the posterior pole of the eyeball). AMD can lead to a marked decrease in visual acuity and loss of central parts of the visual field. The most significant functional impairments are characteristic of subretinal neovascularization followed by atrophy of the RPE, especially if the pathological process involves the central fovea (fovea).

    ICD-10 CODE

    H35.3 Degeneration of the macula and posterior pole.

    If it is necessary to identify the drug that caused the damage, use an additional code of external causes (class XX).

    EPIDEMIOLOGY

    AMD most often develops in patients over 65 years of age. The overall prevalence of the population increases with age: if the proportion of people with early manifestations of this pathology at the age of 65-74 years is 15%, then at the age of 75-84 years it is already 25%, and at the age of 85 years and older - 30%. Accordingly, the proportion of people with late manifestations of AMD aged 65-74 years is 1%; at the age of 75-84 years - 5%; aged 85 years and older - 13%. The predominant gender of patients is female, and in women over 75 years of age this pathology is noted 2 times more often. In Russia, the incidence of AMD is more than 15 per 1000 population.

    PREVENTION

    Patients with AMD are recommended stop smoking, fatty foods, and be less exposed to direct sunlight. If there is concomitant vascular pathology, measures aimed at its correction are necessary. Recommended vitamin therapy and treatment with microelements will be discussed below. The question of the advisability of preventive laser coagulation of the retina in the presence of multiple drusen has not yet been resolved.

    SCREENING

    No screening is carried out. However, in patients over 55 years of age, during routine medical examinations it is necessary to examine the macular zone of the retina, especially if there are characteristic complaints. If patients cannot achieve high visual acuity after uncomplicated cataract extraction, one must remember the likelihood of AMD.

    The examination includes determining visual acuity, biomicroscopy (to identify other possible causes of symptoms, for example, the presence of age-related cataracts), ophthalmoscopy (including a slit lamp using aspheric lenses) and perimetry. We can also recommend a study of color perception (monocularly), the Amsler test.

    CLASSIFICATION

    When defining the main clinical forms of AMD, the following terms are most often used in practical ophthalmology:

    • “dry” (or non-exudative or atrophic) form;
    • “wet” (or exudative or neovascular) form.
    For the “dry” form characterized primarily by slowly progressive atrophy of the RPE in the macular zone and the choroid located underneath it, which leads to local secondary atrophy of the photoreceptor layer of the retina. In addition, drusen are present in this zone (Fig. 31-49).

    

    Thus, The “dry” (non-exudative) form is characterized by:

    • drusen in the macular zone of the retina;
    • RPE defects;
    • redistribution of pigment;
    • atrophy of the RPE and choriocapillaris layer.
    Under the "wet" form As a rule, they understand the growth of newly formed vessels, originating in the inner layers of the choroid, through Bruch’s membrane into the resulting (normally absent) space between the pigment epithelium and the retina. Neovascularization is accompanied by exudation into the subretinal space, retinal edema and hemorrhages.

    The exudative form is characterized by the following stages:

    • exudative detachment of the RPE;
    • exudative detachment of the retinal neuroepithelium;
    • neovascularization (under the pigment epithelium and under the retinal neuroepithelium);
    • exudative-hemorrhagic detachment of the RPE and/or retinal neuroepithelium;
    • scarring stage.
    Sometimes there are early and late stages of AMD. This is argued by the fact that the terms “exudative form” and “non-exudative form” do not characterize the severity of the process: for example, both drusen and geographic atrophy can be classified as “dry” form.

    The early stage is characterized by:

    • local drusen;
    • uneven pigmentation of the RPE.
    The late stage is characterized by:
    • RPE detachment; RPE rupture;
    • disc-shaped (fibrovascular) scar;
    • geographic atrophy of the RPE.

    ETIOLOGY

    The etiology is not determined.

    PATHOGENESIS

    AMD- a chronic degenerative (dystrophic) process in the RPE, Bruch’s membrane and choriocapillaris layer (J.D.M. Gass, 1977). The RPE is involved in the metabolism of vitamin A, the synthesis of melanin, the production of basal and apical extracellular matrix, and the transport of various substances between photoreceptors. One of the most important functions of the RPE is its constant participation in phagocytosis and removal of thousands of discarded distal segments (discs) of photoreceptors. The breakdown products pass through Bruch's membrane and are removed by the choriocapillaris.

    All RPE cells accumulate lipofuscin with age in the form of round yellowish granules with a brown tint, surrounded by lipid membranes and possessing autofluorescence. Lipofuscin is considered a marker of aging; with age, it accumulates not only in the pigment epithelium, but also in other tissues.

    The retina is very sensitive to damage associated with oxidation processes, which is due to the constant high tissue demand for oxygen, the presence of polyunsaturated fatty acids, and exposure to light. The “yellow” macular pigment plays the role of natural sunglasses: it absorbs the short-wavelength part of blue light, thus participating in the antioxidant protection of the macula. This pigment, consisting of lutein and zeaxanthin, is located in the inner layers of the retina.

    During a cascade of biochemical processes under the influence of oxygen, free radicals are formed, which play an important role in the development of AMD. Lipid peroxidation leads to the formation of large molecular chains that are not recognized by the enzymes of pigment epithelial cells, do not disintegrate and accumulate with age, forming drusen.

    Besides, Bruch's membrane thickness increases with age, its permeability to blood serum proteins and lipids (phospholipids and neutral fats) decreases. Increased lipid deposits reduce the concentration of growth factors necessary to maintain normal choriocapillaris structure. The density of the choriocapillaris network decreases, and the supply of oxygen to RPE cells deteriorates. Such changes lead to increased production of growth factors and matrix metalloproteinases. Growth factors promote the growth of newly formed vessels, and metalloproteinases cause defects in Bruch's membrane.

    Thus, AMD begins with the “dry” form, that is, with changes in the RPE and with the appearance of hard drusen. On later stage soft drusen appear, then they turn into confluent drusen. Progressive damage to the pigment epithelium leads to atrophic changes in the retinal neuroepithelium and choriocapillaris. When defects appear in Bruch's membrane, CNV spreads under the pigment epithelium and neurosensory retina. As a rule, this is accompanied by retinal edema, fluid accumulation in the subretinal space, subretinal hemorrhages and hemorrhages into the retinal tissue. Sometimes a breakthrough hemorrhage occurs in the CT. The final stage of the development of the process is the formation of a subretinal disc-shaped fibrous scar in the central part of the retina and a significant loss of visual functions.

    CLINICAL PICTURE

    Clinical manifestations of AMD:

    • hard drusen;
    • soft drusen;
    • strengthening or weakening of RPE pigmentation:
    • atrophic lesions in the macula (geographic atrophy);
    • choroidal neovascularization;
    • serous or hemorrhagic detachment of the RPE;
    • scar lesions in the macular area.

    Druze

    Druze- extracellular deposits of eosinophilic material between the inner collagen layer of Bruch's membrane and the basement membrane of the RPE. The material of drusen is the products of metabolism of RPE cells. The presence of drusen indicates the likelihood of developing more severe macular degeneration. As a rule, patients who do not have other manifestations of this pathology do not notice a deterioration in central vision. Drusen are divided into hard, soft and confluent (Fig. 31-49).

    

    Hard drusen visible in the fundus as small, clearly defined patches of yellowish color; their diameter usually does not exceed 50 microns. Biomicroscopy reveals the hyaline structure of drusen. With FA, characteristic early hyperfluorescence is detected, drusen are filled simultaneously, and the fluorescence stops late. There is no sweating from the druzes. They are considered a relatively benign manifestation of the process, however, if we consider the possibility of disease progression over a period of up to 10 years, the presence of a large number of hard drusen (>8) may predispose to the appearance of soft drusen and more severe manifestations of macular degeneration.
    
    Soft drusen They are large in size and usually have unclear boundaries. They have a granular structure that can be detected histologically. With FA, early accumulation of fluorescein is determined in the absence of sweating, but they can also be hypofluorescent due to the accumulation of lipids and neutral fats. The risk of disease progression to an advanced stage is significantly higher. Soft drusen may coalesce and cause detachment of the RPE.

    Drain druses can lead to detachment of the RPE; to atrophic changes in the retina or to the development of subretinal neovascularization.

    In dynamics, drusen may undergo the following changes:

    • hard drusen can increase in size and turn into soft ones;
    • soft drusen can also enlarge and form confluent drusen, which can lead to detachment of the RPE;
    • calcifications can form inside the drusen, which look like shiny crystals during ophthalmoscopy;
    • Spontaneous regression of drusen is also possible, although most often they tend to progress.

    Redistribution of pigment in the macula

    The appearance of areas of hyperpigmentation is associated with changes occurring in the RPE: proliferation of cells in this layer, accumulation of melanin in them or migration of melanin-containing cells into the subretinal space. Focal hyperpigmentation is considered one of the factors predisposing to the appearance of subretinal neovascularization.

    Localized hypopigmentation often corresponds to the location of the drusen, as the RPE layer overlying them becomes thinner. However, local hypopigmentation can also be determined by atrophy of RPE cells, independent of drusen, or a decrease in the content of melanin in cells.

    Geographic atrophy of the retinal pigment epithelium

    Geographic atrophy of the RPE- an advanced form of dry AMD. Foci of geographic atrophy are detected in the fundus in the form of clearly defined zones of depigmentation with clearly visible large choroidal vessels. With geographic atrophy, not only the RPE is affected, but also the outer layers of the retina and the choriocapillaris layer in this area. With FA, atrophy zones form a “window” type defect. Already in the early phase, choroidal fluorescence is clearly visible, since there is no pigment in the corresponding zones of the pigment epithelium. Fluorescein does not accumulate and does not extend beyond the edges of the atrophic lesion. Geographic atrophy can be not only an independent manifestation of AMD, but also a consequence of the disappearance of soft drusen, flattening of the focus of RPE detachment, and can even occur as a result of regression of the CNV focus.

    Serous (exudative) detachment of the retinal pigment epithelium

    Serous detachment of the RPE- accumulation of fluid between Bruch's membrane and the RPE. Most often, detachment is detected in the presence of drusen and other manifestations of AMD (including CNV). The size of the detachment may vary. In contrast to serous detachment of the sensory retina, RPE detachment is a rounded dome-shaped local formation with clear contours. Visual acuity may remain quite high, but there is a shift in refraction towards gynermetropia. In FA, abruption is characterized by rapid and uniform accumulation of fluorescein, usually occurring in the early (arterial) phase. The dye is retained in the lesions during the late phases and during the recirculation phase, and there is no leakage into the surrounding retina.

    Serous detachment of the neuroepithelium is often combined with detachment of the pigment epithelium. At the same time, a greater prominence of the lesion, which has a disc-shaped shape and less clear boundaries, is noted.

    During the development of the pathological process, a flattening of the lesion may occur with the formation of local atrophy of the RPE or rupture of the RPE with the formation of a subretinal neovascular membrane.

    Hemorrhagic detachment of the pigment epithelium or neuroepithelium

    Hemorrhagic detachment of the pigment epithelium or neuroepithelium is usually a manifestation of CNV. It can be combined with serous detachment.

