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What does glaucoma suspect mean: Glaucoma suspects: A practical approach


Do you treat glaucoma suspects?

January 01, 2011

2 min read


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Treatment means patients will not be lost to follow-up

Anton Hommer

“Glaucoma suspect” describes a person who has borderline signs
of glaucoma. It might be the appearance of the optic disc or retinal nerve
fiber layer. If only the pressure is elevated, we call it ocular hypertension.
The decision of treating or not treating these patients depends on the risk
profile. I always prescribe treatment (preferably with prostaglandins or, as a
second choice, beta-blockers) when IOP approaches 30 mm Hg, even with normal
pachymetry and no other risk factors. I also consider a family history of
glaucoma as a good reason to treat. But there are also other patient-related
and physician-related factors that, in my opinion, are equally important in the

We all agree that regular monitoring of a glaucoma suspect is mandatory.
If you are sure that your patient trusts your judgment, serenely accepts to
wait and see, and will come back for regular visits, treatment can be postponed
to when it is definitely needed. But not many patients react in this way to the
uncertainty of a “suspect” disease. Some of them, if you send them
back without any treatment, get very anxious and afraid to become blind.
Others, at the opposite end of the spectrum, underestimate their condition and
do not come back for visits. In all these patients, the benefits of treatment
outweigh the disadvantages. Medications nowadays are safer; we even have
preservative-free options that can conveniently be taken in once-a-day doses.
They have very few systemic side effects, and so there are fewer concerns about
treating. It is known that patients are more compliant with screening schedules
if they are on medical therapy, and this, together with the appropriate
information on the critical importance of a regular follow-up, will work in
favor of not losing and regularly monitoring glaucoma suspects.

Anton Hommer, MD, is a senior consultant, Hera Hospital,
Vienna, Austria.

Eye needs to show clear evidence of progression

Masaki Tanito

There are several reasons for not treating a glaucoma suspect. First of
all, the possible side effects of medications in patients who possibly do not
need them. Then, the inconvenience of time-consuming everyday instillations and
the burden of more frequent visits to the clinic. Last but not least, glaucoma
medications are expensive. In Japan, public insurance covers 70% of the cost,
while patients need to cover 30%.

We must take into account that all the problems associated with the use
of medications are going to be there for life. Once medications are started,
there are very few chances to quit them. Bearing this in mind, we never rush
into treatment. The true priority in the case of a glaucoma suspect, for both
patients and physicians, is not to miss a possible conversion to glaucoma, and
therefore I perform sequential examinations every 6 to 12 months. I consider
treatment, usually with topical prostaglandins, only when the risk of
developing glaucoma is remarkably high, ie, when there is glaucoma in the
fellow eye or when there is a clear rise of IOP to more than 23 mm Hg. In the
Japanese population, the average IOP is 14.5 mm Hg, and most cases of glaucoma
suspects are expected to show no IOP rise because of the high rate of
normal-tension glaucoma. Otherwise, I will not start any therapy until the eye
shows clear evidence of visual field decline progression by sequential visual
field testing or morphological changes such as rim thinning, widening of RNFL
defect or RNFL thinning.

Masaki Tanito, MD, PhD, is an associate professor, Department
of Ophthalmology, Shimane University, Shimane, Japan.


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Glaucoma Suspect – Vista Eye Care

What is a “glaucoma suspect?”

Let us start off by defining glaucoma.  Glaucoma is an eye disease where the internal fluid of the eye increases and causes a build-up of pressure.  This increased pressure causes damage to the optic nerve.  If left untreated, the disease will cause peripheral and, subsequently, central vision loss.  Glaucoma is one of the leading causes of blindness in the United States.

Glaucoma suspects have no proven optic nerve damage, but they have risk factors for the disease.  The great news is that the majority of glaucoma suspects will never develop glaucoma.  However, vision loss from glaucoma cannot be restored, so early detection is extremely important.

Why did your eye doctor diagnose you as a glaucoma suspect?

Your eye doctor at Vista Eye Care may diagnose you as a glaucoma suspect if you have one or more of these risk factors:

  • Optic nerves that appear suspicious
  • Elevated eye pressures
  • Visual field defects
  • Having eye conditions that may increase the risk of developing high eye pressures such as pseudoexfoliation syndrome or pigment dispersion syndrome

Other factors that can increase your risk for glaucoma include:

  • Family history of glaucoma
  • Thin corneas
  • African-American ethnicity
  • Myopia (nearsightedness)
  • Corticosteroid use
  • Age (although glaucoma can occur at any age, the older the patient the higher the risk)
  • Narrow anterior chamber angle (narrow drainage channel)
  • Existing systemic conditions such as sleep apnea, diabetes, and hypertension

What symptoms will a glaucoma suspect experience?

