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THE DIAGNOSIS AND TREATMENT OF GLAUCOMA
Shodmanov Abbos
Samarkand State Medical University, 1st year clinical
residents of the Department of Ophthalmology
Sattorov Bobur Urol o'g'li
Samarkand State Medical University, 1st year clinical
residents of the Department of Ophthalmology
Saydullayev Dilshod Mirzohid o’g’li
Samarkand State Medical University, 1st year clinical
residents of the Department of Ophthalmology
Abstract
Background
Glaucoma is a group of chronically progressive disorders of the
optic nerve. In this article, we present the epidemiology of and risk factors for
glaucoma, as well as the diagnostic work-up and treatment options.
Methods
This review is based on pertinent publications retrieved by a selective search in
Medline and the Cochrane Library, supplemented by further articles chosen by the
authors.
Results
In Central Asia, the prevalence of glaucoma is 2.93% among persons aged 40 to
80 years. The prevalence rises with age, reaching 10% in persons over 90 years old.
The available diagnostic methods include ophthalmoscopy, tonometry, perimetry, and
imaging techniques. The treatment of glaucoma is focused on lowering the intraocular
pressure with topical drugs, laser therapy, and glaucoma surgery. In patients with
manifest glaucoma, lowering the intraocular pressure prevents the progression of
visual field defects, with a number needed to treat of 7.
Conclusion
The diagnostic evaluation of glaucoma rests on multiple pillars, all of which
must be considered for establishing the diagnosis and defining the desired target
pressure: these are, among others, the intraocular pressure and ocular function and
morphology. Individually tailored pressure-lowering treatment should be evaluated
in regularly scheduled follow-up visits for assessment of function and morphology
and adjusted as necessary to minimize the risk of progression.
Glaucoma (from the Greek
glaukós,
a nonspecific term for green or light gray
is a group of disorders that differ in their pathophysiology, risk factors,
manifestations, treatments, and prognoses. Their common feature is progressive
degeneration of the optic nerve, with loss of retinal ganglion cells, thinning of the
retinal nerve fiber layer, and progressive excavation of the optic disc .
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Annotatsiya
Glaukoma - bu ko‘ruv nervining surunkali progressiv kasalliklari guruhi. Ushbu
maqolada biz glaukomaning epidemiologiyasi va xavf omillarini, shuningdek,
diagnostika va davolash usullarini taqdim etamiz.
Usullar
Ushbu sharh Medline va Cochrane kutubxonasida tanlab olingan tegishli
nashrlarga asoslangan bo‘lib, mualliflar tomonidan tanlangan qo‘shimcha maqolalar
bilan to‘ldirilgan.
Natijalar
Markaziy Osiyoda glaukomaning tarqalishi 40 yoshdan 80 yoshgacha bo‘lgan
odamlar orasida 2,93% ni tashkil qiladi. Yosh ulg‘aygan sari tarqalish darajasi ortib
boradi va 90 yoshdan oshgan odamlarda 10% ga yetadi. Oftalmoskopiya,
tonometriya, perimetriya va vizualizatsiya usullari mavjud. Glaukomani davolash
mahalliy dorilar, lazer terapiyasi va glaukoma jarrohligi yordamida ko‘z ichi bosimini
pasaytirishga qaratilgan. Yaqqol namoyon bo‘lgan glaukoma bilan og‘rigan
bemorlarda ko‘z ichi bosimini pasaytirish ko‘rish maydoni nuqsonlarining
rivojlanishiga to‘sqinlik qiladi, davolash uchun zarur bo‘lgan soni 7 tani tashkil qiladi.
Xulosa
Glaukomaning diagnostik bahosi bir nechta ustunlarga asoslanadi, ularning
barchasi tashxis qo‘yish va kerakli maqsadli bosimni aniqlash uchun hisobga olinishi
kerak: bular boshqalar qatori ko‘z ichi bosimi va ko‘z funksiyasi va morfologiyasidir.
Bosimni pasaytiruvchi individual davolash funksiyasi va morfologiyasini baholash
uchun muntazam rejalashtirilgan keyingi tashriflarda baholanishi va rivojlanish
xavfini minimallashtirish uchun zarur bo‘lganda tuzatilishi kerak.