    Choroidal (subretinal) neovascularization

    It is typical for CNV ingrowth of newly formed vessels through defects in Bruch’s membrane under the RPE or under the neuroepithelium. Pathological permeability of newly formed vessels leads to fluid sweating, its accumulation in the subretinal spaces and the formation of retinal edema. Neovascularization can lead to the appearance of subretinal hemorrhages, hemorrhages into the retinal tissue, sometimes breaking into the CT. This may cause significant functional impairment.

    Risk factors for the development of subretinal neovascularization are:

    • confluent soft drusen;
    • areas of hyperpigmentation;
    • the presence of extrafoveal geographic atrophy of the RPE.
    The following ophthalmoscopic manifestations should raise suspicion of the presence of subretinal neovascularization:
    • retinal edema in the macular area:
    • RPE detachment;
    • accumulation of pigment in the form of a ring or plaque;
    • subretinal hemorrhages and/or hemorrhages into the retinal tissue:
    • presence of hard exudates.
    Hemorrhages may be small. Hard exudates are rare and usually indicate that the subretinal neovascularization is relatively old.

    CNV, based on FA data, is divided into:

    • classical;
    • hidden:
    • mixed.
    Classic CNV found in approximately 20% of patients. Typically, a pigmented or reddish structure beneath the RPE is clinically detected, and subretinal hemorrhages are common. With FA, the newly formed subretinal vessels fill earlier than the retinal vessels (in the prearterial phase). These vessels quickly begin to glow brightly and look like a network in the form of lace or a cart wheel. Hemorrhages, if present, may partially mask subretinal neovascularization. Sweating of fluorescein from newly formed vessels may be observed, increasing as the study progresses. In late phases of FA, the dye usually accumulates within the serous retinal detachment located above the choroidal neovascular membrane.

    Hidden CNV suspected when ophthalmoscopy reveals focal dispersion of pigment with simultaneous thickening of the retina, which does not have clear boundaries. Gradually, 2-5 minutes after fluorescein injection, “speckled” fluorescence becomes visible. The degree of hyperfluorescence increases with the addition of sweating; even accumulations of dye in the subretinal space are noted that do not have clear boundaries. Repeated assessment of the same area in the early phases of FA does not allow finding the source of sweating.

    Mixed CNV in recent studies they are divided into:
    
    
    When choosing a treatment method, it is necessary to apply a classification of CNV based on the type of location of CNV in the macular zone:

    • subfoveal- the choroidal neovascular membrane is located under the center of the foveal avascular zone;
    • juxtafoveal- the edge of the choroidal neovascular membrane, the zone of fluorescence blockade by pigment and/or hemorrhage, is within 1-199 μm from the center of the foveal avascular zone;
    • extrafoveal- the edge of the choroidal neovascular membrane, the area of ​​fluorescence blockade by pigment and/or hemorrhage, is located 200 μm or more from the center of the foveal avascular zone.

    Formation of a disc-shaped scar

    Disc scar- the final stage of development of subretinal neovascularization. Ophthalmoscopically in such cases, a disc-shaped lesion of gray-white color is determined, often with pigment deposition (Fig. 31-51). The size and location of the lesion are of fundamental importance for the preservation of visual functions.

    

    DIAGNOSTICS

    Anamnesis

    When collecting anamnesis, it is necessary to consider:

    • patient complaints of decreased visual acuity, difficulty reading, especially in low light conditions: sometimes patients notice the loss of individual letters when reading fluently, metamorphopsia;
    • duration of symptoms;
    • unilateral or bilateral nature of the lesion;
    • the presence of concomitant pathology of the cardiovascular system (in particular, arterial hypertension, atherosclerotic vascular lesions), lipid metabolism disorders, diabetes, excess body weight;
    • smoking;
    • heredity.
    It is advisable to evaluate the impact of visual impairment on the patient’s quality of life.

    Physical examination

    Physical examination includes:

    • Determination of visual acuity with optimal correction:
    • Amsler test;
    • assessment of color perception using the Yustova or Rabkin tables (monocular);
    • biomicroscopy (to identify other possible causes of symptoms, for example, age-related cataracts);
    • biomicroscopy of the retina using aspherical lenses 60 and/or 90D, as well as Gruby lenses and various CLs (Goldmann lenses, Meinster lenses, etc.), after pupil dilation with short-acting mydriatics.

    Laboratory research

    Instrumental studies

    For assessment of the functional state of the organ of vision use:

    • perimetry, especially computer static perimetry, in particular macular test and determination of foveal sensitivity (in case of low visual acuity, conventional kinetic perimetry is used, with an appropriate choice of the size and brightness of the object);
    • electrophysiological studies (ganzfeld ERG, rhythmic ERG, pattern ERG, macular ERG, multifocal ERG).
    For identifying and documenting anatomical changes in the macula The following methods are used.
    
    

    Differential diagnosis

    In the “dry” form of AMD, differential diagnosis is carried out with:

    • peripherally located drusen;
    • degeneration with high complicated myopia (with it, in addition to changes in the macula, characteristic atrophic changes around the optic disc are noted, but drusen are absent; a pronounced refractive error is observed).
    In the “wet” form of AMD, differential diagnosis is carried out with:
    • high complicated myopia (significant refractive error, varnish cracks in the posterior pole, myopic changes in the optic disc);
    • traumatic retinal rupture (usually in one eye; a history of eye trauma, most often the rupture occurs concentrically with the optic disc);
    • angioid stripes, when in both eyes curved lines of red-brown or gray color diverge subretinal from the optic disc;
    • syndrome of presumed ocular histoplasmosis, when small yellowish-white chorioretinal scars are detected in the middle periphery and in the posterior pole of the retina, as well as foci of scarring in the optic disc;
    • drusen optic nerve disc;
    • choroidal tumors;
    • scar areas after laser coagulation;
    • inflammatory chorioretinal pathology.

    Indications for consultation with other specialists

    • cardiologist/therapist- in the presence of arterial hypertension and other diseases of the cardiovascular system;
    • neurologist- in the presence of severe cerebral atherosclerosis;
    • endocrinologist- in the presence of uncompensated diabetes.

    An example of a diagnosis formulation

    Right eye- age-related macular degeneration, “wet” form (classical subretinal neovascularization).

    Left eye- age-related macular degeneration, “dry” form.

    TREATMENT

    Treatment Goals

    • Achieving stabilization of the pathological process, rather than improving vision, in the presence of choroidal neovascular membranes.
    • Prevention of complications (in the “dry” form - the appearance of subretinal neovascularization, in the “wet” form - the occurrence of hemorrhages of various localizations, increased retinal edema, etc.).
    • Prevention of severe vision loss leading to disability.
    • Preservation of visual acuity, allowing the patient to care for himself independently - in case of advanced pathology.

    Indications for hospitalization

    In the vast majority of cases, patients with AMD can be evaluated and treated on an outpatient basis. In those countries where the intravitreal use of angiogenesis inhibitors is permitted, injections into the CT are also performed on patients without hospitalization (of course, such an injection is performed under aseptic and antiseptic conditions).

    Drug treatment

    General principles

    In the “dry” form In order to prevent the progression of the disease, it is recommended to take biologically active food supplements containing vitamins, lutein, and zinc.

    In “wet” form intravitreal administration of angiogenesis inhibitor drugs is possible. The main advantage of this approach is that these drugs are effective against all types of subretinal neovascular membranes. Accordingly, a decision on intervention can be made even without a preliminary angiographic study. Currently, there are no registered drugs from this group in our country; the drugs pegaptanib (Macugen) and ranibizumab (Lucentis) are being prepared for registration. In some countries, these drugs are already used to treat patients with retinal neovascularization.

    Pegaptanib (Macugen)- a small RNA-like molecule with high affinity for the vascular endothelial growth factor VEGF (vascular endothelial growth factor). By selectively binding isoform 165 of this growth factor, pegaptanib prevents the growth of newly formed vessels and increased permeability of the vascular wall - two main manifestations of the exudative form of AMD. The drug is intended for intravitreal administration. The results of one clinical trial show that there is probably no significant loss of visual acuity during treatment with pegaptanib, compared with the control group. In this study, pegaptanib was administered intraviterally at various doses (0.3, 1.0, and 3.0 mg) every 6 weeks for 54 weeks; the effect of stabilizing visual acuity was achieved in a large percentage of cases even with the minimum dose used.

    For the same purpose - to inhibit angiogenesis - another drug is used - ranibizumab (Lucentis). Ranibizumab is a monoclonal antibody that blocks all isoforms of the growth factor VEGF. Intravitreal injections of the drug are performed once every 4 weeks. In randomized clinical trials (ANCHOR and MARINA), ranibizumab was administered intravitreally at a dose of 0.3 and 0.5 mg. In most cases, not only stabilization was noted, but also some improvement in visual acuity.

    In addition, in world ophthalmology there is a tendency to prefer a cheaper drug related to ranibizumab - bevacizumab (Avastin). This antibody with anti-VEGF activity was initially used intravenously for the treatment of colorectal cancer. Currently, in addition to debates about the ethics of treating patients with a drug that was not developed for the treatment of ophthalmopathology, various attempts are being made to compare the effectiveness and safety of ranibizumab and bevacizumab.

    Another direction of treatment using blockade of angiogenesis continues to develop - intravitreal administration of crystalline glucocorticoids. Currently, triamcinolone injections (kenalog-40) have begun to be used quite actively. Despite the fact that throughout the world this drug is used intravitreally “off-label” (that is, without official approval), such treatment has become widespread. The drug is administered intravitreally, most often in a dose of 4 mg. One pilot study showed that a single intravitreal injection of this glucocorticoid led to a reduction in lesion size but did not affect the likelihood of significant vision loss.

    Much more attention today given to combined treatment: photodynamic therapy in combination with intravitreal administration of triamcinolone. However, the effectiveness of such treatment still needs to be confirmed by appropriate clinical studies.

    When triamcinolone is administered, the likelihood of side effects is quite high, primarily ocular hypertension (about 40% of cases) and cataracts. In addition, the relatively low and temporary effect in improving visual acuity has led to the fact that today more attention is paid to angiogenesis inhibitors in the world. It is possible that over time, schemes for the sequential use of intravitreal injections of glucocorticoids and angiogenesis inhibitors will be developed.

    There is also traditional therapy used in our country for AMD, but such treatment requires additional large clinical studies.

    • In the “dry” form of AMD, drugs are used to improve regional blood circulation, but today their use fades into the background, since many authors question the theory of circulatory failure as the main etiopathogenetic factor in the development of AMD. In this form of AMD, stimulant therapy is also used.
    • In the “wet” form of AMD, subconjunctival injections of glucocorticoids and oral acetazolamide can be used to reduce swelling. This treatment can be used before laser coagulation.
    • The use of drugs with a different mechanism of action, for example, peptide bioregulators, and in particular polypeptides from the retina of livestock eyes (retinalamine), also seems promising.