Glaucoma suspects usually do not experience any symptoms.   Primary open angle glaucoma develops slowly and during early stages there are no obvious symptoms or warning signs.  Individuals with possible angle-closure glaucoma, secondary to blockage of the drainage channel in the eye, may experience visual “haloes” around lights, blurred vision, pain, intermittent headaches, and red eyes.   By the time patients notice vision loss from glaucoma, significant irreversible optic nerve damage has likely occurred.

What additional tests are performed for glaucoma suspects? 

During your comprehensive eye exam at Vista Eye Care, your eye doctor will extensively assess your eye health, including your risk factors for glaucoma.  If risk factors are present, your eye doctor may diagnose you as a glaucoma suspect and ask you to return for further testing.

During this follow-up visit, thorough baseline glaucoma testing will be performed.  We will measure your eye pressures in more detail, assess your corneal thickness and anterior chamber (drainage) angle, and evaluate the optic nerve structure via digital photography and more extensive imaging.   Automated visual field testing will also be performed to assess for any visual field loss secondary to glaucoma.

What are the treatment options for a glaucoma suspect?

The diagnosis of glaucoma is usually made over time, as the progression of the most prevalent types of glaucoma (primary open angle glaucoma) is generally slow.  Therefore, the most important “treatment” for a glaucoma suspect is follow-up care.  Low-risk glaucoma suspects typically require follow-up visits every 6-12 months.  The frequency increases with increased risk.

The majority of glaucoma suspects may never require medical treatment.  Initial treatment for some patients involves prescription eye drops.  In certain cases, laser treatment or surgery is required.  The purpose of these treatments is to lower eye pressure.  If treatment is required and initiated early, the risk for significant vision loss is minimal.

If you have been told that you are a glaucoma suspect, the next step is to return to your eye doctor at Vista Eye Care to assess and monitor for changes of your optic nerve and visual field.



What is a glaucoma suspect?

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  • Renard JP, Rouland JF, Bron A, et al. Nutritional, lifestyle and environmental factors in ocular hypertension and primary open-angle glaucoma: an exploratory case-control study. Acta Ophthalmol. 2012 Mar 6. [Medline].

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  • Andersen JS, Pralea AM, DelBono EA, et al. A gene responsible for the pigment dispersion syndrome maps to chromosome 7q35-q36. Arch Ophthalmol. 1997 Mar. 115(3):384-8. [Medline].

  • Kass MA, Heuer DK, Higginbotham EJ, et al. The Ocular Hypertension Treatment Study: a randomized trial determines that topical ocular hypotensive medication delays or prevents the onset of primary open-angle glaucoma. Arch Ophthalmol. 2002 Jun. 120(6):701-13; discussion 829-30. [Medline].

  • Quigley HA, Addicks EM. Chronic experimental glaucoma in primates. II. Effect of extended intraocular pressure elevation on optic nerve head and axonal transport. Invest Ophthalmol Vis Sci. 1980 Feb. 19(2):137-52. [Medline].

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  • Landers J, Ullrich K, Craig JE. Ibopamine challenge testing differentiates glaucoma suspect, stable glaucoma and progressive glaucoma cases. Clin Experiment Ophthalmol. 2015 Dec. 43 (9):808-14. [Medline].

  • Lichter PR. Variability of expert observers in evaluating the optic disc. Trans Am Ophthalmol Soc. 1976. 74:532-72. [Medline]. [Full Text].

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  • Zeyen TG, Caprioli J. Progression of disc and field damage in early glaucoma. Arch Ophthalmol. 1993 Jan. 111(1):62-5. [Medline].

  • Weinreb RN, Zangwill LM, Jain S, et al. Predicting the onset of glaucoma: the confocal scanning laser ophthalmoscopy ancillary study to theOcular Hypertension Treatment Study. Ophthalmology. 2010 Sep. 117(9):1674-83. [Medline].

  • Jansonius NM, Heeg GP. The Groningen Longitudinal Glaucoma Study. II. A prospective comparison of frequency doubling perimetry, the GDx nerve fibre analyser and standard automated perimetry in glaucoma suspect patients. Acta Ophthalmol. 2009 Jun. 87(4):429-32. [Medline].

