Glaucoma - Information Overview

Glaucoma is a chronic eye disease, the most important symptoms of which are increased intraocular pressure, as well as deterioration of visual functions (field and visual acuity, adaptation, etc.) and the development of marginal excavation of the optic nerve papilla.

Glaucoma is a very common and dangerous eye disease. Glaucoma accounts for 4% of all eye diseases. Now glaucoma is the main cause of incurable blindness and very deep disability. 25% of all blinded from various eye diseases are patients who lost their sight from glaucoma.

The main cause of irreversible blindness in the world is various forms of glaucoma. All types of glaucoma can be divided into primary (damage to both eyes, no data on previous damage) and secondary (damage to the eye as a result of an infectious process, mechanical impact or neovascularization, often only one eye is affected, sometimes the damage is bilateral).

Primary glaucoma is divided into separate forms depending on the width of the angle of the anterior chamber of the eye. In closed-angle glaucoma, there is an increase in intraocular pressure as a result of a violation of the outflow of intraocular fluid during the formation of synechiae between the iris and the trabecular meshwork, and in open-angle glaucoma, intraocular fluid freely enters the trabecular meshwork. There are also different types of primary glaucoma depending on the age of manifestation of the disease. Glaucoma that develops soon after birth is called congenital; juvenile glaucoma develops from childhood to 40 years; glaucoma that manifests after 40 years is called open-angle glaucoma of adults.

The main symptoms of glaucoma were described by A. Graefe (1857):

1. increased intraocular pressure;
2. decreased visual function;
3. changes in the fundus of the eye.

Glaucoma occurs at any age (even in newborns), but a significant prevalence of glaucoma is observed in old and senile age.

Definition of glaucoma

Since the term was first used in ancient Greece, the definition of glaucoma has changed dramatically; it now means different things to different people. The classification is still being refined, which sometimes causes confusion when discussed. Until the second half of the 19th century, glaucoma was diagnosed based on the presence of symptoms: blindness or, later, pain. The development of statistics, the availability of a tonometer, and the development of the concept of the disease as an abnormality led to the definition of glaucoma as an increase in intraocular pressure of more than 21 mm Hg (exceeding double the standard deviation from the mean) or more than 24 mm Hg (exceeding triple the standard deviation from the mean).

Numerous studies conducted in the 1960s showed that only 5% of people with intraocular pressure above 21 mmHg develop optic nerve damage and visual field narrowing, while 1/2 of patients with optic nerve and visual field changes characteristic of glaucoma have intraocular pressure levels within the normal range. This led to a global rethinking of the definition of glaucoma. Many authors began to use the terms "low-tension glaucoma", "normal-tension glaucoma" and "high-tension glaucoma". More and more attention is paid to the optic nerve, and many researchers do not take into account the characteristic changes caused by angle-closure glaucoma (pain and associated changes in the cornea, iris and lens), focusing all their attention only on the optic nerve. This led to the definition of glaucoma as a characteristic optic neuropathy. Later, some authors divided glaucoma into IOP-dependent and IOP-independent. Glaucoma is defined as a process that leads to characteristic changes in the tissues of the eye, partly caused by intraocular pressure, regardless of the level of intraocular pressure. Since almost all the signs and symptoms of early and advanced glaucoma were observed in people who did not suffer from glaucoma, it is very important to identify signs that are characteristic only (or almost only) of glaucoma.

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Epidemiology of glaucoma

Glaucoma occurs in people of all ages and in all geographic areas. Estimates of its prevalence vary widely because of differences in how glaucoma is defined, methods of testing, and the prevalence of a family of loosely related conditions called primary open-angle glaucoma in the population. Congenital glaucoma is an extremely rare, separate entity. Most types of juvenile glaucoma are genetically determined and, although more common than congenital types of open-angle glaucoma, are considered relatively rare forms of the disease. Most patients with glaucoma are over 60 years of age. The prevalence of glaucoma in African Americans over 80 years of age may exceed 20%.

Generalizing the prevalence of blindness due to glaucoma is difficult because glaucoma is a group of diseases and is defined in different ways. However, the prevalence of blindness due to glaucoma clearly increases with age, especially in African American populations.

It is estimated that glaucoma affects 2.5 million people worldwide each year. Three million people are blind due to open-angle glaucoma. In the United States, about 100,000 people are blind in both eyes due to glaucoma.

