Glaucoma. Classification, treatment

GLAUCOMA - comes from the ancient Greek meaning
green, light blue.
Glaucoma is a serious disease that occurs throughout
world and usually affects people over 40 years of age, but
occasionally occurs at younger ages.
Glaucoma accounts for about 4% of all eye diseases. How
evidenced by the results of mass preventive
examinations, among the healthy population aged 40 years and
older, the disease occurs in 1-2% of cases.
In all countries of the world, glaucoma is one of the first
places as a cause of blindness.
The problem of successfully combating blindness from glaucoma is not
only the task of eye doctors, but also a general medical one
task. Therefore, doctors of all specialties should know
signs of this disease and how to treat glaucoma.
The duty of doctors of all specialties is to participate in
carrying out active preventive measures
facilitating early detection of the disease and treatment,
which prevents blindness from glaucoma.

Classification of glaucoma

Primary glaucoma is one of the most common causes of irreversible blindness. In its development, there are 2 main pathophysiological mechanisms:

Direction of action of intraocular pressure

Open angle glaucoma (OAG)

Pseudoexfoliation glaucoma

Angle-closure glaucoma (ACG)

Intraocular fluid flow in angle-closure glaucoma

Acute attack of glaucoma

Accumulation of fluid behind the vitreous in malignant glaucoma - ciliary block

Differential diagnosis of an acute attack of glaucoma and acute iritis (iridocyclitis).

Classification of primary glaucoma

Additional classification scheme for primary glaucoma

Clinical signs of the disease

In diagnosing the form of glaucoma, in addition to the clinical picture, gonioscopy is important - a method of examining the angle of the anterior chamber

Three-mirror Goldmann lens. It is used for gonioscopy - examination of the angle of the anterior chamber.

Degree of opening of the anterior chamber angle (Grade 0 – angle closed, Grade 4 – angle open)

The degree of opening of the anterior chamber angle according to Shaffer

Gonioscopic picture in open-angle glaucoma

Gonioscopic picture of the anterior chamber angle in angle-closure glaucoma

Scheme of the gonioscopic picture in pigmentary glaucoma

Gonioscopic picture in pigmentary glaucoma

Anterior chamber angle in congenital glaucoma

Phacolytic glaucoma

Automatic perimetry

This is what glaucoma patients see

Physiological excavation of the optic disc

Expansion of physiological excavation at the initial stage of glaucoma.

Marginal glaucomatous excavation in advanced stages of glaucoma

Tonometry is an objective method of measuring intraocular pressure

Congenital glaucoma

Congenital iridocorneoendothelial syndrome

Classification of secondary glaucomas

Rubeosis of the iris. Secondary neovascular glaucoma

Phacolytic glaucoma

Conservative treatment

TREATMENT OF ACUTE AND SUBACUTE ATTACK OF GLAUCOMA

Intraocular fluid flow after iridectomy

Laser trabeculoplasty. Effective in the early stages of open-angle glaucoma. The procedure is painless and performed on an outpatient basis

Iridectomy is a fistulizing operation effective for closed-angle glaucoma.

Sclerectomy is a fistulizing operation in which an additional pathway for the outflow of intraocular fluid into the intrascleral veins is created.

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Truth is an error that we temporarily believe to be correct. . .

“Yellow-green water” (Russian)Grun. Star (German) Glaucoma (French, English) Jaskra (pol.) “Blakytna water” (Ukrainian)

Glaukomas - the owl-eyed Heinrich Schliemann (Troy)

HISTORY OF THE ISSUE Avicenna (980-1037), having begun to heal at the age of 18, described glaucoma a thousand years ago. . . at the turn of the 1st millennium In his “Canon of Medical Science,” republished in 1994, there is a description of an eye disease - “cold inflammation” associated with a violation of fluids in the body

1000 years ago - Avicenna There is a type of inflammation of the eyes, which has periods and attacks, periods of change in matter and periods of time of its formation. The severity of pain during inflammation of the eye depends either on the burning juice, which corrodes the membranes, or on the abundance of juice, WHICH STRETCHES THEM. The matter that causes inflammation of the eyes comes either from the body in general, or from the head or from the vessels that bring bad matter to the eye, and sometimes the bad juices are in the eye itself.

in the world: 7.8 million blind in both eyes with glaucoma. According to the International Society of Glaucomatology for 2008

Incidence rates Statistical studies show that 1 in 200 over 40 years of age in the general population suffers from open-angle glaucoma. The overall prevalence of the population in this age group is 1.5%. The number of patients increases with age and reaches 12% in the group over 80 years of age.