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  • Johnson CA, Adams AJ, Casson EJ, Brandt JD. Progression of early glaucomatous visual field loss as detected by blue-on-yellow and standard white-on-white automated perimetry. Arch Ophthalmol. 1993 May. 111(5):651-6. [Medline].

  • Jansonius NM, Heeg GP. The Groningen Longitudinal Glaucoma Study. II. A prospective comparison of frequency doubling perimetry, the GDx nerve fibre analyser and standard automated perimetry in glaucoma suspect patients. Acta Ophthalmol. 2009 Jun. 87(4):429-32. [Medline].

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  • Bozic M, Hentova Sencanin P, Brankovic A, Marjanovic I, Dordevic Jocic J, Sencanin I. [Effect of a tight necktie on intraocular pressure]. Med Pregl. 2012 Jan-Feb. 65(1-2):13-7. [Medline].

  • De Moraes CG, Demirel S, Gardiner SK, et al. Effect of treatment on the rate of visual field change in the ocular hypertension treatment study observation group. Invest Ophthalmol Vis Sci. 2012. 53(4):1704-9. [Medline]. [Full Text].

  • Higginbotham EJ. Ocular Hypertension Treatment Study. Arch Ophthalmol. 2009 Feb. 127(2):213-5. [Medline].

  • Rhee DJ. Preventing glaucoma in a high-risk population: impact and observations of the Ocular Hypertension Treatment Study. Arch Ophthalmol. 2009 Feb. 127(2):216-8. [Medline].

  • Doshi A, Singh K. Cost-effective evaluation of the glaucoma suspect. Curr Opin Ophthalmol. 2007 Mar. 18(2):97-103. [Medline].

  • Lim JH, Park JS, Lee SY, Hong YJ. Incidence of and risk factors for glaucoma in lost-to-follow-up normal-tension glaucoma suspect patients. BMC Ophthalmol. 2016 May 25. 16 (1):62. [Medline].

  • Blini M, Rossi GC, Trabucchi G, et al. Ocular hypotensive efficacy and safety of travoprost 0.004% in inadequately controlled primary open-angle glaucoma or ocular hypertension: short-term, multicenter, prospective study. Curr Med Res Opin. 2009 Jan. 25(1):57-63. [Medline].

  • Shazly TA, Latina MA, Dagianis JJ, Chitturi S. Effect of Central Corneal Thickness on the Long-Term Outcome of Selective Laser Trabeculoplasty as Primary Treatment for Ocular Hypertension and Primary Open-Angle Glaucoma. Cornea. 2012 Apr 19. [Medline].

  • National Advisory Eye Counsel Vision Research. A National Plan. NIH. 1982. 1:12-13.

  • h50.011-023 Open-Angle Glaucoma Suspect, Low Risk

    When initiating treatment, assume that the pre-treatment measurement of intraocular pressure (IOP) is the level that produced damage to the optic nerve.  If the IOP remained at this level, additional damage to the optic nerve would follow.

    To treat glaucoma, an IOP level is identified below which further optic nerve damage is unlikely to occur.  This IOP level is the target pressure range and it is selected based on the following:

    • Pre-treatment level of IOP
    • The rapidity with which the damage to the optic nerve occurred, if that is known
    • Patient age
    • General health of the patient

    Treatment should maintain the IOP at or below the target level.  The status of the optic nerve, visual fields, electrodiagnostics, and the retinal nerve fiber layer are monitored over time for evidence of stability or deterioration.   In the event of further damage, the target pressure range is reset to a lower level.

    Pharmacologic Treatment

    Select your initial medication based upon target pressure range, medical history, and ocular history.  If the initial medication fails to achieve the target pressure range within one month, discontinue the initial medication and substitute another.

    If the second medication fails to achieve the target pressure, begin combination therapy by using two different medications.  If this strategy fails, you could add still a third class of glaucoma medications to the regimen.  With three different eye drops, non-compliance becomes common and laser surgery may be a better treatment option.

    Prostaglandins are the most popular class of medications for glaucoma therapy due to their excellent efficacy, safety index and tolerability.  They flatten the diurnal curve significantly and achieve the greatest IOP reduction of any class of topical medication.