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Risk factors for developing glaucoma

1. Organization of genetic material
Family history of vision loss due to glaucoma Identifying the Glaucoma Gene
2. Intraocular pressure data
Mm Hg	The likelihood of eventually developing glaucoma
>21	5%
>24	10%
>27	50%
>39	90%
3. Age
Years	Glaucoma prevalence rate
<40	Rarely
40-60	1%
60-80	2%
>80	4%
4. Vascular factors
Migraine Vasospastic disease Raynaud's disease Hypotension Hypertension
5. Myopia
6. Obesity

Risk factors for blindness due to glaucoma

1. The course of the disease can cause blindness*
2. Low availability of care:
   • geographic;
   • economic;
   • unavailability of care
3. Low self-care ability
   • intellectual disability;
   • emotional limitation;
   • socio-economic disadvantage

* The severity of primary open-angle glaucoma can vary greatly: in some patients, the disease does not progress even without treatment, while in others, despite treatment, blindness quickly occurs.

Glaucoma - Causes

Pathophysiology of glaucoma

The hallmark of glaucoma is damage to the tissues of the eye, especially the optic nerve. Toxic substances and autoimmune mechanisms cause damage and, ultimately, death of retinal ganglion cells, leading to tissue atrophy and structural damage, which can increase the damaging effects of intraocular pressure.

The final stage of the pathogenesis of all types of primary open-angle glaucoma is the death of retinal ganglion cells due to apoptosis or sometimes necrosis. This can lead to further damage to the retina, optic nerve and brain. The existing feedback loops complement the simplified scheme.

Pathogenesis of eye tissue damage in glaucoma

A. Intraocular pressure (any level) → Mechanical deformation of tissue (cornea, cribriform plate, neuron, blood vessels) → Cell damage - vascular damage → Cell death due to necrosis, more often apoptosis → Tissue atrophy (thinning of the nerve fiber layer, etc.) →

B. Increased cytotoxicity, growth factor deficiency, autoimmune mechanisms → Cell damage → Cell death (especially retinal ganglion cells) → Tissue atrophy → Structural changes

Some factors involved in tissue damage in glaucoma

• Mechanical damage
  • Stretching of the cribriform plate, blood vessels, posterior corneal epithelial cells, etc.
• Abnormal structure of glial, nervous or connective tissue
• Metabolite deficiency
  • Direct compression of neurons, connective tissue and vascular network of intraocular pressure.
  • Neurotrophil deficiency:
    • secondary, as a result of mechanical blockade of axons;
    • genetically determined;
    • Nerve growth factor deficiency
  • Ischemia and hypoxia:
    • violation of autoregulation of the vessels of the retina and choroid;
    • decreased perfusion:
      • acute / chronic,
      • primary / secondary;
    • oxygen transport disorder
• Autoimmune mechanisms
• Violation of defense mechanisms
  • Deficiency or inhibition of NO synthase
  • Abnormal heat shock protein
• Toxic agents for retinal ganglion cells and other tissues
  • Glugamat
• Genetic predisposition
  • Abnormal optic nerve structure:
    • large holes in the lattice plate;
    • large scleral canal;
    • connective tissue anomaly;
    • vascular bed anomaly
  • Trabecular meshwork anomaly:
    • decreased permeability of the intercellular matrix;
    • endothelial cell abnormality;
    • abnormal molecular biology

Symptoms of Glaucoma

An acute attack of glaucoma can develop at any stage of the disease. An acute attack of glaucoma can develop without any externally visible causes. In other cases, the appearance of an acute attack of glaucoma is facilitated by severe emotional shock, an infectious disease, errors in eating or drinking, erroneous instillation of atropine or other means of dilating the pupil into the eye. Therefore, when treating elderly patients prone to increased intraocular pressure, it is necessary to refrain from prescribing these means.

An acute attack of glaucoma in a healthy eye often occurs without any apparent reason.

An acute attack of glaucoma begins suddenly, most often at night or in the morning. There is a sharp pain in the eye, orbit. The headache is accompanied by vomiting, general weakness of the body. Patients lose sleep and appetite. Such general symptoms of an acute attack of glaucoma can be the cause of diagnostic errors.

An acute attack of glaucoma is accompanied by pronounced symptoms from the eye: swelling of the eyelids and conjunctiva, and lacrimation often appears.

Glaucoma - Symptoms and Signs

Diagnosis of glaucoma

The emphasis of clinical examination of a patient with suspected primary open-angle glaucoma differs from the emphasis of standard examination. The most important stage is careful detection of the afferent pupillary defect (APD). The afferent pupillary defect can be detected before changes in the visual fields occur. In addition, the afferent pupillary defect indicates damage to the optic nerve, which allows you to begin searching for the causes of this damage. Searching for the afferent pupillary defect is an integral part of the examination of a patient suffering from glaucoma.