In the general population, primary OAG accounts for slightly less than 1%. Today in Russia there are more than 500 thousand patients with glaucoma, in the USA the number of patients with POAG is 2.47 million (out of a total population of 276.6 million people). According to the American Academy of Ophthalmologists (1996), 116 thousand Americans became blind as a result of glaucoma Incidence rates

In the USA, 4% of the white population are blind in both eyes, 8% are black. Blind in one eye are 8% of the white population, 16% of the black population. The rate of blindness due to OAG in European countries averages 12% of all cases of blindness.

PDA width options (Shaffer, Nesterov) 4 3 2 1 0 45 o 35 o 20 o 10 o

Anatomical and physiological features of the drainage system of the eye The tissues of the drainage system are avascular Their metabolism is ensured by aqueous humor The trabecula contains an array of endothelial cells covering collagen fibers. In the cells, during metabolic processes, free radicals and lipid peroxidation products are formed that pass to the trabecula and damage it

Etiological classification of glaucoma (D. Vaughan, T. Asbury, P. Riordan-Eva, 1999) A. Primary glaucoma 1. Vidkritokutova a. Primary glaucoma b. Glaucoma with normal (low) grip 2. Zakritokutova a. gostra b. podgostra v. chronic B. Congenital glaucoma 1. Primary congenital glaucoma 2. Congenital glaucoma is associated with another eye pathology 3. Congenital glaucoma is associated with an advanced congenital pathology C. Secondary glaucoma 1. Pigmented 2. Exfoliation syndrome 3. Phacogenic 4. Uveal 5 Iridocorneoendothelial syndrome 6. Traumatic 7. Postoperative 8. Neovascular 9. Advancing episcleral venous pressure 10. Steroid D. Absolute glaucoma Kintsevsky heritage of all species uncontrolled and glaucoma - important eye strain, blindness, often - pain

Clinical classification developed by A.P. Nesterov and A.Ya. Bunin and adopted at the III All-Russian Congress of Ophthalmologists (1975). ACUTE ATTACK OF GLAUCOMA Form of glaucoma Stage IOP condition Dynamics of visual function Closed-angle Open-angle Initial I Developed II Unstabilized Stabilized. Normal (A) Moderately elevated (B) Far advanced III High (C) Mixed Terminal IV

The hereditary form of congenital glaucoma is an autosomal recessive disease, which is based on underdevelopment of the drainage zone of the eye

CAUSES OF CONGENITAL GLAUCOMA Unresolved embryonic tissue in the angle of the anterior chamber Anterior attachment of the iris root Underdevelopment of the trabecula Absence of Schlemow's canal Underdevelopment of intrascleral outflow tracts

Clinical signs of congenital glaucoma Photophobia, blepharospasm, lacrimation Increase in the size of the cornea (from 9 to 22 mm) Edema, swelling, clouding of the cornea. Ruptures of Descemet's membrane Expansion of the limbus (from 1 mm to 3-4 mm) Staphylomas of the sclera Increase in the size of the eyeball (from 16 to 35 mm) Changes in the structures of the APC > IOP Glaucomatous excavation

OBJECTIVE CHANGES IN OAG (in advanced and late stages of the disease) Emmysary symptom Cobra symptom Pathological pigmentation of the optic disc Dispersion of the iris pigment Atrophy of the iris stroma Leaching of the pigment border Presence of pseudoexfoliations Glaucomatous excavation of the optic disc Changes in the hydrodynamics of the eye Changes in the visual field

Clinic of o/u glaucoma: Arises and progresses unnoticed Absence of pain and discomfort Complaints of periodic appearance of rainbow circles, blurred vision, sometimes headache in the superciliary area

Risk factors for an acute attack of glaucoma Nervous tension Fatigue Staying in the dark Drug-induced mydriasis Prolonged head tilt Stress Taking large amounts of fluid