    Classes of Glaucoma Medications


    • Lumigan
    • Travatan Z
    • Zioptan
    • Xalatan


    • Timolol
    • Betagan
    • Betimol
    • OptiPranolol

    Adrenergic Agonists

    • Alphagan P 0.1% and 0.15%
    • Brimonidine 0.2%
    • Propine

    Carbonic Anhydrase Inhibitors

    Cholinergic Agonists

    • Pilocarpine
    • Carbachol
    • Echothiophate

    Combination Glaucoma Medications

    • Cosopt – carbonic anhydrase inhibitor / beta-blocker
    • Cosopt PF – carbonic anhydrase inhibitor / beta-blocker
    • Combigan – adrenergic agonist / beta-blocker
    • Simbrinza – adrenergic agonist / carbonic anhydrase inhibitor

    Changing the Treatment due to Side Effects


    • Red eye
    • Eye color change
    • Excessive eyelash growth
    • Uveitis
    • Macular edema


    • Bronchospasm
    • Pulmonary edema
    • Heart failure
    • Headache
    • Weakness
    • Depression
    • Lethargy
    • Itching
    • Stinging
    • Blurred vision
    • Photophobia
    • Loss of libido

    Adrenergic Agonist       

    • Red eye
    • Allergic follicular conjunctivitis
    • Dry mouth
    • Drowsiness

    Carbonic Andydrase Inhibitors   

    • Sulfa allergy
    • Red eye
    • Ocular itching
    • Metallic taste
    • Paresthesia of fingers or toes
    • Headache
    • Blood dyscrasias
    • Depression
    • Loss of libido
    • Impotence

    Cholinergic Agonists      

    • Red eye
    • Induced myopia
    • Reduced vision in low illumination
    • Headaches
    • Lens opacities
    • Iris cysts
    • Increased risk of angle closure
    • Increased risk of retinal detachment
    • Sweating
    • Salivation
    • Diarrhea
    • Bradycardia
    • Dyspnea


    • Eye color change
    • Stinging
    • Increase in periocular eyelid pigmentation
    • Increase in upper eyelid sulcus deepening

    The definition and classification of glaucoma in prevalence surveys

    An appropriate case definition is the keystone of epidemiological research whether measuring prevalence, studying risk factors, or conducting clinical trials. This reconsideration of the definition and classification of glaucoma was prompted by our experiences of cross sectional prevalence research in Africa and Asia, and by the difficulty we experienced in identifying and classifying cases and in making valid comparisons with previously published data. The proposed definition of glaucomatous optic neuropathy has evolved from one initially developed for the Kongwa Eye Study in Tanzania.1 At the same time, work in Mongolia and Singapore,2,3 where there was a high prevalence of primary angle closure glaucoma (PACG), had prompted a re-examination of the definition of this condition. We were concerned that in previous reports subjects with “latent angle closure glaucoma” had been classified as cases of established glaucoma, despite having normal visual function. This may result in misinterpretation of the estimates of visual morbidity attributable to glaucoma, especially as PACG is believed to be at least as prevalent as primary open angle glaucoma (POAG).4

    At the biennial congress of the International Society for Geographical and Epidemiological Ophthalmology held in Leeuwenhorst, the Netherlands, in June 1998, a group interested in glaucoma epidemiology met to discuss the prototype system. This has since been discussed further, and various experts in the fields of glaucoma research and clinical practice consulted. (The appendix lists participants and co-opted advisers.) The views presented here are, however, those of the authors. Our aim has been to present a practical framework which can be tested and discussed further.


    The fundamental concept of the proposed classification for cross sectional epidemiological research is that the term glaucoma is reserved for people with established, visually significant, end organ damage. In the public health context, glaucoma can be seen as an optic neuropathy associated with characteristic structural damage to the optic nerve and associated visual dysfunction that may be caused by various pathological processes.

    Structural damage—optic neuropathy

    The feature that differentiates glaucoma from other causes of visual morbidity is a characteristic pattern of damage to the optic nerve head. This is most easily recognised at the superior and inferior poles of the optic disc. The vertical cup:disc ratio (VCDR) has proved to be a simple, relatively robust index of glaucomatous loss of the neuroretinal rim. As with intraocular pressure, VCDR is a continuous variable within the population.