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External examination and biomicroscopy

A biomicroscopic examination of a patient with glaucoma differs from a standard examination in that the physician pays attention to local side effects of medications the patient may be using and signs characteristic of glaucoma, such as Krukenberg spindles.

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Gonioscopy

Gonioscopy is mandatory for all patients with glaucoma. During the examination, attention should be paid to signs of pigment dispersion syndrome, exfoliation syndrome, and signs of recession of the anterior chamber angle. Gonioscopy should be performed annually, since the initially open angle of the anterior chamber of the eye may narrow with age, ultimately leading to chronic or, rarely, acute closure of the anterior chamber angle. Gonioscopy should be performed after the start of miotics or after a change in their concentration, due to the fact that they can cause significant narrowing of the anterior chamber angle. The Specf scale of gonioscopic changes is a valuable clinical method that allows for a rapid quantitative description and recording of the state of the anterior chamber angle of the eye.

Posterior pole

Primary open-angle glaucoma is initially a disease of the optic nerve head. Correct assessment of the optic nerve is an essential part of the examination and subsequent management of a patient with suspected glaucoma. Assessment of the optic nerve is the most important aspect in the diagnosis of primary open-angle glaucoma. In the management of a patient with glaucoma, the optic nerve head is second in importance after a thorough anamnesis.

The optic disc is best examined with a dilated pupil. After dilating the pupil, a stereoscopic examination of the optic disc is performed using a slit lamp and powerful converging lenses of 60 or 66 D. The best method of examination is with a light beam in the form of a narrow slit at high magnification (1.6 or 16X) using a Haag-Streit 900 series slit lamp. This method provides the physician with an idea of the topography of the optic disc. The disc is also measured. To measure the vertical size of the disc, the light beam is expanded until the horizontal dimension of the beam coincides with the width of the disc. Then the beam is vertically narrowed until the vertical dimension of the beam coincides with the vertical diameter of the disc. Then the value is marked on the slit lamp scale, which, after appropriate correction, corresponds to the vertical diameter of the disc. The values obtained differ slightly when using Volk and Nikon lenses. It is accepted that when using 60 diopter lenses, the scale value is increased by 0.9, for 66 diopter lenses no correction is required, and for 90 diopter lenses the scale value is multiplied by 1.3. The vertical diameter of the optic nerve disc is normally 1.5-1.9 mm.

The next step is direct ophthalmoscopy. The ophthalmoscope beam is narrowed to produce a spot on the retina that is approximately 1.3 mm in diameter. This size corresponds to the medium beam on some Welch-Allyn ophthalmoscopes and to the smallest beam on other Welch-Allyn ophthalmoscopes. The examiner must know the beam size of the ophthalmoscope he or she is using. This can be calculated by projecting a spot of light on the retina near the optic disc, comparing the vertical diameter of the spot to the vertical diameter of the disc, and then using a high-power converging lens to accurately measure the vertical size of the spot. Once the spot size has been measured, the optic disc can be measured with a single direct ophthalmoscope. When examining eyes that are hyperopic or myopic by more than 5 D, the disc will appear larger or smaller due to its optical magnification or reduction with a high-power converging lens.

The optic disc examination is best performed with a direct ophthalmoscope, with the physician and patient sitting opposite each other. The physician's head should not cover the patient's other eye, since the patient must clearly fix the gaze position with the other eye for the examination to be performed correctly. At first, attention should be paid to the optic disc at the 6 and 12 o'clock positions: the width of the neuroretinal rim, excavation or hemorrhage rupture, peripapillary atrophy, displacement, curvature, plethora, narrowing or "bayonet-shaped" deformation of the vessels. The rim thickness should also be assessed at 1, 3, 5, 7, 9 and 11 o'clock by measuring the rim/rim ratio, which is calculated as the ratio of the rim thickness to the optic nerve diameter along the same axis. Thus, the maximum rim/rim ratio is 0.5.

The area of the cingulum is relatively unchanged in the absence of pathology. Thus, in the case where the patient has a large disc, the cingulum is distributed over a much larger area (as shown above, the cingulum is part of the radius). It turns out that the thickness of the normal cingulum of a large disc without pathology is less than the thickness of the normal cingulum of a small disc without pathology.