    Biologically active food additives

    Okuwait Lutein(contains lutein - 6 mg, zeaxanthin - 0.5 mg, vitamin C - 60 mg, vitamin E - 8.8 mg, selenium - 20 mcg, zinc - 5 mg) 1 tablet 2 times a day. For preventive purposes, they are used in courses of 2 months, 2 times a year. This is the only drug whose effectiveness in the early stages of AMD to prevent progression of the process has been confirmed by extensive multicenter studies.

    Lutein complex(contains lutein - 2 mg, standardized blueberry extract - 130 mg, vitamin C - 100 mg, vitamin E - 15 mg, vitamin A - 1100 IU, beta-carotene - 1.3 mg, zinc - 5 mg, copper - 0. 5 mg, selenium - 15 mg, taurine - 50 mg).

    The usual prophylactic dose is 1 tablet 1 time per day (as directed by the doctor, the dose can be increased to 3 tablets per day). Considering that the drug contains beta-carotene, it should not be prescribed to smokers. For preventive purposes, it is used in courses of 2 months, 2 times a year.

    Vitrum Vision forte(contains vitamin C - 225 mg, vitamin E - 36 mg, beta-carotene - 1.5 mg, lutein - 2.5 mg, zeaxanthin - 0.5 mg, copper (in the form of copper sulfate) - 1 mg, zinc (in form of zinc oxide) - 5 mg) - 1 tablet 2 times a day. This drug, unlike others, is registered in our country as a drug. Many other drugs of similar composition are also used.

    It is important to remember that drugs containing beta-carotene should not be prescribed to smokers due to the risk of stimulating the development of lung cancer.

    Drugs to improve regional blood circulation:

    • vinpocetine 5 mg 3 times a day orally, in courses of 2 months;
    • pentoxifylline 100 mg 3 times a day orally, in courses of 1-2 months;
    • ginkgo biloba leaf extract 1 tablet 3 times a day orally, in courses of 2 months.
    Stimulant drugs:
    • preparations with blueberry extract (for example, myrtilene forte) 1 tablet 2 times a day orally, in courses of 2-3 weeks;
    • Spirulina platensis algae extract, 2 tablets 3 times a day orally, in courses of 1 month.
    Drugs to reduce retinal edema:
    • dexamethasone 0.5 ml in the form of subconjunctival injections (10 injections);
    • acetezolamide 250 mg 1 time per day in the morning half an hour before meals for 3 days, then after a three-day break the course can be repeated.
    Peptide bioregulators- polypeptides of the retina of livestock eyes (retinamine) in the form of subconjunctival injections (5 mg 1 time per day, diluted with 0.5 ml of 0.5% procaine or 0.9% sodium chloride solution, course of 10 injections).

    Laser treatment

    Purpose of laser treatment- reduce the risk of further vision deterioration. The subretinal neovascular membrane within the affected tissues is completely destroyed by coagulation with argon green or cryptopine red (wavelength 647 nm) lasers. The Macular Photocoagulation Study (MPS) showed that laser treatment significantly reduced the risk of significant visual loss in patients with extrafoveal and juxtafoveolar CNV.

    Photodynamic therapy has become an alternative to laser coagulation. When using it, they take vertenorphine (visudine), a derivative of benzoporphyrin.

    Visudin (vertenorphine) is the only drug approved for use in Russia for the treatment of patients with choroidal neovascularization (CNV).

    Indications for use. Age-related macular degeneration in patients with predominantly classic subfoveal CNV or subfoveal CNV with pathological myopia.

    Method of administration and dose. PDT with Visudin is a 2-stage process. Visudin is administered intravenously over 10 minutes. 15 minutes after the start of the injection, Visudin is activated with a non-thermal laser (689 nm) for 83 s.

    Effect of the drug based on the fact that it contains a photosensitive (that is, light-activated) substance whose light energy absorption peak is between 680 and 695 nm. Verteporfin is a liposomal form; when administered intravenously, it quickly reaches the lesion and is selectively captured by the endothelium of newly formed vessels of the neovascular membrane. Irradiation of the focus of neovascularization is carried out using a diode laser with a wavelength of 689 nm, which allows laser energy to freely pass through blood, melanin and fibrous tissue. Thus, it is possible to selectively target target tissue without adversely affecting surrounding tissue. Under the influence of non-thermal laser radiation, verteporfin generates free radicals that damage the endothelium of newly formed vessels, which leads to thrombosis and obliteration of subretinal neovascularization vessels. The procedure must be carried out within a week after performing FA, after which a decision is made on the need for intervention.

    Since recanalization can often occur after vascular occlusion, on average, patients required 5-6 sessions of photodynamic therapy (more than half of them were performed within 1 year after the start of treatment). The first re-examination with FA is usually carried out after 3 months. If sweating is detected, repeat intervention is performed. If the ophthalmoscopic picture and the result of FA remain the same, there is no sweating, then you should limit yourself to dynamic observation, scheduling a re-examination after another 3 months.

    The results of the studies showed that such treatment can be recommended in the following cases:

    • with subfoveal classic subretinal neovascular membrane, with visual acuity of 0.1 or higher (such patients account for no more than 20% of all patients suffering from AMD);
    • with “predominantly classic” or “hidden” subfoveal CNV;
    • with a juxtafoveal lesion located so that when performing laser coagulation the center of the foveal avascular zone would necessarily be affected;
    • for “hidden” CNV with a lesion size greater than 4 areas of the optic disc, photodynamic therapy: only with very low visual acuity (in addition, if the diameter of the lesion exceeds 5400 µm, the patient should be explained that the goal of treatment is to stabilize visual functions);
    • when rapid progression of the lesion is expected or in cases where visual acuity without treatment may soon fall below “useful” (that is, allowing the patient to do without assistance).
    However, approximately 3% of patients experience a decrease in visual acuity within a week after exposure (an average of 4 ETDRS lines).

    In order to reduce the risk of phototoxic reactions, patients are advised to avoid exposure to direct sunlight and bright light for 2 days and wear dark glasses.

    Recently, photodynamic therapy has been used less frequently in countries where intravitreal administration of an angiogenesis inhibitor is permitted.

    Application transpupillary thermotherapy was proposed in the early 90s for the treatment of choroidal melanomas. The method is based on laser coagulation, in which wave energy in the infrared part of the spectrum (810 nm) is delivered to the target tissue through the pupil using a diode laser. Thermal radiation is perceived mainly by the melanin of the RPE and choroid. The exact mechanism of the beneficial effects in the treatment of AMD remains unclear. Perhaps there is a certain effect on choroidal blood flow.

    The indication for transpupillary thermotherapy is occult CNV or occult subretinal neovascular membranes with a minimal classical component. Thus, transpupillary thermotherapy can be used in cases where patients experience virtually no positive effect from photodynamic therapy. The method is easy to use and relatively inexpensive.

    However, when using transpupillary thermotherapy, frequent complications are noted, primarily associated with an overdose of laser energy (normally, the effect should be subthreshold): infarctions in the macular zone, occlusion of retinal vessels, ruptures of the RPE, subretinal hemorrhages and atrophic foci in the choroid are described. Cataracts and the formation of posterior synechiae were also noted. Perhaps this is why the method has not become widespread.

    Surgery

    Removal of subretinal neovascular membranes

    First, vitrectomy is performed according to the standard technique, then retinotomy is performed paramacularly, from the temporal side. A balanced saline solution is injected through the retinotomy hole to detach the retina. After this, the membrane is mobilized using a horizontally curved peak, and the membrane is removed by inserting horizontally curved tweezers through the retinotomy. The resulting bleeding is stopped by lifting the bottle with infusion solution and thereby increasing the IOP. The liquid is partially replaced with air. In the postoperative period, the patient must maintain a forced position face down until the air bubble is completely resolved.

    The main possible complications during and after the intervention:

    • subretinal hemorrhage (from minimal to more massive, requiring mechanical removal);
    • Iatrogenic retinal tears in its periphery:
    • Macular hole formation:
    • formation of the preretinal membrane;
    • unresolved or recurrent subretinal neovascularization.
    Such interventions can reduce metamorphopsia and provide more constant eccentric fixation, which is often regarded by patients as a subjective improvement in vision. The main disadvantage is the lack of improvement in visual acuity as a result of the intervention (in most cases it does not exceed 0.1 after the intervention).

    Methods have been developed for the removal of massive subretinal hemorrhages through their evacuation through retinotomy holes. In case of formed clots, it is recommended to administer subretinal recombinant tissue plasminogen activator during the intervention. If it is necessary to shift hemorrhages from the macular zone, subretinal administration of tissue plasminogen activator is successfully combined with the introduction of gas (perfluoroorganic compound) into the CT cavity. In the postoperative period, the patient maintains a forced position face down.

    In addition, the decision to perform vitrectomy can be made in case of massive non-resorbable hemorrhage in the CT resulting from breakthrough of subretinal hemorrhage.

    Currently, experimental studies are being carried out on transplantation of RPE cells, but issues of tissue compatibility still remain unresolved.

    Also perform surgical interventions for macular translocation. The main idea of ​​such an intervention is to displace the neuroepithelium of the foveal retina, located above the choroidal neovascular membrane, so that the unchanged RPE and choriocapillaris layer are located under it in a new position. To do this, first perform a subtotal vitrectomy, and then completely or partially detach the retina. The operation can be performed by performing a retinotomy along the entire circumference (360°), followed by rotation or displacement of the retina, as well as by forming folds (i.e. shortening) of the sclera. The retina is then “fixed” in its new position using an endolaser, and the neovascular membrane is destroyed using laser coagulation. Pneumoretinopexy is performed, after which the patient must remain in a forced position for 24 hours. During interventions for macular translocation, a number of complications are possible: proliferative vitreoretinopathy (PVR) (in 19% of cases), retinal detachment (in 12-23%), formation of a macular hole (9%), as well as complications encountered during vitrectomy for other types of surgery. indications. In this case, loss of not only central but also peripheral vision may occur. Currently, this technique has not found wide application.

    Approximate periods of incapacity for work

    The duration of incapacity for work is determined by the severity of the process. In some cases, the issue of the visual disability group should be addressed.

    Further management

    After the intervention, patients are advised to monitor their condition daily using an Amsler grid and, if any new symptoms appear, to consult an ophthalmologist. For early detection of persistent or recurrent subretinal neovascular membranes, control FA is performed within the time limits established by the relevant protocols. After this, inspections continue after 1.5; 3 and 6 months from the moment of intervention, and then at least once every 6 months.

    The patient should be advised to lead a healthy lifestyle. Quitting smoking, a diet rich in vitamins and microelements, and limiting the consumption of fatty foods are especially important. Excessive sun exposure should be avoided; it is recommended to wear dark glasses. The patient should be advised of the need to take dietary supplements with antioxidant vitamins, lutein and zinc.

    If soft drusen are detected, the ophthalmologist should recommend that the patient perform daily self-monitoring using the Amsler grid and contact an ophthalmologist if any new symptoms appear, since this type of drusen is accompanied by a high risk of vision loss.