Glaukoma (yunoncha glaukós, yashil yoki och kulrangning o‘ziga xos
bo‘lmagan atamasi patofiziologiyasi, xavf omillari, namoyon bo‘lishi, davolash va
prognozi bilan farq qiladigan kasalliklar guruhidir. Ularning umumiy xususiyati
ko‘ruv nervining progressiv degeneratsiyasi, to‘r parda gangliy hujayralarining
yo‘qolishi, to‘r parda nerv tolalari qatlamining yupqalashishi va ko‘ruv nervi
diskining progressiv ekskavatsiyasidir.
Keywords:
glaucoma, glaucomadrainageimplants, surgical , adult.
Kalit so’zlar:
glaukoma, glaukomadrainajimplantlar, jarrohlik, katallar.
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Figure 1.
Optic disc images: a) normal and b) glaucomatous optic disc; c) and d) the
respective visual field measurements. The findings from one eye (the right eye) are
shown in all images. The optic disc in b) displays, particularly in the upper and lower
temporal quadrants, marked thinning of the neuroretinal edge zone (black arrows),
with a large excavation. The corresponding visual field examination d) reveals
marked defects with central sparing. Darker shading represents the areas in which
light is less well perceived; a normal visual field is shown for comparison (c). Visual
field measurements depend on the patient’s concentration and cooperation, which can
be quantified, for example, with automatic fixation detection and trick questions.
Definition.
Glaucoma is a group of disorders whose common feature is progressive
degeneration of the optic nerve, with loss of retinal ganglion cells, thinning of the
retinal nerve fiber layer, and increasing excavation of the optic disc.
Learning objectives
After reading this article, the reader should know:
How the various types of glaucoma differ from one another
How a targeted diagnostic evaluation should be structured
What treatment options are available for each of the disease entities
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Pathophysiology.
Elevated intraocular pressure and low perfusion pressure increase the gradient
across the lamina cribrosa and cause papillary hypoperfusion, leading to structural
changes and remodeling of the lamina cribrosa and to impaired axonal transport in
the optic nerve fibers.
Resulting disturbances.
The progressive loss of retinal ganglion cells leads to increasing impairment of
the visual field. Further functional disturbances include impaired contrast and color
perception and difficulty in reading.
The retinal ganglion cells are neurons of the central nervous system that
receive signals from the photoreceptors, process them, and transmit them in axons
through the optic nerve to further centers in the brain. These axons run from the
ganglion cell nuclei in the retina to the optic disc , and then together with the retinal
vessels through the lamina cribrosa, a sieve-like structure composed of collagen.
Behind the lamina cribrosa, the axons, surrounded by a myelin sheath, continue as the
optic nerve. Elevated intraocular pressure, low perfusion pressure, and/or low
cerebrospinal fluid pressure increase the gradient across the lamina cribrosa and cause
papillary hypoperfusion, leading to structural changes and remodeling of the lamina
cribrosa and to impaired axonal transport in the optic nerve fibers . In particular, the
pores in the anterior region of the lamina cribrosa are elongated in open-angle
glaucoma .
The increasing loss of retinal ganglion cells leads to progressive impairment of
the visual field, generally beginning in the mid-periphery and then advancing until
only a central or peripheral island of intact vision remains. Further functional
disturbances include impaired contrast and color perception and difficulty in reading
. The mechanisms by which retinal ganglion cells are lost are not yet fully understood.
The different types of glaucoma are classified according to the respective
structural changes in the anterior segment of the eye. The aqueous humor is mainly
drained in the chamber angle via the trabecular meshwork and the canal of Schlemm,
and partly via the uveoscleral outflow (root of the iris, ciliary div). The chamber
angle lies between the iris and the peripheral posterior surface of the cornea, and at
its end the canal of Schlemm lies under the trabecular meshwork. While in open-angle
glaucoma the chamber angle is macroscopically open, in acute angle closure it is
occluded by the iris (
); this suddenly blocks the outflow of aqueous humor via
the trabecular meshwork and the canal of Schlemm, causing a marked elevation of
intraocular pressure. In secondary open-angle glaucoma, there are changes of the
chamber angle that are visible under the microscope (gonioscope), such as pigment
deposition (in pigmentary glaucoma) or protein deposition (in pseudoexfoliation
glaucoma) , that elevate the intraocular pressure. The mechanisms leading to elevated
intraocular pressure in primary open-angle glaucoma are not fully understood.