    One approach would be to determine the range of CDR in people with normal visual function (normal visual field) in a population. This group of individuals will therefore be “hypernormal,” as those with visual dysfunction due to causes other than glaucoma would be excluded. The choice of where to place the division between “normal” and “abnormal” is, for the time being, arbitrary and partially flawed by the fact that there is overlap between the range of CDRs in those with and without glaucomatous visual loss. Faced with this dilemma, we propose that the statistical convention that a probability of <5% representing a significant deviation from normal be invoked. Therefore, the CDR above which 2.5% of the normal population lie defines the “upper limit of normal” (the other 2.5% falling below the normal distribution). By using the 97.5th percentile, one avoids making the assumption that CDR is normally distributed (it has been found to be Gaussian in some studies, but not in others). We also suggest using the 97.5th percentile value for CDR asymmetry as a second criterion for abnormality. Examples of what these criteria might be for some populations are shown in Table 1.

    Table 1

    Vertical cup:disc ratio (VCDR) distribution in people with normal visual fields in one African and three Asian countries

    Functional damage

    While most published definitions of glaucoma include the presence of “characteristic visual field defects,” many authors fail to provide quantitative, clearcut descriptions of what this means. The broadly accepted principles are summarised in Table 2.

    Table 2

    Characteristics of glaucomatous field defects

    These principles fail to account for the possibility of diffuse damage to the visual field in glaucoma. While some diffuse loss clearly must occur, its magnitude and importance in specific glaucoma diagnosis are difficult to determine.5 Following consultation with a group of researchers interested in the psychophysics of glaucoma, we have adopted the following as the “gold standard” of glaucomatous visual field loss. The glaucoma hemifield test graded “outside normal limits” and a cluster of three contiguous points at the 5% level on the pattern deviation plot, using the threshold test strategy with the 24-2 test pattern of the Zeiss-Humphrey field analyser 2. This is not intended to indicate that this device is the only acceptable tool for field analysis. However, we consider it the standard against which others should be validated.


    The relation between VCDR and proved visual field abnormalities is complex. Some eyes have reproducible visual field defects although they have a CDR that lies within the range defined as normal by the criteria we have selected. Figure 1 shows the relation between CDR and the cumulative probability of a reproducible field defect CDR among Chinese Singaporeans (unpublished data, Paul Foster, Steve Seah, Singapore National Eye Centre, 2001).

    Figure 1

    The cumulative percentage of vertical CDR distribution among subjects able to complete visual field testing in a population survey3 in whom a reproducible visual field defect (glaucoma hemifield test “outside normal limits” and a four point cluster (p<5%) on the pattern deviation plot) was identified. The data shown here are based on 61 of 67 eyes. Fives eyes were excluded because lens opacity was sufficient to account for the field defect. One eye was excluded because diabetic retinopathy was present. Several eyes with severe visual field loss were not able to produce a reliable visual field test result.

    We further propose that an individual with field loss who meets the stated criteria (and optic disc meeting criteria for abnormality) in one eye has glaucoma. This takes account of the fact that damage is often present in one eye before the other. However, we appreciate that this monocular based definition may not be representative of a subject’s functional capacity.6

    We have not sought to specify that the visual field defect should be “consistent” with the pattern of structural damage to the optic nerve—for example, requiring that inferior field loss must be matched with superior optic disc rim loss. This may lower the specificity of the definition, although we believe the interobserver variation in making this judgment is potentially so great as to introduce greater weakness to the scheme. We therefore suggest that structural features exceeding the specified limits, combined with a field defect that meets the above criteria, will constitute the definition of glaucoma damage.

    Levels of evidence

    It is therefore envisaged that cases of glaucoma would be classified according to three levels of evidence. The highest level of certainty requires optic disc abnormalities (VCDR >97.5th percentile in the normal population) and visual field defect compatible with glaucoma. In the second, if a visual field test could not be performed satisfactorily, a severely damaged optic disc (VCDR > 99.5th percentile of the normal population) would be sufficient to make the diagnosis. Lastly, if the optic disc could not be examined because of media opacity (and, hence, no field test was also possible), an IOP exceeding the 99.5th percentile of the normal population, or evidence of previous glaucoma filtering surgery, may be taken as sufficient for a diagnosis of glaucoma (see Table 3 for summary).

    Table 3

    The diagnosis of glaucoma in cross sectional prevalence surveys (The diagnosis is made according to three levels of evidence)


    POAG and the role of IOP

    Although the level of intraocular pressure (IOP) is one of the most consistent risk factors for the presence of glaucoma, the concept that statistically raised IOP is a defining characteristic for glaucoma has been almost universally discarded. This is based on several population based studies that document the typical disc and field damage of glaucoma in people with a statistically normal IOP and, conversely, people with statistically elevated IOP and no evidence of optic neuropathy. We propose to follow this current convention except for category 3 diagnosis, as detailed above.