    In the presence of CNV, the patient must strictly adhere to the recommended schedule of repeated examinations, since even with treatment, relapses of the pathological process are not excluded. The patient must understand that the goal of treatment is to stabilize the state of the visual organ, including visual acuity, and not to improve vision. The patient needs to be explained: most likely, he will retain peripheral vision.

    It should be emphasized that many patients with severe central vision loss in both eyes can independently cope with many of their daily activities, especially with the use of assistive devices, and still have a good quality of life.

    Sick with low visual acuity We can recommend so-called aids for the visually impaired. These are devices that magnify images in various ways and enhance the illumination of objects. Among such devices can be named special magnifying glasses, magnifying glasses with various types of mounting, closed-circuit television systems, various digital cameras with image projection on the screen. Low vision aids are especially important for patients with low visual acuity in both eyes.

    FORECAST

    If there are manifestations of late-stage AMD in one eye, the risk of minor pathological changes in the other eye is, according to various estimates, from 4 to 15%. Moreover, in approximately 1/4 of such patients, visual acuity in the absence of treatment may decrease to hundredths over the next 12 months.

    According to various data, laser coagulation and transpupillary thermotherapy can reduce the number of cases of severe vision loss to 23 - 46% (depending on the localization of the process), photodynamic therapy with verteporfin - on average up to 40%, submacular surgery - up to 19% (it must be taken into account that the treatment was applied to patients with different characteristics of the pathological process, so the comparison is very conditional).

    Article from the book: .

    Angioid stripes of the macula

    Drusen (degenerative) macula

    Age-related macular degeneration (atrophic) (exudative)

    Retinal degeneration:

    • lattice
    • microcystic
    • palisade
    • resembling a cobblestone street in appearance
    • reticular

    Excludes: with retinal tear (H33.3)

    Dystrophy:

    • retinal (albipunctate) (pigmented) (yolk-like)
    • taperetinal
    • vitreoretinal

    Central serous chorioretinopathy

    Detachment of the retinal pigment epithelium

    In Russia, the International Classification of Diseases, 10th revision (ICD-10) has been adopted as a single normative document for recording morbidity, reasons for the population's visits to medical institutions of all departments, and causes of death.

    ICD-10 was introduced into healthcare practice throughout the Russian Federation in 1999 by order of the Russian Ministry of Health dated May 27, 1997. No. 170

    The release of a new revision (ICD-11) is planned by WHO in 2017-2018.

    With changes and additions from WHO.

    Processing and translation of changes © mkb-10.com

    Retinal diseases - classification according to ICD-10 (codes)

    According to the ICD, there are several categories of retinal diseases.

    Chorioretinal inflammation (H30)

    Chorioretinal inflammation includes the following specific nosologies:

    • Focal chorioretinal inflammation (H30.0);
    • Disseminated chorioretinal inflammation (H30.1);
    • Posterior cyclitis (H30.2);
    • Chorioretinal inflammation of other etiology (H30.8);
    • Unspecified type of chorioretinal inflammation (H30.9).

    Diseases of the choroid of the eyeball, not included in other sections (H31)

    This section of the ICD includes:

    • Chorioretinal scars (H31.0);
    • Degenerative changes in the choroid (H31.1);
    • Dystrophic processes in the choroid of a hereditary nature (H31.2);
    • Ruptures of the choroid, hemorrhages in this area of ​​the eye (H31.3);
    • Choroidal detachment (H31.4);
    • Other pathologies of the choroid (H31.8);
    • Unspecified diseases of the choroid (H31.9).

    Secondary chorioretinal changes (H32)

    Such pathologies include:

    This pathology combines:

    • Retinal detachment accompanied by a rupture (H33.0);
    • Retinal cysts, retinoschisis (H33.1);
    • Serous retinal detachment (H33.2);
    • Retinal tear not accompanied by detachment (H33.3);
    • Ordinary retinal detachment (H33.4);
    • Other forms of retinal detachment (H33.5).

    Retinal vascular occlusion (H34)

    Occlusion of retinal vessels can be of the following types:

    • Transient occlusion of the retinal arteries (H34.0);
    • Central retinal artery occlusion (H34.1);
    • Occlusion of other retinal arteries (H34.2);
    • Other types of retinal vascular occlusions (H34.8);
    • Unspecified type of retinal vascular occlusion (H34.9).

    Other retinal pathologies (H35)

    Other retinal diseases include:

    • Background retinopathy or retinal vascular pathologies (H35.0);
    • Preretinopathy (H35.1);
    • The remaining pretinopathy is of the proliferative type (H35.2);
    • Degenerative changes in the macula or posterior pole (H35.3);
    • Degeneration of the peripheral retina (H35.4);
    • Hereditary retinal dystrophy (H35.5);
    • Hemorrhage into the retinal substance (H35.6);
    • Splitting of cell layers in the retina (H35.7);
    • Other specified disorders of the retina (H35.8);
    • Unspecified diseases of the retina (H35.9).

    Secondary retinal lesions (H36)

    Retinal diseases can occur with other pathologies:

    • Diabetic retinopathy (H36.0);
    • Other disorders in the retina (H36.8).

    Eye diseases. Classification according to ICD-10.

    H00-H59 DISEASES OF THE EYE AND ITS ACCIDENTAL APPARATUS

    diseases of the endocrine system, nutritional disorders and metabolic disorders (E00-E90),

    congenital anomalies, deformations and chromosomal disorders (Q00-Q99),

    neoplasms (C00-D48), complications of pregnancy, childbirth and the postpartum period (O00-O99),

    certain conditions arising in the perinatal period (P00-P96),

    symptoms, signs and abnormalities identified during clinical and laboratory tests, not classified elsewhere (R00-R99),

    injuries, poisoning and some other consequences of external causes (S00-T98)

    H00.0 Hordeolum and other deep inflammations of the eyelids

    H01 Other inflammations of the eyelids

    Excludes: blepharoconjunctivitis (H10.5)

    H01.1 Non-infectious dermatoses of the eyelid

    H01.8 Other specified inflammations of the eyelid

    H01.9 Inflammation of eyelid, unspecified

    H02 Other eyelid diseases

    Excludes: congenital malformations of the eyelid (Q10.0-Q10.3)

    H02.0 Entropion and trichiasis of the eyelid

    H02.1 Ectropion of the century

    H02.5 Other diseases affecting the function of the eyelid

    Excludes: blepharospasm (G24.5), tic (psychogenic) (F95.-)

    H02.6 Xanthelasma of the eyelid

    H02.7 Other degenerative diseases of the eyelid and periocular area

    H02.8 Other specified diseases of the eyelid

    H02.9 Disease of the eyelid, unspecified

    H03* Lesions of the eyelid in diseases classified elsewhere

    H03.1* Lesions of the eyelid in other infectious diseases classified elsewhere

    H03.8* Lesions of the eyelid in other diseases classified elsewhere

    H04 Diseases of the lacrimal apparatus

    Excludes: congenital malformations of the lacrimal apparatus (Q10.4-Q10.6)

    H04.1 Other diseases of the lacrimal gland

    H04.3 Acute and unspecified inflammation of the lacrimal ducts

    Excludes: dacryocystitis of the newborn (P39.1)

    H04.4 Chronic inflammation of the tear ducts

    H04.5 Stenosis and insufficiency of the lacrimal ducts

    H04.6 Other changes in the tear ducts

    H04.8 Other diseases of the lacrimal apparatus

    H04.9 Disease of the lacrimal apparatus, unspecified

    H05 Diseases of the orbit

    Excludes: congenital malformations of the orbit (Q10.7)

    H05.0 Acute inflammation of the orbit

    H05.1 Chronic inflammatory diseases of the orbit

    H05.2 Exophthalmic conditions

    H05.3 Orbital deformity

    H05.5 Unremoved, long-standing foreign body in the orbit due to penetrating injury to the orbit

    H05.8 Other diseases of the orbit

    H05.9 Disease of the orbit, unspecified

    H06* Lesions of the lacrimal apparatus and orbit in diseases classified elsewhere

    H06.0* Lesions of the lacrimal apparatus in diseases classified elsewhere

    H06.2* Exophthalmos due to dysfunction of the thyroid gland (E05.-+)

    H06.3* Other disorders of the orbit, in diseases classified elsewhere

    H10.0 Mucopurulent conjunctivitis

    H10.1 Acute atopic conjunctivitis

    H10.2 Other acute conjunctivitis

    H10.3 Acute conjunctivitis, unspecified

    Excludes: ophthalmia of the newborn NOS (P39.1)

    H10.4 Chronic conjunctivitis

    H10.8 Other conjunctivitis

    H10.9 Conjunctivitis, unspecified

    H11 Other diseases of the conjunctiva

    Excludes: keratoconjunctivitis (H16.2)

    Deleted: pseudopterygium (H11.8)

    H11.1 Conjunctival degeneration and deposits

    H11.2 Conjunctival scars

    H11.3 Conjunctival hemorrhage

    H11.4 Other conjunctival vascular diseases and cysts

    H11.8 Other specified diseases of the conjunctiva

    H11.9 Disease of the conjunctiva, unspecified

    H13* Lesions of the conjunctiva in diseases classified elsewhere

    H13.0* Filarial infestation of the conjunctiva (B74.-+)

    H13.1* Acute conjunctivitis in diseases classified elsewhere

    H13.2* Conjunctivitis in diseases classified elsewhere

    H13.3* Ocular pemphigoid (L12.-+)

    H13.8* Other lesions of the conjunctiva in diseases classified elsewhere

    H15.8 Other scleral lesions

    Excludes: degenerative myopia (H44.2)

    H15.9 Disease of the sclera, unspecified

    H16.0 Corneal ulcer

    H16.1 Other superficial keratitis without conjunctivitis

    H16.3 Interstitial (stromal) and deep keratitis

    H16.4 Corneal neovascularization

    H16.8 Other forms of keratitis

    H16.9 Keratitis, unspecified

    H17 Scars and corneal opacities

    H17.0 Adhesive leukoma

    H17.1 Other central corneal opacities

    H17.8 Other corneal scars and opacities

    H17.9 Corneal scars and opacities, unspecified

    H18 Other corneal diseases

    H18.0 Pigmentation and deposits in the cornea

    If it is necessary to identify the drug that caused the lesion, use an additional external cause code (class XX).