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Figure 2.
Slit-lamp examination a) of an occluded chamber angle in acute angle closure
and b) after successful treatment (laser iridotomy). There is marked enlargement of
the chamber angle (white arrow) and deepening of the anterior chamber from a) to b),
as well as corneal clearing and regression of conjunctival hyperemia and scleral
vascular distention.
Chamber angle.
The chamber angle lies between the iris and the peripheral posterior surface of
the cornea, and at its end the canal of Schlemm lies under the trabecular meshwork.
The normal intraocular pressure has an average value of 15.7 mm Hg but
displays marked chronobiological and interindividual variation even in healthy
persons. It is regulated by the balance between the secretion of aqueous humor by the
ciliary div and its outflow. Central Asia intraocular pressure may thus be a
consequence of increased outflow resistance. This can be due to gonioscopically
visible changes in the chamber angle in secondary open-angle glaucoma, as
mentioned above, but it can also arise without any such changes, as in primary open-
angle glaucoma. Glaucomatous changes in the optic nerve may arise even when the
intraocular pressure is within normal limits (normal-pressure glaucoma). Among
persons of European ancestry, the intraocular pressure is normal in 30% of all cases
of glaucoma , with regional variation in prevalence. This disorder is apparently caused
by an intraocular pressure that, although within normal limits, nonetheless exceeds
the pressure sensitivity of the optic disc. The importance of the pressure sensitivity of
the optic disc is also indicated by the fact that a 25% pressure reduction lowers the
risk of glaucoma progression by 50% . Moreover, vascular changes seem to play a
role in the pathophysiology of open-angle glaucoma, and of normal-pressure
glaucoma in particular , e.g., an excessive nocturnal drop in blood pressure in
otherwise normotensive persons .
Risk factors
Advanced age
Elevated intraocular pressure
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High myopia
A positive family history of glaucoma
The risk also depends on ethnicity . Moreover, excavation of the optic disc is
particularly hard to assess in highly myopic eyes. It is thought that enlargement of the
optic disc due to myopia, with consequent thinning of the lamina cribrosa, may
predispose to glaucoma . Increased shear forces in the lamina cribrosa caused by eye
movements in persons with highly myopic (long) eyes have been mentioned as
another possible pathogenetic factor .
Elevated intraocular pressure, or an elevated translaminar pressure gradient , is
the sole modifiable risk factor for open-angle glaucoma that has been identified so
far. The randomized, controlled Ocular Hypertension Treatment Study led to the
conclusion that lowering elevated intraocular pressure (21–32 mm Hg) by 22.5% can
decrease the 5-year risk of developing open-angle glaucoma from 9.5% to 4.4% .
Diagnostic evaluation
Symptoms
Acute angle closure can manifest itself with pain radiating from the eye, visual
impairment, conjunctival hyperemia, and sometimes nausea and vomiting with a
tense, rock-hard globe. This is an ophthalmological emergency that demands
immediate treatment to prevent severe ocular damage and blindness.
Risk reduction.
Lowering an elevated intraocular pressure (21–32 mm Hg) by 22.5% can lower
the 5-year risk of developing open-angle glaucoma from 9.5% to 4.4%.
In contrast, open-angle glaucoma usually does not become symptomatic until it
has reached an advanced stage. If visual field defects are present, they usually do not
lie in the same part of the fields of the two eyes and are therefore well compensated
by binocular vision. Thus, persons with open-angle glaucoma generally report no
symptoms , and many are completely unaware that they have the condition . One-
third of patients already have the condition in an advanced or late stage in at least one
eye at the time of diagnosis . Gramer et al. reported that 10–20% of patients were
already unable to drive a vehicle at the time of presentation at the clinic because of
binocular visual field defects .