Scheme of the development of an acute attack of glaucoma. C h a r t T i t l e A c u c t u r e o f gla u co m a F u l l B l o c k S h i p t i v e i d i d o x p U s t a l d i a ph r a g m O f t e x t e x t o f t h e vitreous body o c l u s i o n a b e c u l a r y Z o n e B o m b a r i r iris I n c e l e r i n g I n g d R e a r c h a m m e r W e r d e r i n g i n g flow S h e n t i n g r i d o x r u s t i l a l d i a f r a g m

links in the pathogenesis of glaucoma Specific atrophy of the optic nerve head with excavation. Hemodynamic disturbances in the optic nerve system OPTIC NEUROPATHY decreased perfusion Impaired autoregulation increased IOP apoptosis

Control of IOP IOP - pressure of the contents of the eyeball on its walls Function of eye rigidity and its volume Depends on - production of intraocular fluid - outflow of intraocular fluid - volume of anatomical structures - resistance and blood supply of the vessels of the eye

Volumetric model of normal and pathological differential light sensitivity as a function of localization in the visual field (Bebie. H., Fankhauser F., 1983) “Visual Island”

Features of glaucomatous changes in the visual field Changes in the peripheral visual field in glaucoma. a - narrowing of the field of view on the nasal side, breakthrough of Bjerrum’s scotoma to the periphery; b - concentric narrowing; c - tube field of view; d - residual island of the visual field.

In the first stage, a relative arcuate defect is detected. Isopter depression is often detected in the region from 5 to 25 degrees. from the fixation point, it is possible to identify a small scotoma in the same area. Five stages of development of glaucomatous visual field defects (Authorn, 1978) I

In the second stage, the appearance of deep round-shaped defects, or scotomas, that do not merge with the blind spot is noted; they are often detected in the nasal region and an increase in the size of the blind spot. Five stages of development of glaucomatous visual field defects (Authorn, 1978) II

In the third stage, an arcuate scotoma appears, often with a breakthrough to the periphery in the nasal region, which leads to the formation of a classic nasal step. Five stages of development of glaucomatous visual field defects (Authorn, 1978) III

In the fourth stage, a widespread circular or semicircular scotoma may appear, leaving an island of vision in the center, as well as peripheral vision. Five stages of development of glaucomatous visual field defects (Authorn, 1978) I V

In the fifth stage, the center of the optic hill practically collapses and only residual vision on the temporal side remains. Five stages of development of glaucomatous visual field defects (Authorn, 1978) V

The number of capillaries in the layer of the cribriform plate is 3300. 1 bundle of axons is supplied with blood by 8 capillaries. There are 2500 capillaries in 1 mm of the optic nerve; 1 capillary supplies blood to 312 axons. Biological vulnerability of the optic nerve

Biological vulnerability of the optic nerve absence of capillaries inside the axon bundles of the optic nerve insufficiency of blood supply to the axons decrease in the partial pressure of oxygen in post-capillary venules disproportion between the length of the axon (15 cm) and its thickness (15 mm)

Biological vulnerability of the optic nerve extreme compression of axons in the cribriform plate absence of the myelin sheath absence of lymphatic capillaries in the optic nerve absence of sensory innervation in the optic nerve

Anatomy of the blood supply to the optic nerve disc The main source is the posterior short ciliary arteries shown on the left side of the figure [according to Cioffi, van Buskrik, 1996].

Quantitative criteria for the stage of glaucoma with a uniform expansion of the visible zone of axonal atrophy in all directions (type I excavation), if the E/D is:< 0, 4 — преглаукома; 0, 4 — 0, 5 — начальная глаукома; 0, 6 — 0, 7 — развитая глаукома; 0, 8 — 0, 9 — далеко зашедшая стадия. Достоверность показателей верифицируется меньшими размерами экскавации на парном глазу и наличием характерных для глаукомы нарушений зрения:

Approximate forms for recording and sketching ophthalmoscopy data of the optic disc in the presence of signs of glaucoma are as follows. Example 1. Slight deflection of the temporal half of the optic disc of the left eye with an atrophy sector within one (inferotemporal) quadrant with moderate thinning of the disc with the presence of a beta zone in the disc atrophy sector with a width of about 0.1 (to the diameter of the disc). There are no hemorrhages.

Approximate forms for recording and sketching ophthalmoscopy data of the optic disc in the presence of signs of glaucoma are as follows. Example 2. A barely noticeable total sagging of the optic disc of the right eye, emphasized by the course of the vessels, with a rounded zone of blanching in the center measuring E/D 0.7. In the 7 o’clock meridian there is a streak-like hemorrhage along the edge of the disc.