    H18.1 Bullous keratopathy

    H18.2 Other corneal edema

    H18.3 Changes in corneal membranes

    H18.4 Corneal degeneration

    Excludes: Moray ulcer (H16.0)

    H18.5 Hereditary corneal dystrophies

    H18.7 Other deformities of the cornea

    Excludes: congenital malformations of the cornea (Q13.3-Q13.4)

    H18.8 Other specified diseases of the cornea

    H18.9 Disease of the cornea, unspecified

    H19* Lesions of the sclera and cornea in diseases classified elsewhere

    H19.0* Scleritis and episcleritis in diseases classified elsewhere

    H19.1* Herpes simplex virus keratitis and keratoconjunctivitis (B00.5+)

    H19.2* Keratitis and keratoconjunctivitis in other infectious and

    H19.3* Keratitis and keratoconjunctivitis in diseases classified elsewhere

    H19.8* Other lesions of the sclera and cornea in diseases classified elsewhere

    H20.0 Acute and subacute iridocyclitis

    H20.1 Chronic iridocyclitis

    H20.2 Iridocyclitis caused by lenses

    H20.8 Other iridocyclitis

    H20.9 Iridocyclitis, unspecified

    H21 Other diseases of the iris and ciliary body

    Excludes: sympathetic uveitis (H44.1)

    Excludes: traumatic hyphema (S05.1)

    H21.1 Other vascular diseases of the iris and ciliary body

    H21.2 Degeneration of the iris and ciliary body

    H21.3 Cyst of the iris, ciliary body and anterior chamber of the eye

    Excludes: miotic cyst of the pupil (H21.2)

    H21.4 Pupillary membranes

    H21.5 Other types of adhesions and tears of the iris and ciliary body

    Excludes: corectopia (Q13.2)

    H21.8 Other specified diseases of the iris and ciliary body

    H21.9 Disease of the iris and ciliary body, unspecified

    H22* Lesions of the iris and ciliary body in diseases classified elsewhere

    H22.0* Iridocyclitis in infectious diseases classified elsewhere

    H22.1* Iridocyclitis in diseases classified elsewhere

    H22.8* Other lesions of the iris and ciliary body in diseases classified elsewhere

    Excludes: capsular glaucoma with false lens detachment (H40.1)

    H25.0 Initial senile cataract

    H25.1 Senile nuclear cataract

    H25.2 Senile Morgani cataract

    H25.8 Other senile cataracts

    H25.9 Senile cataract, unspecified

    H26 Other cataracts

    Excludes: congenital cataract (Q12.0)

    H26.0 Childhood, juvenile and presenile cataract

    H26.1 Traumatic cataract

    If it is necessary to identify the cause, use an additional external cause code (class XX).

    H26.2 Complicated cataract

    H26.3 Drug-induced cataracts

    If it is necessary to identify the drug that caused the lesion, use an additional external cause code (class XX).

    H26.4 Secondary cataract

    H26.8 Other specified cataracts

    H26.9 Cataract, unspecified

    H27 Other lens diseases

    Excludes: congenital lens defects (Q12.-), mechanical complications associated with implanted lens (T85.2)

    H27.1 Lens luxation

    H27.8 Other specified diseases of the lens

    H27.9 Lens disease, unspecified

    H28* Cataracts and other lesions of the lens in diseases classified elsewhere

    H28.0* Diabetic cataract (E10-E14+ with common fourth digit.3)

    H28.1* Cataracts in other diseases of the endocrine system, nutritional disorders and metabolic disorders classified elsewhere

    H28.2* Cataract in other diseases classified elsewhere

    H28.8* Other lesions of the lens in diseases classified elsewhere

    H30.0 Focal chorioretinal inflammation

    H30.1 Disseminated chorioretinal inflammation

    Excludes: exudative retinopathy (H35.0)

    H30.2 Posterior cyclitis

    H30.8 Other chorioretinal inflammations

    H30.9 Chorioretinal inflammation, unspecified

    H31 Other diseases of the uvea

    H31.0 Chorioretinal scars

    H31.1 Uveal degeneration

    Excludes: angioid streaks (H35.3)

    H31.2 Hereditary dystrophy of the choroid

    Excludes: ornithinemia (E72.4)

    H31.3 Hemorrhage and rupture of the choroid

    H31.4 Choroidal detachment

    H31.8 Other specified diseases of the uvea

    H31.9 Choroid disease, unspecified

    H32* Chorioretinal disorders in diseases classified elsewhere

    H32.8* Other chorioretinal disorders in diseases classified elsewhere

    H33 Retinal detachment and tears

    Excludes: retinal pigment epithelial detachment (H35.7)

    H33.0 Retinal detachment with retinal break

    H33.1 Retinoschisis and retinal cysts

    Excludes: congenital retinoschisis (Q14.1), microcystic retinal degeneration (H35.4)

    H33.2 Serous retinal detachment

    Excludes: central serous chorioretinopathy (H35.7)

    H33.3 Retinal tears without retinal detachment

    Excludes: peripheral retinal degeneration without break (H35.4), chorioretinal scars after surgery for retinal detachment (H59.8)

    H33.4 Tractional retinal detachment

    H33.5 Other forms of retinal detachment

    H34 Retinal vascular occlusions

    H34.0 Transient retinal arterial occlusion

    H34.1 Central retinal arterial occlusion

    H34.2 Other retinal arterial occlusions

    H34.8 Other retinal vascular occlusions

    H34.9 Retinal vascular occlusion, unspecified

    H35 Other retinal diseases

    H35.0 Background retinopathy and retinal vascular changes

    H35.2 Other proliferative retinopathy

    H35.3 Macular and posterior pole degeneration

    If it is necessary to identify the drug that caused the lesion, use an additional external cause code (class XX).

    H35.4 Peripheral retinal degenerations

    Excludes: with retinal tear (H33.3)

    H35.5 Hereditary retinal dystrophies

    H35.6 Retinal hemorrhage

    H35.7 Retinal layer splitting

    H35.8 Other specified retinal disorders

    H35.9 Retinal disease, unspecified

    H36* Retinal lesions in diseases classified elsewhere

    H36.0* Diabetic retinopathy (E10-E14+ with common fourth digit.3)

    H36.8* Other retinal disorders in diseases classified elsewhere

    Excludes: absolute glaucoma (H44.5), birth glaucoma (Q15.0), traumatic glaucoma due to birth injury (P15.3)

    H40.0 Suspicion of glaucoma

    H40.1 Primary open-angle glaucoma

    H40.2 Primary angle-closure glaucoma

    H40.3 Glaucoma secondary post-traumatic

    H40.4 Glaucoma secondary to inflammatory disease of the eye

    H40.5 Glaucoma secondary to other eye diseases

    H40.6 Glaucoma, secondary, drug-induced

    H40.8 Other glaucoma

    H40.9 Glaucoma, unspecified

    H42* Glaucoma in diseases classified elsewhere

    H42.0* Glaucoma in diseases of the endocrine system, nutritional disorders and metabolic disorders

    H42.8* Glaucoma in other diseases classified elsewhere

    H43.0 Vitreous loss (prolapse)

    Excludes: vitreous syndrome after cataract surgery (H59.0)

    H43.1 Vitreous hemorrhage

    H43.2 Crystalline deposits in the vitreous

    H43.3 Other vitreous opacities

    H43.8 Other diseases of the vitreous

    Excludes: proliferative vitreoretinopathy with retinal detachment (H33.4)

    H43.9 Vitreous disease, unspecified

    H44 Diseases of the eyeball

    Includes: disorders affecting multiple structures of the eye

    H44.0 Purulent endophthalmitis

    H44.1 Other endophthalmitis

    H44.2 Degenerative myopia

    H44.3 Other degenerative diseases of the eyeball

    H44.4 Hypotony of the eye

    H44.5 Degenerative conditions of the eyeball

    H44.6 Unremoved (long-standing in the eye) magnetic foreign body

    H44.7 Unremoved (long-term in the eye) non-magnetic foreign body

    H44.8 Other diseases of the eyeball

    H44.9 Disease of the eyeball, unspecified

    H45* Lesions of the vitreous body and eyeball in diseases classified elsewhere

    H45.0* Vitreous hemorrhage in diseases classified elsewhere

    H45.1* Endophthalmitis in diseases classified elsewhere

    H45.8* Other lesions of the vitreous body and eyeball in diseases classified elsewhere

    Excludes: ischemic optic neuropathy (H47.0), optic neuromyelitis [Devic's disease] (G36.0)

    H47 Other diseases of the optic nerve and visual pathways

    H47.0 Diseases of the optic nerve, not elsewhere classified

    H47.1 Papilledema, unspecified

    H47.2 Optic atrophy

    H47.3 Other optic disc diseases

    H47.4 Optic chiasm lesions

    H47.5 Lesions of other parts of the visual pathways

    H47.6 Lesions of visual cortex

    H47.7 Diseases of the visual pathways, unspecified

    H48* Disorders of the optic nerve and visual pathways in diseases classified elsewhere

    H48.0* Optic nerve atrophy in diseases classified elsewhere

    H48.1* Retrobulbar neuritis in diseases classified elsewhere

    H48.8* Other lesions of the optic nerve and visual pathways in diseases classified elsewhere

    Supranuclear progressive (G23.1)

    H49.0 3rd [oculomotor] nerve palsy

    H49.1 4th [trochlear] nerve palsy

    H49.2 6th [abducens] nerve palsy

    H49.3 Complete (external) ophthalmoplegia

    H49.4 Progressive external ophthalmoplegia

    H49.8 Other paralytic strabismus

    H49.9 Paralytic strabismus, unspecified

    H50 Other forms of strabismus

    H50.0 Convergent concomitant strabismus

    H50.1 Concomitant divergent strabismus

    H50.2 Vertical strabismus

    H50.3 Intermittent heterotropia

    H50.4 Other and unspecified heterotropies

    H50.6 Mechanical strabismus

    H50.8 Other specified types of strabismus

    H50.9 Strabismus, unspecified

    H51 Other concomitant eye movement disorders

    H51.0 Gaze paralysis

    H51.1 Convergence insufficiency [insufficient and excessive convergence]

    H51.2 Intranuclear ophthalmoplegia

    H51.8 Other specified disorders of conjugal eye movement

    H51.9 Concomitant eye movement disorder, unspecified

    H52 Impairments of refraction and accommodation

    Excludes: malignant myopia (H44.2)

    H52.3 Anisometropia and aniseikonia

    H52.5 Accommodation disorders

    H52.6 Other refractive errors

    H52.7 Refractive error, unspecified

    H53.0 Amblyopia due to anopsia

    H53.1 Subjective visual disturbances

    Excludes: visual hallucinations (R44.1)

    H53.3 Other disturbances of binocular vision

    H53.4 Visual field defects

    H53.5 Color vision abnormalities

    Excludes: day blindness (H53.1)

    H53.6 Night blindness

    Excluded: due to vitamin A deficiency (E50.5)

    H53.8 Other visual disturbances

    H53.9 Visual impairment, unspecified

    H54 Blindness and decreased vision

    Excludes: transient blindness (G45.3)

    H54.0 Blindness in both eyes

    H54.1 Blindness in one eye, reduced vision in the other eye

    H54.2 Reduced vision in both eyes

    H54.3 Unspecified loss of vision in both eyes

    H54.4 Blindness in one eye

    H54.5 Reduced vision in one eye

    H54.6 Unspecified loss of vision in one eye

    H54.7 Unspecified vision loss

    H57 Other diseases of the eye and its adnexa

    H57.0 Abnormalities of pupillary function

    H57.1 Eye pain

    H57.8 Other unspecified diseases of the eye and adnexa

    H57.9 Disorder of the eye and adnexa, unspecified

    H58* Other lesions of the eye and its adnexa in diseases

    nyakhs classified in other headings

    H58.0* Abnormalities of pupillary function in diseases classified elsewhere

    H58.1* Visual impairment in diseases classified elsewhere

    H58.8* Other disorders of the eye and its adnexa in diseases classified elsewhere

    H59 Lesions of the eye and its adnexa after medical procedures

    Excluded: mechanical complication from:

    Intraocular lens (T85.2)

    Other ocular prosthetic devices, implant and graft (T85.3)

    H59.0 Vitreous syndrome after cataract surgery

    H59.8 Other lesions of the eye and adnexa following medical procedures

    H59.9 Damage to the eye and its adnexa following medical procedures, unspecified

    What is retinal angiopathy, and what is the disease code according to ICD 10,

    Angiopathy is a change in the condition of the vessels of the retina, which can lead to the development of dystrophic changes (retinal dystrophy), myopia, optic nerve atrophy, etc.