    POAG is therefore optic nerve damage meeting any of the three categories of evidence above, in an eye which does not have evidence of angle closure on gonioscopy, and where there is no identifiable secondary cause.

    Primary angle closure and narrow drainage angles

    The current classification of PACG is largely based on clinical observations in European derived people, among whom the condition is scarce. While the acute, symptomatic phase is dramatic, it occurs in only a minority of those with PACG diagnosed in population based surveys in African and Asian settings.2,3,7,8 Rather, a chronic, asymptomatic form of PACG predominates. Thus, a full re-evaluation of the definition of this disease is appropriate, with emphasis placed on visual loss rather than symptomatic disease.

    We propose that it would be useful to distinguish between the mechanism by which IOP becomes elevated and the resultant damage that is caused by PACG. To do this, people meeting gonioscopic criteria for narrow angles and with evidence of significant obstruction of the functional trabecular meshwork by the peripheral iris would be classified as having primary angle closure (PAC). Those in whom PAC had led to significant glaucomatous damage to the optic nerve would be defined as having PACG. This is not intended to indicate that those with PAC do not require treatment. It is intended to differentiate between those with and without damaged visual function attributable to glaucomatous optic neuropathy. People with PAC and other causes of visual loss, such as iris damage, non-glaucomatous optic atrophy, lens opacity, and corneal endothelial failure should be separately identified.

    This approach to classification differs from the scheme found in most textbooks in which people with a narrow drainage angle and either raised IOP or peripheral anterior synechiae (PAS) are said to have primary angle closure “glaucoma.” Thus, in this new concept, PAC includes both asymptomatic people with occludable angles who have not had an acute attack, and those with PAC who have had an attack that was treated promptly but suffered no detectable nerve damage. As many as 60–75% of people suffering an acute, symptomatic episode of angle closure recover without optic disc or visual field damage,9,10 at least in the short term. If one intends the term glaucoma to signify a disease characterised by an irreversible defect in visual function, then many people suffering symptomatic episodes of high IOP or those with narrow drainage angles who are as yet asymptomatic do not meet this criterion for nerve injury. They share anatomical and physiological characteristics with those whose angle closure has led to field loss, but they deserve to be considered separately for the purposes of the definitions we have intended to construct. This classification scheme is summarised in Table 4.

    Table 4

    Classification of primary angle closure (PAC)

    Glaucoma with secondary ocular pathology

    Not all prevalence studies of glaucoma have separated primary and secondary glaucoma in consistent fashion, if they have done so at all. None the less, the estimated proportion of glaucoma damage that is clearly secondary to other ocular or systemic disease, or to trauma, may represent as much as 20% of all glaucoma. While we argue above for elimination of IOP as a defining feature of primary OAG or ACG, secondary glaucoma is properly considered to represent those eyes in which a second form of ocular pathology has caused IOP above the normal range, leading to optic nerve damage. We propose that the diagnosis of secondary glaucoma only be based on the presence of optic neuropathy, in so far as it is possible to determine this, in the presence of a second ocular pathological process. These processes may include one of the following:

    1. neovascularisation

    2. uveitic

    3. trauma

    4. lens related.

    There are arguments for and against including people with glaucoma and pigment dispersion syndrome or pseudoexfoliation syndrome as cases of secondary glaucoma. They have been omitted from the list above, on the premise that they represent a variant of POAG, although this view remains to be fully vindicated. It must be recognised that many eyes with secondary glaucoma have opaque media, precluding optic disc and visual field examinations. Hence, many of the secondary glaucoma examples will be diagnosed with the category 3 information detailed above, when optic neuropathy is inferred from reduced visual acuity and a relative afferent pupil defect, in the presence of raised IOP. Furthermore, a substantial number of these people are affected unilaterally compared to bilateral involvement in primary glaucoma.

    On the other hand, there will be eyes with processes such as pseudoexfoliation or uveitis with IOP above the normal range, but in which the disc is visible and seen to be normal. For consistency, people with eyes with these features will be categorised as secondary ocular hypertensives, or secondary glaucoma suspects.

    Glaucoma suspects

    Our categorisation aims to separate an examined population into those who did not have glaucoma, those who had one of the defined forms of glaucoma, and those who had some suspicion of glaucoma. The various reasons that a person would be considered as a glaucoma suspect are summarised in the Table 5.