Approximate forms for recording and sketching ophthalmoscopy data of the optic disc in the presence of signs of glaucoma are as follows. Example 3. The optic disc of the left eye in the entire temporal half with a transition below to part of the nasal half is grayish-white, excavated. The zones of sagging and blanching coincide. Over a long distance (in a sector of more than 6 hours), IU fishing is completely absent. The adjacent beta zone reaches a width of 0.3 (to the disc diameter).

Approximate forms for recording and sketching ophthalmoscopy data of the optic disc in the presence of signs of glaucoma are as follows. Example 4. Total atrophic deep excavation of the optic disc of the right eye. Circular halo (Halo).

GBOU RM SPO (SSUZ)Saransk Medical College

Methodological development

for an open theoretical lesson on the topic:

« Violations of the hydrodynamics of the eye. Etiology, clinical manifestations, treatment. Emergency care for an acute attack of glaucoma"

Item - Eye diseases

Speciality - General Medicine

Qualification - paramedic

The level of education - increased

Completed by Rev. Shamshetdinova G.Kh.

Saransk 2012

Explanatory note

This lesson is devoted to the most pressing topic of our time, glaucoma. PAccording to literature data (including WHO), the number of glaucoma patients in the world reaches 100 million people. Glaucoma ranks first among the causes of visual disability.

The methodological development is intended for the training of paramedical workers in the specialty “General Medicine”, qualification “Paramedic” (advanced level of education) in the subject “Eye Diseases”.

This lesson is theoretical and is conducted in accordance with the lecture plan. To facilitate the perception of lecture material in class, multimedia illustrations are used.

During the lesson, in order to better perceive the material, fragments of techniques are used:critical thinking technology (compiling clusters and syncwines), which allowsorganizedtprocesstraining, aimed at the active activity of understanding, applying, analyzing, summarizing or evaluating information obtained or created through observation, experience, reflection, reasoning or communication as a guide to action or the formation of beliefs; case method allowingconsolidate the knowledge acquired in previous classes,develop skills in the practical use of conceptual schemes and familiarize students with schemes for analyzing practical situations, as well as develop skills in group problem analysis and decision-making (as part of training procedures);health saving technologies Anddevelopmental learning technologies .

To control and consolidate the acquired knowledge, situational tasks are carried out at the end of the lesson. Great importance is attached to the independent work of students; it was proposed to prepare short messages, reflecting their opinion on the topic under consideration.

Tasks:

1. To study the anatomical and physiological features and functions of the visual analyzer, their changes in glaucoma.

2.Study the research methods used in diagnosing glaucoma.

3.Study the clinical manifestations of glaucoma.

4. To study emergency care for acute and subacute attacks of glaucoma and the tactics of managing a patient with glaucoma.
5. Study the rules of dispensary observation of glaucoma patients.

Purpose of the lesson:

Educational - study the concept of etiopathogenesis, clinical manifestations, principles of treatment of glaucoma.

Developmental - promote the development of clinical thinking, memory, attention; instill the ability to work with educational and technical literature.

Educating - to promote the development of hard work, accuracy, a sense of responsibility and honesty, to influence the aesthetic views of students, to contribute to the formation of professional qualities in the work of a paramedic.

Interdisciplinary connections:

anatomy;

physiology;

therapy;

obstetrics;

pediatrics;

psychology.

Lesson timing:

1. Organizational moment: checking students’ attendance, checking readiness for the lesson, announcing the topic of the lesson, tasks and goals of the lesson, introductory word from the teacher - motivation for the lesson - 5 minutes.

2. Presentation of new material - 50 min.

2.1 Presentation of the material - 25 min.

2.2 Physical education minute - 3-5 min.

2.3 Presentation of the material - 20 min.

3. Student messages - 15 min.

4. Reinforcing the material (compiling clusters, syncwines, situational tasks) - 15 min.

5. Summing up - 5 min.________________________________

Total: 90 min.

Progress of the lesson.

1 Introductory word (5 minutes).

This lesson is devoted to a pressing topic of our time, namely the disease that ranks first among the causes of blindness and visual disability, glaucoma.Between 1% and 2% of the population over 40 years of age is affected by this disease.According to WHO, there are more than 100 million patients with glaucoma in the world, and their number is steadily increasing every year. According to the forecast, by 2030 this number could double.