    Retinal vascular angiopathy is not a disease and ophthalmologists often focus on this, but a condition that can occur against the background of other diseases. Pathological changes in blood vessels appear during injuries and damage, and are also observed in diabetes mellitus.

    ICD-10 code

    Angiopathy does not have a code according to the international classification, since it is not considered an independent disease. The code is assigned to the disease that led to the development of the pathological condition.

    This is what retinal angiopathy looks like

    Causes and classification

    Angiopathy has several causes. The names in the vessels appear against the background of:

    1. Traumatic injuries to the chest or cervical spine. Which leads to impaired blood flow and hypoxia.
    2. Arterial hypertension is, simply put, high blood pressure. When blood pressure levels increase, the small capillaries of the retina cannot withstand the load and burst. Hemorrhages occur, which can lead to a decrease in visual acuity, changes in the vessels and their course.
    3. Arterial hypotension is low blood pressure that occurs against the background of significant dilation of veins and large vessels, leading to the formation of blood clots in the vessels of the retina.
    4. Cervical osteochondrosis is a disease that leads to impaired blood flow to the brain and increased intracranial pressure.
    5. Diabetes mellitus is a pathology of the endocrine system, characterized by increased blood sugar levels. In the absence of adequate therapy, diabetes mellitus leads to thickening of the membrane walls and affects the condition of the retinal vascular network.
    6. Traumatic brain injury - leads to disruption of brain function, increased intracranial pressure, and the development of hypoxia. In this case, angiopathy occurs as a consequence of the injury.
    7. Pregnancy and childbirth - changes in blood vessels can appear during pregnancy or occur after a difficult birth. In this case, the condition is subject to correction, but only if the cause of the pathology has been established.
    8. Autoimmune diseases and diseases of the hematopoietic system are nonspecific causes. Against the background of such diseases, changes in the retinal vessels occur quite rarely.

    But this information will help you understand what presbyopia and retinal angiopathy is and how it is treated.

    The video shows a description of the disease:

    There are several types of angiopathy, it happens:

    • hypertensive - occurs when blood pressure or intracranial pressure increases;
    • hypotonic – develops against the background of low blood pressure and blood clots;
    • diabetic - the main cause is diabetes mellitus or an increase in blood sugar levels (can be diagnosed in children of the first year of life or newborns);
    • background – occurs against the background of changes in the condition of the vessels of the retina of the eyes, with a long course it is dangerous for complications;
    • traumatic – a consequence of injuries suffered, injuries that occur when blood flow to the brain is disrupted;
    • juvenile - appears in children during puberty. The exact cause has not been established. It manifests itself as a sharp loss of visual acuity, develops quickly and can cause glaucoma or retinal dystrophy.

    Angiopathy of both eyes is diagnosed more often. But there are cases when the vessels change in only one eyeball. This may indicate a slow progression of the pathology.

    Description of symptoms

    Angiopathy has a number of specific signs that a person can notice, but leave without proper attention. Attributing the condition to stress or fatigue.

    In most cases, patients complain:

    1. For the appearance of “flies” in the eyes.
    2. To reduce visual acuity.
    3. The appearance of flashes or fog before the eyes.
    4. For pain or colic in the eyeball area.
    5. For rapid fatigue of the visual organs.
    6. For the appearance of pinpoint hemorrhages or burst red blood vessels in the area of ​​proteins.

    It is necessary to pay attention to decreased visual acuity, the appearance of floaters or lightning before the eyes. Temporary, but complete or partial loss of vision. When, when getting out of bed or during heavy physical exertion, there is a sharp clouding in the eyes, an acute attack of dizziness.

    This indicates that the person has problems with blood circulation in the brain, hypoxia or high intracranial pressure. Against the background of these pathologies, retinal angiopathy develops.

    Symptoms may change and occur periodically (only when blood pressure levels increase), but these signs should not be ignored. If alarming symptoms appear, you should consult a doctor as soon as possible.

    Diagnostics

    It is not particularly complicated; you just need to contact an ophthalmologist. The doctor will examine the vessels of the fundus.

    To detect changes, it is enough to conduct only one examination, but if necessary, the doctor may recommend an ultrasound of the eyes. Intraocular pressure is also measured, which helps eliminate the possibility of developing glaucoma. But this information will help you understand how retinal angiopathy is diagnosed in a child.

    Treatment

    Therapy is aimed at eliminating the root cause of the pathological condition. If angiopathy occurs against the background of arterial hypertension, the doctor writes a referral to a cardiologist. The doctor prescribes medications that can stabilize blood pressure levels and reduce the risk of bleeding in the retinal vessels and small capillaries.

    If angiopathy is associated with diabetes mellitus, then the underlying disease is treated and attempts are made to prevent the development of complications.

    So, what medications can an ophthalmologist prescribe:

    • vasodilators (Cinnarizine, Vinpocetine, etc.);

    Cinnarizine

  • vitamin complexes (narrowly targeted drugs, vitamins for the eyes are used). But what vitamins should be used first for age-related farsightedness are outlined here.
  • drugs that improve blood microcirculation (mainly drops, Taufon eye drops).

    List of medications that improve blood microcirculation in the eyeballs:

    Does retinal angiopathy have an ICD 10 code?

    For such a complex eye disease as retinal angiopathy, there is no ICD-10 code. And this does not mean that this pathology of the visual organs does not deserve the close attention of ophthalmologists. What are the symptoms of this disease and how to treat it?

    Let us remind you. that ICD-10 is the International (adopted by WHO for doctors of all categories and countries) classification of diseases in the tenth revision.

    In medical terms, angiopathy is a vascular disorder of the eye, manifested in a violation of the tone of the retinal vessels and the capillary bed of the fundus. Against the background of this pathology, a decrease in blood flow and nervous regulation is observed. There is no separate classification of this condition in ICD-10, since it is a consequence of much more serious diseases. Most often, angiopathy occurs against the background of such diseases:

    1. Intracranial hypertension.
    2. Damage to the cervical segments.
    3. Osteochondrosis of the cervical spine.
    4. Various blood infections.
    5. Diabetes mellitus.
    6. Abuse of smoking and alcoholic beverages.
    7. Congenital anomalies.

    And these are just some of the possible causes of retinal blood supply disorders. The danger of this pathology is that against the background of angiopathy, more serious pathologies may occur, such as retinal dystrophy and/or myopia. Moreover, in the absence of timely and adequate treatment, this disorder in the trophism of the retina can lead to complete loss of vision.

    It is characteristic that angiopathy, including diabetic retinopathy, affects both eyes simultaneously. This serves as a distinctive sign when carrying out differential diagnosis. Angiopathy is detected when examining the fundus of the eye by an ophthalmologist.

    Retinal angiopathy: ICD-10 code, treatment, types

    What it is?

    Angiopathy is a condition of retinal vessels in which capillary circulation changes due to disturbances in their nervous innervation. This occurs due to low blood filling of the vessels or their prolonged spasm.

    Medicine does not distinguish angiopathy as an independent disease; modern scientific approaches classify it as one of the manifestations of the underlying disease. Such a symptom complex can be a consequence of metabolic or hormonal disorders, injuries and intoxications, as well as the consequences of such bad habits as smoking or drug addiction.

    This condition, if detected and treated in a timely manner, is reversible. Only in advanced cases does the disease lead to serious complications:

    Stages of retinal angiopathy

    Treatment of angiopathy is prescribed by an ophthalmologist after a thorough examination. The success of therapy directly depends on procedures aimed at getting rid of the underlying disease.

    ICD-10 code

    According to the international typology of diseases, angiopathy does not have its own code, since it is not assigned the status of an independent disease. Therefore, coding is based on the pathology that caused vascular imbalance in the retinal tissue.

    These can be various diseases:

    • traumatic injuries to the eyes, face, neck, head;
    • high intracranial or blood pressure;
    • osteochondrosis, cervical spondylosis;
    • diabetes;
    • hypo- or avitaminosis;
    • blood diseases;
    • atherosclerosis, vasculitis;
    • intoxication with microbial toxins or poisoning with chemicals (radiation);
    • strong physical and psycho-emotional stress, causing prolonged spasms of the capillaries;
    • presbyopia or tissue degeneration in the eye apparatus.

    Angiopathy has its own classification:

    1. Juvenile (Eales disease), refers to rare pathologies with unknown etiology. The disease affects young people and manifests itself:

    • inflammation of capillaries and veins and proliferation of connective fibers in the retina;
    • hemorrhages in the tissue of the eye;

    The prognosis of the disease is serious, as it can provoke retinal detachment and partial or complete loss of vision, as well as the development of cataracts or glaucoma.

    2. Retinal angiopathy of the hypertensive type is caused by high blood pressure in patients; because of this, the vessels of the eyes are often in a narrowed state, which prevents normal blood supply to the retina, and often occurs with pronounced changes in the fundus.

    3. Traumatic angiopathy develops with injuries to the head, neck or chest. Here, mechanical compression of veins and capillaries or increased intracranial pressure is possible. The pathology causes temporary or long-term loss of visual acuity, damage to the nerve plexuses innervating the eyes, and degenerative changes in the cells of the retina and vitreous body.

    4. The hypotonic type of the disease is characterized by overflow of blood vessels and their pathological expansion, therefore there is a risk of increased thrombus formation and hemorrhages in the eye tissue.

    5. Diabetic angiopathy is a consequence of the progression of this disease. Improper cellular metabolism causes changes in the structure of blood vessels (thinning or obesity), so normal blood circulation through them is disrupted.

    6. The age-related form of the disease occurs due to the aging of the body, worn-out vessels can no longer cope with the loads, their tone decreases, and degenerative changes appear.

    Retinal angiopathy in a child

    Changes in the tone of blood vessels in the eyes in children in infancy can be observed with a change in body position or hysterical crying. This occurs due to the immaturity of the circulatory and nervous system of babies and is not a pathology. The painful condition of the blood vessels in the eyes in children is indicated by a prolonged spasm of the veins and capillaries, diagnosed during examination in a hospital (maternity hospital, children's hospital) or in an outpatient setting.