    Table 5

    Criteria for classification as glaucoma suspect


    The proposed scheme provides a framework for classifying cases of glaucoma in cross sectional population based research. It places the emphasis of the diagnosis on glaucomatous optic neuropathy with a reproducible visual field defect, but includes criteria for some eyes in which visual field testing or disc evaluation are impossible.

    Limiting the use of the term “glaucoma” for those people with established end organ damage—that is, a visually significant optic neuropathy, provides a uniform definition across the various causal mechanisms: primary open angle, primary angle closure, and secondary to other pathology. The “glaucoma as damage” approach is attractive for a number of reasons. Firstly, it is conceptually simple. Secondly, it limits the features required to make the diagnosis to direct measurements of the structure and function of the optic nerve. Thirdly, it is also less arbitrary in specifying divisions between what constitutes normality and disease, because we have considerable information on the distribution of optic nerve structural and functional traits in the population of developed countries.

    Potential weaknesses in the use of VCDR as a defining feature for glaucoma include variation in the size of the optic disc between individuals,11,12 variation in the number of axons in the optic nerve, from a minimum of 816 000 to a maximum of 1 502 000 (mean 1 159 000 plus or minus 196 000) in Europeans13 and the observation that larger optic nerves have a larger neuroretinal rim area14 and contain more axons.15 Correction for variation in disc size when assessing the CDR has been suggested.16–18

    However, the precise VCDR and degree of asymmetry that denote statistical abnormality cannot necessarily be extrapolated to other populations without justification from further data. For example, there is evidence that the disc size and CDR in African-Americans is larger than in European-Americans, although the area of the neuroretinal rim is similar.19–21 However, a recent report cited 97.5th and 99.5th percentile figures for VCDR distribution in a population in the Netherlands as 0.73 and 0.78 respectively.22 These are remarkably similar to those found in Asian populations (Table 1).

    The emphasis on end organ damage as the defining characteristic of glaucoma has led to the separation of people with an angle closure into (1) primary angle closure suspects, (2) primary angle closure (where there are signs of disturbed structure or function but no visually significant optic nerve damage), and (3) primary angle closure glaucoma (where optic nerve damage is present). The diagnostic criteria employed in eight major population based studies of glaucoma in areas with a high prevalence of PACG are shown in Table 6. Only three out of eight allowed for optic disc and visual field abnormalities in considering the diagnosis of PACG. In all eight studies, a raised IOP with gonioscopic abnormalities was sufficient to diagnose PACG. The logic of this convention is questionable since natural history data in Europeans suggest that many such people never lose vision.23 The Inuit people of Greenland have the highest rate of primary angle closure of any ethnic group.24 Follow up over 10 years suggests that even “high risk” individuals within this population have less than a 1% annual risk of suffering a symptomatic episode or developing ocular damage from angle closure.25

    Table 6

    Diagnostic criteria for PACG in population based research

    Thus, the diagnostic criteria proposed here are likely to lead to alterations in prevalence estimates, particularly for PACG. Since some of those with narrow angles but normal discs will now be classified as PAC, the population with PACG may be lower than in previous surveys that included both in one category. Both are likely to benefit from iridectomy, but the former (PAC) are likely to be cured, while the latter will require more intensive follow up and treatment—indeed much like the treatment for POAG.

    Published glaucoma surveys in different populations have varied widely in the availability and sophistication of the instruments available for measurement and diagnosis, in the time available for repeat testing (for example, of a suspect visual field test), and in the money available for an adequate number of examiners and assistants. The optic disc cupping may have been assessed by direct ophthalmoscopy, binocular indirect ophthalmoscopy at the slit lamp, with or without an eye piece graticule, stereoscopic disc photography, a scanning laser ophthalmoscope, or other imaging device. Surveys can thus be arranged in a hierarchy of degrees of completeness and sophistication of the examination.

    We do not know the true effect that differences in the methodology may have on the calculated prevalence using the proposed definition. This could be estimated by careful analysis of previous survey data and future glaucoma surveys in which more than one methodological approach is used and comparisons are made.

    Considering field testing for the purposes of our definition standards, tests, and instruments other than the Humphrey field analyser (HFA) 2 may be used, but each should be individually validated against this standard. Good equivalence has already been demonstrated for the Zeiss-Humphrey 1 instrument with the newer HFA 2 instrument, and for the SITA testing strategy compared with the standard test algorithm.26,27

    Reliability of test results is an important consideration. The standards for check trials provided by the Zeiss-Humphrey instrument may not be appropriate. Fixation loss scores may bear little relation to fixation accuracy,28 and are especially sensitive to mis-plotting of the blind spot. Furthermore, the precision of false negative and false positive indices is very poor, given the number of test points. The 95% CIs around a 33% false negative rate may be from 13% to 53%.29 The software for calculation of false negative and positive responses in the newer HFA 2 machine has been modified, although only limited independent evaluation of this is currently available.