Even at the level of modern knowledge, it remains unclear what triggers the occurrence of glaucoma. Many diseases inherent in old age contribute to its development. These include diseases of the cardiovascular system (atherosclerosis, hypertension), the endocrine system (diabetes mellitus, thyroid diseases), and the nervous system.

Hereditary factors play a huge role in the occurrence of glaucoma. It is 35%. Blood relatives of patients with glaucoma constitute the main risk group and should undergo an annual preventive eye examination.

2 Presentation of new material (50 minutes):

Glaucoma - a large group of eye diseases, each of which is characterized by a constant or periodic increase in intraocular pressure caused by impaired outflow of aqueous humor from the eye, resulting in the development of a special form of optic nerve atrophy with excavation in the disc area. Characterized by a triad of signs:

1 increase in intraocular pressure.

2 progressive glaucomatous optic atrophy.

3 progressive decrease in central and peripheral vision.

Etiological factors the occurrence of glaucoma: heredity, metabolic disorders, hemodynamic and endocrine disorders, local degenerative changes.

Classification:

By origin: primary, secondary and combined with developmental defects of the eye and other structures.

By patient age: congenital, infantile, juvenile and adult glaucoma.

According to the mechanism of increase in intraocular pressure: open-angle, closed-angle, dysgenesis of the anterior chamber angle, pretrabecular block and peripheral block.

By IOP level: hypertensive and normotensive.

According to the degree of damage to the optic nerve head: initial, developed, advanced and terminal.

Downstream: stable and unstable.

Pathogenesis associated with impaired outflow of aqueous humor - with the development of trabeculopathy and functional canalicular block, and is common to all forms of primary open-angle glaucoma. Violation of the hydrodynamics of the eye leads to an increase in IOP above the normal level and the development of optic disc atrophy of the glaucomatous type.

Congenital glaucoma.

The cause of congenital glaucoma is unresolved embryonic mesodermal tissue, anterior attachment of the iris, dysgenesis of the aqueous humor, leading to difficulty in the outflow of aqueous humor, and then to an increase in IOP.

Clinic. Congenital glaucoma is characterized by an inconspicuous course. You can suspect glaucoma based on mild photophobia, lacrimation, restless behavior, and the child’s sleep. The cornea, anterior chamber of the eye and pupil increase in size. The cornea may look like fogged glass or white porcelain. This appearance is most often caused by edema or dystrophy of the cornea.

Edema can be distinguished from dystrophy when one of the hypertonic solutions (glucose, urea, glycerin and even saline solution) is instilled onto the cornea: the edema disappears or decreases after instillation. But not only the size of the cornea can be increased to about 11 mm (and not 9 mm), the depth of the anterior chamber is 3-4 mm (and not 2 mm), the pupil width is 3-4 mm (and not 2 mm), but also the entire eyeball , and this increase reflects the stage of the glaucomatous process.

Enlargement of the entire eye is the so-called buphthalmos (bulls eye) or hydrophthalmos (dropsy of the eye). High ophthalmotonus is also evidenced by the presence of congestive eye injection with characteristic symptoms of “emissary”, “cobra’s head”, and processed “body of the medusa”. The magnitude of the increase in intraocular pressure is determined by palpation as T+2 and even higher (T+3).

If the cornea is transparent, then with ophthalmoscopy one can detect in the area of ​​the optic nerve disc (papilla) a shift of the vascular bundle to the nasal side and pathological atrophic excavation of the disc itself.

All of the listed glaucomatous changes in various structures of the eye cannot but affect visual functions: they are reduced according to the stage of the process and the severity of symptoms.

Treatment: Surgical - goniotomy operation. The purpose of goniotomy is to destroy the mesodermal tissue in the angle of the anterior chamber and open the outflow of moisture from the anterior chamber through Schlemm's canal; or goniotonia with goniopuncture - + creation of additional outflow of intraocular fluid under the conjunctiva

If help is not provided, optic nerve atrophy will result; by one year the eye will go blind.

Open angle glaucoma accounts for more than 90% of all cases of this disease. With this form of glaucoma, the iridocorneal angle is open, which is why it gets its name. For reasons not yet fully understood, the outflow of intraocular fluid is disrupted. This leads to a buildup and a gradual but constant increase in pressure, which can ultimately destroy the optic nerve and cause vision loss.