    Clinical signs of the disease appear:

    • in decreased visual acuity;
    • in the appearance of flickering, white or dark spots before the eyes, “fiery flashes, lightning, flashes”;
    • increased eye fatigue when reading, watching TV or working on a PC;
    • in the formation of a network of capillaries on the mucous membrane of the eyes, in redness of the conjunctiva, in the detection of pinpoint hemorrhages;
    • in reducing the fields of lateral vision;
    • a feeling of pulsation inside the eyes;
    • in pathological changes in the fundus (during an objective examination by a doctor).

    Treatment

    Angiopathy therapy is carried out according to the underlying disease:

    1. The diabetic form of pathology requires strict adherence to a diet and (or) systematic administration of insulin.
    2. Hypertensive angiopathy of the retina of both eyes is treated primarily with drugs that lower blood pressure and vasoconstrictors.
    3. Traumatic angiopathy involves treatment in a surgical hospital, the use of special manipulations (splints, casting) or operations.

    To improve blood circulation in the ocular vessels in all forms of angiopathy, the following may be prescribed:

    Physiotherapy is usually added to medicinal methods:

    General restorative procedures for this condition include:

    • following a low-carbohydrate diet;
    • walks in the open air;
    • light physical activity (swimming, gymnastics);
    • reduction of visual stress;
    • use of vitamins.

    Why is retinal angiopathy dangerous today and how to treat it correctly?

    The human eye is a rather vulnerable organ and deterioration in the quality of vision is not the only ailment that can befall a person. Moreover, some eye diseases are independent diseases, others are only symptoms of others. And in both cases, it is important to be able to recognize the problem and begin to solve it correctly. Indeed, often in the absence of action you can lose the opportunity to see well. Angiopathy does not always pose a serious threat to the health of the body, but its treatment is as necessary as the treatment of any eye disease.

    Definition of disease

    As a rule, retinal angiopathy appears against the background of a disorder of the nervous system and is a pathological change in the circulatory system with a deterioration in blood movement. This pathology is not an independent disease and appears against the background of a general deterioration in the condition of the body’s blood vessels, caused by various diseases and abnormalities. Sometimes angiopathy can be accompanied by deterioration and complete loss of vision.

    Causes

    Angiopathy can develop due to many reasons and factors. Among the main ones:

    • Increased intracranial pressure;
    • Decreased tone of vascular walls;
    • Diabetes;
    • Various blood diseases;
    • Age-related changes;
    • Damage and injury to the eyes.

    The causes of the disease can also be divided according to its types.

    • Hypertensive. Due to the development of hypertension, the body may lose the general tone of the veins and blood vessels, and at the same time, the movement of blood in the retina of the eyes is disrupted. Blurred vision is observed, myopia progresses. Degeneration occurs in the tissues of the retina.
    • Juvenile (Iles disease). It is an inflammation of blood vessels and can lead to the development of cataracts, glaucoma and retinal detachment.
    • Hypotonic. Along with the expansion of veins and arteries, the vessels of the eyes also expand, and their general tone is lost. As a result, blood clots can form, and the patient, in turn, feels pulsation in the eye area.
    • Traumatic. Angiopathy may appear due to vascular damage in the cervical spine. There may be a narrowing of the blood vessels in the eyes and, as a result, hypoxia.
    • Dystonic. Accompanied by the rapid development of myopia. The disease manifests itself against the background of general dysfunction of the body's blood vessels; hemorrhages into the eyeball are possible.
    • Diabetic. Develops in the absence of proper treatment for diabetes. In this case, the blood vessels narrow and, as a result, the blood begins to move more slowly.
    • Background. It occurs against the background of the appearance of various diseases and the presence of hereditary abnormalities associated with the vascular system. Possible chronic circulatory problems.
    • Venous. Throughout the body, veins lose their tone and shape, blockages and blood clots occur. At the same time, vision deterioration and blurred vision may occur.

    Symptoms

    The main symptoms of retinal angiopathy include:

    • Deterioration in the quality of vision;
    • Progressive retinal dystrophy;
    • Myopia;
    • Lightning in the eyes;
    • Bleeding and hemorrhage;
    • Tortuosity of blood vessels;
    • Proliferation of defective capillaries.

    With microangiopathy, thinning of the capillary walls and deterioration of blood circulation are observed. The development of macroangiopathy is accompanied by degradation of large vessels, diabetic - by clogging and blockage of them with mucopolysaccharides.

    Angiopathy and the individual causes of its occurrence are diagnosed by an ophthalmologist using ophthalmoscopy, as well as based on data on the patient’s general health.

    Possible complications

    Without timely intervention in angiopathy, a reversible change in the retina, tissue hypoxia and hemorrhage can be expected. The retinal vessels themselves also undergo changes. In turn, they become severely deformed and lose blood conductivity. In some cases, complete loss of vision is possible.

    Complications can be caused by various bad habits, high blood pressure, hereditary vascular diseases, obesity, and high cholesterol.

    Treatment

    Retinal angiopathy is an unpleasant phenomenon, but treatable. If it is built correctly, the condition of the retina can return to normal. Only a qualified ophthalmologist can prescribe a course.

    Self-medication can be detrimental in the case of angiopathy, since specific procedures and medications are prescribed for each cause.

    Simultaneously with the treatment of angiopathy, therapy is carried out for the diseases that resulted from it, so observation by other doctors is often necessary. It is important to follow the prescribed diet during this period.

    By medication

    When treating a disease, the first step is to restore proper blood circulation. For this, as a rule, they prescribe:

    The main set of medications also includes vascular strengtheners (Calcium Dobesilate, Parmidine, etc.), as well as drugs that prevent platelet aggregation (Aspirin, Ticlodipine, Dipyridamole, etc.). If necessary, vitamins C, E, P and group B elements can be prescribed.

    Eye drops such as Taufon, Emoxipi, Anthocyan Forte are also widely used.

    During the treatment of disorders of the vascular system, it is necessary to give up bad habits. If they were one of the reasons for the development of the disease, they will have to be completely excluded from everyday life.

    Surgical methods

    If angiopathy has become advanced, surgical intervention may be required. Photocoagulation is performed to prevent retinal detachment, the formation of fibrous tissue and reduce the appearance of defective vessels, as well as treatment with a surgical laser. Physiotherapeutic methods are also widely used.

    Night blindness - symptoms in humans, as well as treatment methods are described here.

    Folk remedies

    When treating retinal disease, the use of folk remedies is also permissible, but only in combination with basic methods of therapy and only after consultation with doctors.

    Treatment with folk remedies is usually carried out using infusions: rowan fruits, currant leaves, dill seeds and caraway seeds.

    Collection No. 1. It is necessary to collect one hundred grams of yarrow, chamomile, St. John's wort, immortelle and birch buds. The infusion must be prepared based on the proportion: half a liter of boiling water per tablespoon of the collection. After infusing for twenty minutes, the mixture must be filtered and diluted with hot water in the amount of half a liter. Take twice a day – one glass in the morning and evening. The course of treatment is carried out until the collection is completely used up.

    Collection No. 2. Fifteen grams of lemon balm and valerian must be mixed with fifty grams of yarrow. A quarter liters of boiling water is needed to brew every two teaspoons of the resulting mixture. The infusion must be kept for three hours, then heated in a water bath and strained. This amount of herbal medicine must be spread throughout the day. Treatment is carried out over three weeks.

    Prevention

    In order to prevent the appearance and development of retinal vascular disease, it is necessary to follow the basic rules:

    1. Promptly treat diseases that cause retinal angiopathy.
    2. Avoid serious physical overload.
    3. Regularly undergo examinations with an ophthalmologist.
    4. Lead a healthy lifestyle and follow a proper diet.
    5. To refuse from bad habits.
    6. If you have hereditary diseases of the cardiovascular system, follow the regimen and recommendations of your doctor.

    Levomycytin eye drops: instructions for use are described here.

    Video

    conclusions

    Retinal angiopathy is not an independent disease, which can complicate its treatment program depending on the identified causes. It is not recommended to allow complications and let the situation arise, as this can lead to serious consequences, including complete loss of vision. At the same time, with the right choice of treatment for angiopathy and the underlying disease, it is possible to achieve a complete return to the previous healthy state of the retina and return to normal life.

    Many diseases can impair eye health! How to distinguish retinal angiopathy?

    You are viewing the Angiopathy section.

    A disease characterized by disruption of the blood vessels and capillaries of the eye is called angiopathy.

    It is not considered an independent disease, since it is only a symptom of other diseases that affect the blood vessels of the body. In order to get rid of angiopathy, it is necessary to cure the disease due to which it develops.

    Retinal vascular angiopathy: what is it, classification, ICD 10 code

    Angiopathy is a pathology that is the result of diseases affecting blood vessels; it usually develops in both eyes at once. This disease does not have a code in ICD-10, since it is not considered a separate disease.

    Photo 1. Fundus of the eye with a healthy organ of vision (left) and with retinal angiopathy (right).

    Primary or hypotonic in children and adults

    For newborns, the cause of angiopathy can be injuries during childbirth.

    Reference. There are also cases when angiopathy is not caused by a number of problems, but appears due to the specific structure of the blood vessels of the eyes.

    The appearance of primary angiopathy in an adult indicates that he has a malfunction in the vegetative-vascular system.

    Secondary or background

    • Hypertensive or hypertensive - appears due to high blood pressure for a long time. There is a slight hemorrhage and dilatation of the veins of the eye.
    • Diabetic - the main cause of this type of angiopathy is diabetes mellitus.

    Important! This type of pathology manifests itself gradually, which means that its development can be prevented by consulting a doctor in a timely manner!

    • Mixed type is the simultaneous development of several types of disease.
    • The hypotonic form is expressed by pathological dilation of blood vessels, which impairs blood circulation and, as a result, reduces vision.
    • Traumatic - the cause of the appearance is vascular disorders in the spine and an increased level of cerebrospinal fluid pressure in the brain, resulting from injuries to the chest, as well as injuries to the brain and cervical spine.
    • Juvenile, or Eales' disease, manifests itself through hemorrhages in the retinal tissue, as well as through inflammation of blood vessels. This type of angiopathy occurs at a young age, when teenagers do not pay attention to their health, so it is important for parents to pay more attention to the health of their child, since this pathology can lead to glaucoma, cataracts or retinal detachment.

    Reasons for appearance

    Doctors identify the following reasons for the development of the disease:

    • brain injuries, cervical vertebrae;
    • arterial hypertension and hypotension;
    • increased intracranial pressure;
    • eye damage;
    • specific structure of the retina;
    • smoking;
    • toxic work environment;
    • old age.

    Symptoms

    To preserve vision and prevent the development of the disease, you should consult a doctor if you notice the following manifestations:

    • blinking, dots and glare before the eyes;
    • accelerated growth of myopia;
    • repeated bleeding;
    • drop in visual acuity.

    With hypotensive angiopathy the following appear:

    • feeling of throbbing in the eyes;
    • cardiopsychoneurosis.

    For hypertensive angiopathy:

    • spots form before the eyes;
    • blood pressure rises.