In young patients or in patients with glaucoma whose disc involvement is at relatively early stages (especially stages 0-III), evaluation of the nerve fiber layer is useful. The examination is performed with a direct ophthalmoscope by focusing light (preferably without the red part of the spectrum) on the surface of the retina and tracing the course of the nerve fibers. In most cases, the topography of the optic disc provides more valuable information than the state of the nerve fiber layer.

The optic nerves of both eyes should be symmetrical. With asymmetry, there is almost always a pathology of one optic nerve, unlike the situation when the optic nerves are of different sizes

Particular attention should be paid to the breakthrough of the excavation of the disc - a local defect with a depth to the outer edge of the cingulum on the temporal side near the upper or lower pole of the disc, a pathognomonic change for glaucoma. Attention should also be paid to the presence of hemorrhages in the retina, above the cingulum. Hemorrhages, as a rule, indicate the lack of control of the glaucoma process.

Special research methods

The examination of the visual fields on a red object provides information on the absence or presence of defects. Changes in the visual fields obtained with the Esteman test on the Humphrey perimeter provide valuable information on the functional changes associated with glaucoma. A mandatory examination method for assessing the damage to the visual field of each eye and confirming the absence of changes is standard perimetry performed monocularly, preferably with an automatic perimeter, such as Octopus or Humphrey.

The Disk Damage Likelihood Scale (DDLS)

	The thinnest part of the girdle (girdle/disk ratio)
DDLS	For small disc <1.5 mm	For medium sized disc 1.5-2.0 mm	For large disc >2.0 mm	DDLS stage
0a	0.5	0.4 or more	0.3 or more	0a
0b	From 0.4 to 0.5	From 0.3 to 0.4	From 0.2 to 0.3	0b
1	From 0.3 to 0.4	From 0.2 to 0.3	From 0.1 to 0.15	1
2	From 0.2 to 0.3	From 0.1 to 0.2	From 0.05 to 0.1	2
3	From 0.1 to 0.2	Less than 0.1	From 0.01 to 0.05	3
4	Less than 0.1	0<45°	0 to 45°	4
5	No belt at <45°	0 at 45°-90°	0 at 45°-90°	5
6	No belt at 45°-90°	0 at 90°-180°	0 at 90°-180°	6
7	No belt at >90°	0 to >180°	0 to >180°	7

DDLS is based on the assessment of the neuroretinal zonule thickness at its thinnest point. The zonule/disc ratio is calculated as the ratio of the radial zonule thickness to the disc diameter along the same axis. If the zonule is absent, the zonule/disc ratio is considered to be 0. The extent of the absence of the zonule (zonule/disc ratio equals 0) along the circumference is measured in degrees. Caution should be exercised in assessing the zonule thickness and differentiating its true absence from its bending, which may occur, for example, in the temporal parts of discs in patients with myopia. A bend in the zonule is not considered its absence. Since the zonule thickness depends on the disc size, it should be measured before using the DDLS scale. The measurement is performed using 60 or 90 diopter lenses with the appropriate correction. The Volk 66D lens distorts the disc size to a lesser extent. Correction for other lenses: Volk 60DxO,88, 78Dxl,2,90Dxl,33. Nikon 60Dxl,03, 90Dxl,63.

Diagnosis of glaucoma

Early detection and clinical examination of patients with glaucoma

Glaucoma is a disease of social significance. About 1% of the population aged 40 and above suffers from primary glaucoma alone. This disease is one of the main causes of blindness. Glaucoma cannot be completely cured, as it is a chronic disease, but blindness from it can be prevented if the disease is detected early and the patient is under constant dispensary observation, receiving rational treatment. Early detection of patients with glaucoma is carried out by preventive examinations of the population. Preventive examinations are divided into current and active. As a rule, current examinations are an examination of people who come to the clinic for some other disease. In the clinic, they are carried out in pre-medical examination rooms by nurses who are proficient in ocular tonometry, or in the eye room.

It is recommended that all patients over 40 years of age who visit an ophthalmologist undergo a routine examination, as well as those suffering from endocrine, cardiovascular and neurological diseases.

Active examinations are carried out directly at enterprises, where a doctor and a nurse come, or by calling elderly people living in a certain area or working at a particular enterprise to a clinic according to a special schedule.

Since the incidence of glaucoma is higher in relatives of patients with glaucoma and in individuals with endocrine pathology (especially in patients with diabetes mellitus), this contingent with an increased risk of the disease should be examined first.

It should be noted that active examinations are time-consuming and not always effective. Such examinations must be mandatory and systematically performed on persons who have contact with occupational hazards, and especially close relatives of patients with primary glaucoma.