In most casesopen angle glaucoma arises and progresses unnoticed by the patient, who does not experience any discomfort and consults a doctor already at a late stage of the disease, when he notices worseningvisual acuity. Complaints about the appearancerainbow circlesaround light sources, periodicblurred vision noted only by 15-20% of patients. These are the symptoms that appear whenand may be accompanied by pain in the eyebrow area and head.

Open angle glaucoma As a rule, it affects both eyes, in most cases occurring asymmetrically.

The leading symptom of the disease is increasedintraocular pressure (IOP) . Intraocular pressure at open angle glaucoma increases slowly and gradually as outflow resistance increasesintraocular fluid (IOH) . In the initial period it is unstable, then it becomes persistent.

The most important diagnostic signopen angle glaucoma is a changefield of view. First of all, these defects are determined in the central sections and are manifested by the expansion of the boundaries of the blind spot, the appearance of arched prolapses. These disorders are detected in the early stagesglaucoma, with special studiesfields of view. As a rule, patients themselves do not notice these changes in everyday life.

With further developmentglaucomatous process are revealed peripheral visual field defects . Narrowing field of viewoccurs predominantly on the nasal side, then the narrowing of the field of vision concentrically covers the peripheral parts until it is completely lost. Dark adaptation worsens. These symptoms appear against the background of a persistent increaseintraocular pressure (IOP) . A fall visual acuityspeaks of a severe, advanced stage of the disease, accompanied by almost completeoptic nerve atrophy .

Angle-closure glaucoma - a rarer form of glaucoma. Women get sick more often than men. Predisposing factors for the development of this formglaucoma are:

anatomical predisposition;

functional closure factorsanterior chamber angle ;

age-related changes in the eye.

Anatomical features of the structureeyeball , predisposing to the developmentangle-closure glaucoma serve small eye size, shallow anterior chamber, largelens , narrowanterior chamber angle , farsightedness . Functional factors include increased productionintraocular fluid (IOH) , increased blood supplyintraocular vessels , pupil dilation .

With this form of glaucoma, the pressure in the eye rises quickly. Anything that causes the pupil to dilate, such as dim light, certain medications, and even dilating eye drops given before an eye exam, can cause the iris to block the flow of fluid in the eye. When this form of the disease occurs, the eyeball quickly hardens and the sudden pressure causes pain and blurred vision.

Flowangle-closure glaucoma in most patients it is characterized by periodic, initially short-term, and then increasingly long periods of increaseintraocular pressure (IOP) . In the initial stage, this is due to mechanical closure of the zonetrabeculae iris root , which is due to the anatomical predispositions of the eye. Whereinoutflow of intraocular fluid (IOH) decreases. When fully closedanterior chamber angle a condition calledacute attack of angle-closure glaucoma . In the intervals between attacks, the angle opens.

During such attacks, adhesions gradually form between the iris and the wall of the anterior chamber angle, the disease gradually becomes chronic with a constant increase inintraocular pressure (IOP) .

Duringangle-closure glaucoma The following phases can be distinguished:

preglaucoma;

acute attack of glaucoma;

chronic course of glaucoma.

Preglaucoma occurs in individuals who do not have clinical manifestations of the disease, but upon examinationanterior chamber angle It turns out that it is either narrow or closed. Betweenpreglaucoma Andacute attack of glaucoma possible transient symptoms of visual discomfort, the appearance of rainbow circles when looking at a light source, short-termvision loss . Most often, these phenomena occur during prolonged exposure to darkness or emotional excitement (these conditions contribute to pupil dilation, which completely or partially reducesoutflow of intraocular fluid ) and usually disappear on their own, without causing much concern in patients.

Acute attack of glaucoma occurs under the influence of provoking factors, such as nervous tension, fatigue, prolonged exposure to darkness, drug-induced pupil dilation, prolonged work in a position with the head tilted, and intake of large amounts of liquid. Sometimes an attack appears for no apparent reason. The patient complains abouteye pain and in the head, especially in the back of the head,nausea, often vomiting, general weakness, blurred vision , appearance rainbow circles when looking at a light source. An acute attack of glaucoma is often mistaken for a migraine, hypertensive crisis, or poisoning, which leads to serious consequences, since such a patient must be helped in the first hours of the disease.

Painful sensations are caused by compression of nerve elements inroot of the iris Andciliary body . Visual discomfort is associated with corneal edema.