    In the juvenile form, vision deteriorates sharply in a generally normal condition.

    Diabetic disease is characterized by:

    • presence of diabetes mellitus;
    • damage to other vessels of the body.

    Diagnostic methods

    An ophthalmologist is a doctor who studies and treats eye diseases. In his work he applies additional research:

    • Ophthalmoscopy - study of the fundus of the eye (optic nerve, retina and choroid).
    • Biomicroscopy - study of the structure of the eye. A stereo microscope helps to examine the anterior and posterior parts of the eyeball.
    • Determination of intraocular pressure.
    • Fluorescein angiography, which helps in the study of the vessels of the retina.

    Photo 2. The process of eye diagnostics using fluorescein angiography. Data on the state of the retina is displayed on the monitor.

    • Echoophthalmography - diagnosis of pathologies using the ultrasound method.

    How to treat eyes

    Treatment is divided into four groups:

    Traditional methods

    For angiopathy caused by high blood pressure, therapy is aimed at lowering it and reducing cholesterol in the blood, for which the following are traditionally prescribed:

    • medications aimed at lowering blood pressure;
    • medications that can thin the blood;
    • diuretics.

    For the diabetic type of disease, treatment is aimed at reducing blood sugar. For this use:

    • special diets to reduce carbohydrates;
    • medications;
    • physical exercise in moderation, which helps strengthen the cardiovascular system.

    In case of illness caused by nervous exhaustion, it is obligatory to:

    • minimize stressful situations;
    • spend more time outdoors;
    • Healthy food;
    • attend psychotrainings and aromatherapy;
    • add a vitamin complex to the diet: ginseng, lemongrass, Actovegin, Glycine.

    In case of Eales' disease or juvenile angiopathy, treatment depends on the severity of the process, since this type of disease has not been fully studied by doctors. The following are prescribed as treatment:

    • hormonal drugs;
    • laser intervention and photocoagulation.

    Important! Surgery can also be used for severe hemorrhage.

    Effective drugs for the treatment of eye angiopathy - Pentilin, Vazonit, Arbiflex, Solcoseryl, Trental. They normalize microcirculation. Aspirin, Magnicor or Trombonet prevent blood clots from developing.

    Photo 3. Packaging of the antithrombotic drug Magnikor in the form of tablets, 100 pieces in a pack.

    Diet-based therapy

    This treatment is suitable for diabetic and hypertensive types of disease.

    Dietary order for the prevention of diabetic angiopathy:

    • remove fried and smoked foods from the menu;
    • consume onions as much as possible, adding them to various dishes;
    • eat more fresh vegetables and fruits;
    • steam, bake and boil foods;
    • eat only chicken, turkey, veal, other meat is prohibited;
    • exclude canned food and other food additives.

    Attention! Do not create a menu yourself, only on the recommendation of a doctor!

    In the hypertensive form, fluid intake should be kept to a minimum. It is important to remove foods that contain salt and cholesterol from the menu. You should eat vegetables, fruits, fish, veal, turkey, rabbit, vegetable oils and dairy products.

    Physiotherapeutic treatment

    Effective types of this treatment method:

    • Laser radiation - allows you to purify the blood, reduces toxicity, strengthens the patient's immune system.
    • Magnetic therapy - activates blood circulation, increases cell permeability and enhances enzyme activity, reduces swelling.
    • Acupuncture - people with hypertension and hypotension can resort to this type.

    Folk remedies

    Eliminate deposits in blood vessels:

    • freshly squeezed parsley juice;
    • infusion of dill (seeds);
    • tinctures of blue cornflower stem and caraway seeds;
    • St. John's wort and medicinal chamomile.

    Features of the disease during pregnancy

    During pregnancy, the body adapts to provide the fetus with the necessary amount of oxygen and nutrients.

    Diagnosis of retinal angiopathy during pregnancy is most often carried out using hardware. Such an event is prescribed to all pregnant women without exception in accordance with the standards of medical supervision. Symptoms of retinal angiopathy during pregnancy can be expressed as:

    • burning sensation in the eyes;
    • feelings of slight pressure on the eyeball;
    • drop in visual acuity;
    • regular headaches;
    • appearance of the “red eye” effect.

    The main danger of the disease during pregnancy is an increase in pressure during contractions, which can provoke rupture of blood vessels, which, in turn, will lead to partial or complete loss of vision.

    In this case, medications are prescribed extremely rarely, only for severe cases of the disease. This is due to the fact that the drugs can significantly affect the child’s health.

    Useful video

    Watch the video in which an ophthalmologist talks about such a diagnosis as angiopathy and its features.

    Conclusion

    The causes of angiopathy are different, they depend on the age and lifestyle of the person. There are many treatment methods; it is possible to cure the disease. To do this, it is important to immediately contact an ophthalmologist when you notice the first symptoms and carefully follow all his recommendations.

  Pigmentary degeneration of the retina (abiotrophy, retinitis pigmentosa) is a rare pathology of the visual organs, occurring in one case out of 5 thousand.

  It is associated with dysfunction of cells that are responsible for peripheral vision and the ability to see in poor lighting conditions.

  Pigmentary degeneration It is characterized by a slow course and can lead to complete blindness.

  Causes and symptoms, ICD 10 code

  The main factor causing the development of the disease is- hereditary mutations of genes that are responsible for the nutrition and vital functions of the retina. Due to congenital anomalies, the synthesis of specific proteins is disrupted, which negatively affects the condition of the cells of the visual organs. Inheritance of pathological genes can occur in different ways.

  

  Symptoms of the disease often discovered in childhood, but in some cases develop slowly, for several decades, which is why the disease is diagnosed at an advanced age.

  Signs of retinal pigmentary degeneration include:

  • decreased quality of vision in low light conditions, with both eyes seeing poorly at once;
  • disturbance of orientation in space at dusk (night blindness);
  • reduction of the boundaries of peripheral vision, which progresses over time;
  • rapid eye fatigue;
  • in the later stages there is a short-term improvement, and then a sharp decrease in visual acuity and color perception.

  The disease has been described in 1857, later he was assigned code H35.5 in the International Classification of Diseases.

  Important! The disease is characterized by great variability in development and symptoms, so some patients are affected both eyes, and for others - one or separate segments of the retina.

  Mechanism of disease development

  Pathological process in pigmentary degeneration affects rods and cones- receptor cells located at the edges and in the center of the retina. They are responsible for peripheral and color vision, as well as its acuity. As the disease develops, the layers of the retina where the receptors are located are gradually destroyed.

  

  A person sees poorly at dusk, stumbles and bumps into objects, after which the patient vision narrows.

  Typically, the progression of pigmentary abiotrophy occurs slowly, but with some changes in the body (for example, during pregnancy), the pathology begins to develop faster.

  Types of disease: what it is, signs

  Depending on the characteristics of the clinical course and manifestations, pigment abiotrophy has several forms, and each of them requires appropriate treatment.

  The mechanism of development of the disease is associated with damage to the pigment layer of the retina, as well as the tissues where the photoreceptors are located. This form affects both eyes and most often occurs at the age of 8-16 years. In the first stages, the patient experiences slight photophobia and a slight but progressive decrease in vision, and upon a detailed examination of the eyes, pathological changes can be noticed - pigmented mottling. As the disease progresses, areas of depigmentation appear and visual acuity decreases up to 0.2—0.1.

  Reference. Central pigmentary degeneration has several varieties. The most dangerous of them is Leber's congenital amaurosis, characterized by the spread of the pathological process to the entire retina.

  Whitish punctate retinitis

  White dotted retinal degeneration, or whitish dotted retinitis manifested by the formation of numerous lesions. They have different sizes (most often small), clearly defined boundaries and a white tint. The disease progresses slowly but steadily, and its main symptoms are decreased twilight and night vision. Over time, patients experience narrowing of the retinal vessels and degenerative processes of the optic nerve, which ultimately leads to severe complications.

  

  Photo 1. Fundus image of whitish punctate retinitis. Many lesions can be seen.

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  A non-pigmented form of pigmentary degeneration

  The name of this form of the disease is associated with the absence of characteristic pigment deposits in the fundus. It is characterized by a decrease in visual acuity at dusk and changes in visual fields, subsequently developing atrophy of the optic nerve and deterioration of blood circulation in the retina due to vasoconstriction. The non-pigmented form occurs much less frequently than other types of the disease, and diagnosis can be difficult due to the lack of visible changes in the tissues of the eyes.

  Diagnostics

  The diagnosis of pigmentary abiotrophy is made on the basis of a comprehensive examination, which includes different diagnostic methods:

  • visual acuity test;
  • measurement of intraocular pressure;
  • perimetry, or assessment of visual fields;
  • examination using a slit lamp and an ophthalmoscope.

  

  The most informative way to diagnose a disease is considered ophthalmoscopy- examination of eye tissue using a special device (ophthalmoscope), which allows you to completely examine the entire retina.

  Characteristic signs of retinitis pigmentosa are pigment deposits in the form of white or yellowish spots, vasoconstriction, and changes in the optic nerve.

  Additional diagnostic methods include general blood and urine tests, glucose level tests, etc.

  Important! If there are difficulties in making a diagnosis, it is recommended to examination of the patient's close relatives, since the disease is hereditary.

  Treatment

  Modern medicine does not yet know methods that can completely rid a person of this disease. Treatment methods are aimed to slow down the pathological process, maintain the quality of vision and normal condition of eye tissues. Depending on the stage of the pathological process and the clinical course of the disease, therapy can be carried out with medications, physiotherapeutic methods or surgery.

  Conservative therapy

  To treat retinal pigmentary degeneration, drugs are used that improve blood supply and nutrition to eye tissue. These include intraocular and intravenous injections of metabolic agents ( Mildronate, Emoxipin), drugs containing nucleic acids ( Encad), drops with amino acids ( Taufon), peptide bioregulators ( Retinalamine). Patients are prescribed vitamin therapy, as well as an appropriate diet.

  

  Photo 2. Packaging of the drug Taufon in the form of eye drops with a dosage of 4%, volume 10 ml.

  Physiotherapeutic techniques

  To treat the disease, magnetic and electrical stimulation of the tissues of the organs of vision is recommended. They have a beneficial effect on blood circulation. At home, you can use a device called "Sidorenko's glasses", affecting tissue in several directions at once. In the absence of special devices, you can do simple eye exercises (close and open your eyes) and massage, pressing in a circular motion on the eyeballs.

  Attention! Physiotherapy methods are most effective in the early stages of the disease and cannot replace conservative and surgical treatment.

  Surgical intervention

  In advanced cases, patients with retinal pigmentary degeneration carry out vasoreconstructive operations: During the intervention, the surgeon crosses the superficial temporal artery, which improves blood supply to the optic nerve and retinal tissue.

  It is used to treat the disease laser coagulation affected vessels with subsequent scar formation. Today, ophthalmologists are developing developments in the field of genetic engineering and regenerative medicine, which in the future will make it possible to restore damaged genes and introduce special implants into the eyes that replace retinal tissue.