Early detection
As this condition only becomes symptomatic when it has reached an advanced
stage, the German ophthalmological associations recommend regular screening
examinations for early detection from age 40 onward . Because of the low prevalence
of the disorder ( and the low sensitivity and specificity of the tests , The rate of false
positives is high (> 65%, and even higher in younger patients), and thus any positive
finding must be followed up by further testing. Regular examination is especially
important in risk groups with elevated incidence and prevalence of the disorder, so
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that it can be diagnosed and treated early in its course. No randomized, controlled
trials on this topic have yet been conducted. The recommended screening examination
consists of at least a clinical history, stereoscopic examination of the papilla and
peripapillary nerve layer, tonometry, and slit-lamp examination of the eye . Screening
examinations for glaucoma are not covered by the statutory health insurance providers
in Germany, nor is there any population-wide periodic screening for glaucoma in
other European countries such as the UK, France, or the Netherlands.
Figure 4
Examination of peripapillary nerve fiber layer thickness a) in a normal eye and
b) in a glaucomatous eye. The retinal nerve fiber layer lies between the internal
limiting membrane (red line) and the border between the retinal nerve fiber layer and
the ganglion cell layer (turquoise line). Beyond this layer, reflections from the
vitreous div can be seen.
Topical treatment
Various substance classes are available for topical use to reduce the intraocular
pressure. They differ in their mechanisms of action, in the degree to which they lower
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the intraocular pressure , and in their dosing, side effects, and cost. A network meta-
analysis on topical first-line drugs showed that the intraocular pressure is lowered to
the greatest extent by prostaglandin analogs (bimatoprost by 5.61 mm Hg, latanoprost
4.85 mm Hg, travoprost 4.83 mm Hg, tafluprost 4.37 mm Hg), followed by beta-
blockers (levobunolol 4.51 mm Hg, timolol 3.70 mm Hg, carteolol 3.44 mm Hg,
levobetaxolol 2.56 mm Hg, betaxolol 2.24 mm Hg), alpha
2
-adrenergic agonists
(brimonidine 3.59 mm Hg, apraclonidine 2.52 mm Hg), and carbonic anhydrase
inhibitors (dorzolamide 2.49 mm Hg, brinzolamide 2.42 mm Hg) .
Prostaglandin analogs are usually prescribed for the initial treatment and are
applied once daily, in the evening. These drugs improve the uveoscleral and trabecular
outflow and thereby lower the intraocular pressure. Their side effects include
conjunctival hyperemia, increased growth of the eyelashes, reduction of periorbital
fat, and increased pigmentation of the iris and periocular skin . Systemic conditions
limiting the use of prostaglandin analogs include bronchial asthma, severe
cardiovascular conditions, and diseases of the liver or kidneys.
Target range for intraocular pressure.
The target pressure is set individually and the further course of the intraocular
pressure should be regularly checked to determine whether the disease has stabilized
as desired.
Topically applied beta-blockers are an alternative. These are usually applied
twice per day; they lower the intraocular pressure by diminishing the production of
the aqueous humor. Their main local side effect is dry eye disease, or exacerbation of
existing dry eye disease. Systemic contraindications include bronchial asthma, sinus
bradycardia, second- or third-degree AV block, decompensated congestive heart
failure, severe allergic rhinitis, cerebral hypoperfusion, and muscle weakness. Beta-
blockers can exacerbate hyperglycemia and mask the symptoms of hypoglycemia in
diabetic patients.
Alpha
2
-adrenergic agonists lessen the secretion of aqueous humor and increase
the uveoscleral outflow. The local side effects include initial white discoloration of
the conjunctiva after the drops are applied, and, over the long term, topical intolerance
in more than one-third of patients. Less commonly, there can be lid retraction, dry
mouth, bradycardia, and fatigue . Simultaneous treatment with monoamine oxidase
inhibitors, sympathomimetic drugs, or tricyclic antidepressants, which can affect
noradrenergic transmission, is a systemic contraindication. Topical treatment with
alpha
2
-adrenergic agonists is contraindicated in children under 12 because of
extremely severe side effects (ranging up to coma in toddlers). Conditions requiring
special caution include bradycardia, hypotension, arteriosclerosis, and impaired
hepatic or renal function. Topical carbonic anhydrase inhibitors likewise function by
decreasing the production of aqueous humor; local undesired side effects include
tearing, burning, and corneal endothelial decompensation. Miotic drugs can be a
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further alternative, but are now hardly ever used as the treatment of first resort. Drugs
from these different substance classes may be combined with one another, with due
consideration of their side effect profiles and mechanisms of action. It is
recommended that the eyes should be kept closed for a few minutes after the local,
touch-free application of eyedrops in the lower conjunctival sac; if indicated, the tear
ducts should be manually occluded with the index fingers. This lessens outflow of the
drug through the tear duct system and resorption through the nasal mucosa, thereby
reducing the chance of systemic side effects. Multiple studies have shown that
patients tend to display poor compliance with local antiglaucomatous treatment.