During a visual examination without special instruments, one can only notice a sharp dilation of the vessels on the anterior surface of the eyeball, the eye becomes “red”, somewhat with a bluish tint (congestive vascular injection). The cornea becomes cloudy due to the development of edema. Noteworthy is the dilated pupil that does not respond to light. At the height of the attack, it can sharply decreasevisual acuity . Intraocular pressure can increase to 60-80 mmHg. Art.,drainage of fluid from the eye stops almost completely. The eye feels dense to the touch, like stone.

If, within the next few hours after the onset of an attack, the pressure is not reduced using medications or surgery,eye faces irrevocablevision loss !!! Acute attack of glaucoma is an emergency and requires emergency medical attention!!!

Over time, the disease becomes chronic. This typeglaucoma occurs with a progressive riseintraocular pressure (IOP) , subacute attacks and increasing blockadeanterior chamber angle . These processes naturally end with the developmentglaucomatous optic atrophy , loss of visual function .

Urgent Care:

1 instillation of pilocarpine 1% for the first 2 hours every 15 minutes, then 2 hours. every 30 minutes, during track. 2 hours 1 time per hour. Then 3-6 times per day depending on the degree of IOP reduction.

2 0.5% timolol twice a day.

3 orally or parenterally osmotic diuretics, IM or IV furosemide 20-40 mg.

4 orally acetazolamide 0.25-0.5 g 2-3 times a day.

5 dorzolamide 2% 3 times a day.

6 IM lytic mixture: 1-2 ml 2.5% aminosine + 1 ml 2% diphenhydramine + 1 ml 2% promedol. After administration of the mixture, bed rest for 3-4 hours prevents orthostatic collapse.

7 to relieve an attack and prevent repeated attacks - laser iridectomy in both eyes.

8 if the attack could not be stopped within 12-24 hours, surgical treatment is indicated.

Secondary glaucoma is a complication of inflammatory diseases or injuries of the eye, as a result of which there is an outflow of fluid through the drainage system.

Stages of glaucoma:

Initial: the boundaries of the visual field are normal, but there are changes in the paracentral parts of the visual field (individual scotomas in zone 5-200 , Bjerum's arcuate scotoma, widening of the blind spot). M.b. initial signs of excavation of the optic nerve head.

Developed: pronounced changes in the visual field in the paracentral region combined with a narrowing of its peripheral boundaries by more than 100 in the upper or lower nasal segment. The excavation of the optic disc approaches the marginal one.

Far advanced: the border of the visual field is concentrically narrowed and in one or more segments is less than 150 from the point of fixation, there is a marginal excavation of the optic nerve head.

Terminal: complete loss of vision or preservation of light perception with incorrect light projection. The field of view cannot be examined.

IOP level: a-within normal limits (18-24 mm Hg); c-moderately elevated (25-32 mm Hg); c-high blood pressure (33 mm Hg).

Treatment:

1 first choice drugs: 1% pilocarpine, 0.25% and 0.5% timolol, 0.005% latanoprost. If the drug is ineffective, it is replaced with another drug of first choice or a combination of first and second choice (0.25% and 0.5% betaxolol, 1-2% proxodolol, 2% dorzolamide)

2 enzyme antioxidants - superoxide dismutase-Erisod.

3 1% emoxipine subconjunctival and parabulbar 10 injections. The effect of emoxipine is enhanced when combined with tocopherol. Aevit 1 capsule 2-3 times a day with vitamins gr. IN.

4 antispasmodics - orally xanthinol nicotinate 150 mg 3 times a day after meals for 2 months. or IM 15% 2 ml once a day for 10 days. Theophylline 250 mg 3 times a day for 2 weeks; Cavinton 5 mg 3 times a day for 1 month; pentoxifylline after meals 400 mg 3 times a day.

5 angioprotectors - dicinone 0.25 g 3 times a day for 2-3 months; prodectin0.25g 3-4r/d2-4wk

6 nootropic drugs - nootropil 30-160 mg/kg/day for 6-8 weeks. Picamilon 10 mg 3 times a day; antihypoxants (cytochrome C).

7 vitamin therapy.

8 piracetam - 30-160 mg/kg/day 6-8 weeks.

3.Student messages

Students give a presentation on the topic: “Dispensary observation of a glaucoma patient”- 15 minutes.