Both types of professional phosmograf consist of two stages. The purpose of the first stage is to identify people with suspected glaucoma, the purpose of the second stage is to make a final diagnosis. The second stage of professional examination is carried out in a polyclinic, in a glaucoma room or center, and in some cases - even in a hospital.

Each patient with glaucoma should be registered with a dispensary. There are several links in the dispensary treatment system. The first link is observation by an ophthalmologist, the second is examination and treatment by a glaucoma doctor, and the third is inpatient treatment. It should be noted that initially diagnosed patients with glaucoma are registered with an ophthalmologist. A patient with glaucoma should be called by a doctor for observation of visual functions at least once every 3 months with mandatory examination of the visual fields. In cases where there is no compensation of intraocular pressure, patients should visit an ophthalmologist more often. In the absence of glaucoma offices in the city or region, outpatient observation of patients with glaucoma is carried out by an ophthalmologist at a polyclinic, and if indicated - by a hospital. The role of a hospital in the system of outpatient care is to provide highly qualified diagnostic and therapeutic care to patients with glaucoma.

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Glaucoma treatment

Treatment of glaucoma consists of several directions:

1. hypotensive therapy - normalization of intraocular pressure;
2. improving the blood supply to the optic nerve and the inner membranes of the eye - stabilization of visual functions;
3. normalization of metabolic processes in eye tissues to stop membrane dystrophy. This also includes healthy working and resting conditions, a healthy diet.
4. Surgical treatment (operation) of glaucoma.

Methods of hypotensive treatment of glaucoma - miotics, cholinomimetics, anticholinergics - block factors that break down acetylcholine.

Glaucoma - Treatment

Modern operations used for glaucoma include:

1. improving the outflow of intraocular fluid;
2. decrease in the production of intraocular fluid.

If the production of intraocular fluid decreases, innervation is disrupted, corneal dystrophy develops, etc. On the seeing eye, operations on the ciliary body are undesirable.

Glaucoma - Operations

Lifestyle with Glaucoma

Most people with glaucoma can lead normal lives, but there are some dietary guidelines that should be followed.

Coffee, tea. Within an hour after drinking coffee or strong tea, a moderate increase in intraocular pressure may occur, but this effect is so minimal that no patient with glaucoma ever refuses these drinks.

A glaucoma patient should not limit himself in fluid intake, but it should be taken evenly throughout the day, an adequate amount of fluid should be drunk, but in small portions.

Alcohol. A small amount of alcohol, especially wine, is well tolerated and even has a beneficial effect on the heart and blood circulation. A patient with glaucoma can safely drink small amounts of alcohol even daily. In the case of an acute attack of closed-angle glaucoma, drinking large amounts of strong alcoholic beverages can cause a decrease in intraocular pressure for several hours, but this should not be abused.

Smoking is one of the most serious risk factors threatening human health. Smoking also affects the occurrence of eye diseases. Thus, smokers are much more likely to have eye diseases such as retinal vascular obstruction, maculopathy, cataracts and others, and at an earlier age than non-smokers. In old age, smoking is a risk factor for the development of increased intraocular pressure.

Leisure and sports. Regular physical activity is as important for a patient with glaucoma as mandatory rest and sufficient sleep. Physical activity tends to cause a decrease in intraocular pressure, except in cases of pigmentary glaucoma, in which physical activity increases intraocular pressure. Sports are also recommended for patients with significantly reduced blood pressure to stimulate and stabilize blood circulation. Patients who already suffer from narrowing of the visual fields should be warned about their condition. They can only engage in certain types of sports.

Scuba diving. When diving with a mask, the fluctuation of intraocular pressure is insignificant. Patients who have significant damage to the optic nerve should refrain from scuba diving.

Sauna. Changes in intraocular pressure occur in glaucoma patients in the same way as in healthy people: in a sauna, it decreases and then returns to its original level within an hour. But there is no evidence that a sauna can be useful for glaucoma.

Air travel. Usually, a rapid decrease in atmospheric pressure on board an airplane does not cause problems for glaucoma patients: there is artificial atmospheric pressure inside the airplane, which compensates for a significant part of the natural pressure drop that occurs at high altitude. The eye adapts to the new situation quite quickly. In this regard, a slight decrease in atmospheric pressure does not cause a significant increase in intraocular pressure. However, patients suffering from glaucoma and severe circulatory disorders and who fly frequently should consult their ophthalmologist.

Music. Playing wind instruments may cause a temporary increase in intraocular pressure. Glaucoma patients who play these instruments should consult an ophthalmologist.