Prostaglandin analogs.
These drugs improve the uveoscleral and trabecular outflow and thereby lower
the intraocular pressure. Their side effects include conjunctival hyperemia, increased
growth of the eyelashes, reduction of periorbital fat, and increased pigmentation of
the iris and periocular skin.In the past, most eyedrops contained benzalkonium
chloride as preservative, but in recent years multiple eyedrop preparations have been
developed and approved without this ingredient (so-called preservative-free
eyedrops). These have lessened the undesired side effects, conjunctival hyperemia in
particular, and improved local tolerance . Artificial tears (e.g., hyaluronic acid
preparations) are used to treat side effects such as dry eye.
Laser therapy
Laser therapy may be considered as a supplementary measure if local treatment
does not adequately lower the intraocular pressure or fails to achieve the target
pressure (e.g., because of lacking compliance with treatment). Laser therapy,
however, generally results in a moderate lowering of the intraocular pressure, by way
of increased aqueous humor outflow after laser trabeculoplasty or diminished
aqueous humor production after cyclophotocoagulation . The latter lowers the
intraocular pressure by at least 20% in 47% of the treated eyes ; its potential
complications include inadequate or excessive pressure reduction, inflammation, and
pupillary deformity, which may lead to highly bothersome glare. Micropulse laser
techniques can be used for both applications as well, but their efficacy has not yet
been fully documented.
Glaucoma surgery
Surgery is indicated if nonsurgical treatment options are insufficient to lower the
intraocular pressure to the target pressure, or cause intolerable side effects. Minimally
invasive, filtering, and non-filtering types of glaucoma surgery are available. For
example, in one type of minimally invasive procedure a stent is placed in the canal of
Schlemm to lower the outflow resistance through the trabecular meshwork. In
general, this operation, which can be performed in combination with cataract surgery,
does not lower the intraocular pressure enough, unless the glaucoma is only moderate
; in recent years, the surgical options have expanded markedly. Minimally invasive
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glaucoma surgery seems to have fewer side effects than a filtering procedure , but also
lowers the intraocular pressure by a lesser amount .
Laser therapy.
Laser therapy may be considered as supplementary treatment if local treatment
does not adequately lower the intraocular pressure or fails to achieve the target
pressure (e.g., because of non-compliance). In a filtering operation, an accessory
pathway is created for the aqueous humor to flow out of the eye under the conjunctiva.
Trabeculectomy is now considered the reference standard for this type of procedure.
Various antimetabolites are applied intraoperatively and postoperatively to inhibit
local conjunctival scarring . Patients with advanced glaucoma have less worsening of
their visual fields if they are treated with trabeculectomy than if they undergo laser
trabeculoplasty (hazard ratio [HR] = 3.95 in 10 years for Caucasian patients, HR =
1.62 in 10 years for patients with dark skin) . Other methods include deep sclerectomy
and canaloplasty; these seem to have a lower risk of complications (cataract,
endophthalmitis, etc.) . Treatments for acute angle closure, aside from intraocular
pressure reduction with topical agents and systemic drugs (carbonic anhydrase
inhibitors), include surgical procedures such as lentectomy with intraocular lens
implantation or mechanical opening of the occluded angle (iridotomy, iridectomy) ,
which can be performed as an emergency procedure for persistent acute angle closure.
The other eye should also be treated surgically shortly afterwards, as the risk of acute
angle closure in the second eye is 51%, but can be reduced by successful treatment to
2% .
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