4. Reinforcing the material (compiling clusters and syncwines, situational tasks) - 15 min.

How to create a cluster

1. Write the keyword or sentence in the middle of a large piece of paper or on the board.

2. Write down words or sentences that come to mind about the topic.

3. As you come up with ideas, you write them down.

4. Write down as many ideas as come to your mind.

How to make a syncwine

Sinkwine is a “poem” consisting of five lines. In syncwine, a person expresses his attitude to the problem.

The order of writing a syncwine:

The first line is one keyword that defines the content of the syncwine.

The second line contains two adjectives that characterize this concept.

The third line is three verbs showing the action of the concept.

The fourth line is a short sentence in which the author expresses his attitude.

The fifth line is one word, usually a noun, through which a person expresses his feelings and associations associated with this concept.

Make a cluster for the word:

Glaucoma Congenital glaucoma

Disease

Decreased visual acuity

Limitation of field of view

Disability

Glaucoma attack

Make a syncwine for the word:

Glaucoma Angle-closure glaucoma

Disease

Decreased visual acuity

Limitation of field of view

Disability

Glaucoma attack

TASK No. 1.

A 72-year-old patient was treated in the urology department for urolithiasis. After the injection of atropine, severe pain appeared in the left eye, and vision deteriorated sharply. Objectively: visual acuity of the left eye is 0.01, the eye is dense but painless on palpation, congestive injection of the vessels of the eyeball, the cornea is cloudy. Make a diagnosis.

Prescribe treatment

Acute attack of primary glaucoma of the left eye

TASK No. 2.

During your night duty, the nurse at the second post, an elderly pensioner, suddenly had an attack of sharp headaches radiating to her left eye, which, according to the patient, she had been seeing poorly lately. There was vomiting, the pulse was slow, blood pressure was 180/100 mmHg, which, however, is not uncommon for the patient. During an external examination, you were able to detect a moderate narrowing of the left palpebral fissure, redness of the left eyeball, a cloudy and dilated pupil on the left, which almost does not react to light. The patient sees only the light from a light bulb with this eye.

Taking into account the fact that the patient suffered an acute respiratory illness on her feet a few days before this attack, try to make a presumptive diagnosis.

1. Acute iridocyclitis

2. Hemorrhage into the cavity of the eyeball

3. Acute attack of glaucoma

TASK No. 3.

In the eye department of an interdistrict hospital, a middle-aged woman is being examined, in whom the following was revealed in the left eye: visual acuity 1.0, visual field is normal; periodically - pain in the eye, accompanied by blurred vision, the appearance of rainbow circles around the light source, an increase in intraocular pressure to 43-46 mm Hg. These exacerbations are quickly relieved by instillation of a 1% pilocarpine solution every 2-3 hours in combination with instillations of Armin solution - morning and evening. The second eye is clinically healthy.

What do you decide to do in this case?

1. Discharge the patient for outpatient treatment

2. Offer the patient surgery

5. Summing up - 5 minutes .

List of used literature

Main literature

1. Dubovskaya L.A. Eye diseases, M., 1986.

2. Ruban E.D. Eye diseases, M., Phoenix, 2010.

3. Morozov V.I., Yakovlev L.A. Pharmacotherapy of eye diseases. M., Medicine, 2009.

additional literature

Avetisov E.S. Handbook of ophthalmology, M., 1978.

Broshevsky T.I., Bochkareva A.A. Eye diseases, M., 1983.

Dzhaliashvili O.A., Gorban A.I. First aid for acute diseases and eye injuries, M., 1995.

Zhivkov E., Denev V. Eye symptoms in general diagnostics, M., 2000.

Zolotareva M.M. Eye diseases, M., 1964.

Kapaeva V.G. Eye diseases M.: Medicine 2002.

Kovalevsky E.I. Ophthalmology M.: Medicine 2006.

Kovalevsky E.I. Guide to practical exercises for the courseeye diseases, M., 2007.

Krasnov M.L., Margalis M.G. Ophthalmology outpatient doctor,M., 1969.

Ryabchikova T.V., Nazarova N.A. Nursing process of educational methodstechnical manual, M., 2000.

Sidorenko E.I. Ophthalmology M.: “GEOTAR - MED” 2003.

Shilyaev V.G. Work of paramedical personnel in ophthalmologydepartments of hospitals and clinics, M., 1999.