    The failure to include field testing in some surveys in developing countries is likely to lead to an underestimation of glaucoma prevalence. While reliance on the optic nerve appearance is not ideal, it would identify the more advanced cases and provide at least a minimum estimate of glaucoma prevalence. It would include those at highest risk for total blindness in their lifetimes.

    This scheme is not definitive, but is intended as an operational approach to identifying, in cross sectional surveys, those suffering visual disability from glaucoma and to standardise our enumeration and evaluation of the cause of their disease. The usefulness of the proposed system for comparison between studies must now be validated by subsequent research.


    ISGEO Glaucoma classification working group, 27 and 28 June 1998, Leeuwenhorst, Netherlands: co-chair: Gordon J Johnson, Harry A Quigley; rapporteurs: Ralf Buhrmann, Paul J Foster; group members: Poul-Helge Alsbirk, Michelle Coffey, Lalit Dandona, Paulus TVM de Jong, Fridbert Jonasson, Paul Mitchell, Ian Murdoch, R Pararajasegaram, RS Ramrattan, Poul Roux, Ravi Thomas, Bjorn Thylefors, Roger Wolfs; co-opted advisers: Anders Heijl, David Henson, Roger A Hitchings, Chris A Johnson, Gottfried Naumann, John F Salmon; co-authors of studies from which data are presented: Bangladesh: M Rahman, N Rahman, AU Zahman, A Zia; Mongolia: J Bassanhu, J Devereux, D Uranchimeg, PS Lee, D Machin; Singapore: SKL Seah, F Oen, TP Ng, D Machin, J Devereux, J Hall, J Hee, SJ Chew, PT Khaw; Tanzania: Y Barron, SK West, MS Oliva, BBO Mmbaga.


    We thank all those mentioned in the appendix for participating in this work, and wish to emphasise that the views expressed in this manuscript are solely those of the authors, and not those of the ISGEO or an other organisation or individual.


    1. Buhrmann RR, Quigley HA, Barron Y, et al. Prevalence of glaucoma in a rural East African population. Invest Ophthalmol Vis Sci 2000;41:40–8.

    2. Foster PJ, Baasanhu J, Alsbirk PH, et al. Glaucoma in Mongolia—a population-based survey in Hövsgöl Province, Northern Mongolia. Arch Ophthalmol 1996;114:1235–41.

    3. Foster PJ, Oen FT, Machin DS, et al. The prevalence of glaucoma in Chinese residents of Singapore. A cross-sectional population survey in Tanjong Pagar district. Arch Ophthalmol 2000;118:1105–11.

    4. Quigley HA. Number of people with glaucoma worldwide. Br J Ophthalmol 1996;80:389–93.

    5. Asman P, Heijl A. Diffuse visual field loss and glaucoma. Acta Ophthalmol Scand 1994;72:303–8.

    6. Viswanathan AC, McNaught AI, Poinoosawmy D, et al. Severity and stability of glaucoma. Patient perception compared with objective measurement. Arch Ophthalmol 1999;117:450–4.

    7. Salmon JF, Mermoud A, Ivey A, et al. The prevalence of primary angle-closure glaucoma and open angle glaucoma in Mamre, Western Cape, South Africa. Arch Ophthalmol 1993;111:1263–9.

    8. Congdon N, Quigley HA, Hung PT, et al. Screening techniques for angle-closure glaucoma in rural Taiwan. Acta Ophthalmol 1996;74:113–19.

    9. Douglas GR, Drance SM, Schulzer M. The visual field and nerve head in angle-closure glaucoma. A comparison of the effects of acute and chronic angle closure. Arch Ophthalmol 1975;93:409–11.

    10. Dhillon B, Chew PT, Lim ASM. Field loss in primary angle-closure glaucoma. Asia-Pacific J Ophthalmol 1990;2:85–7.

    11. Jonas JB, Gusek GC, Guggenmoos-Holzmann I, et al. Size of the optic nerve scleral canal and comparison with intravital determination of optic disc dimensions. Graefes Arch Clin Exp Ophthalmol 1988;226:213–15.

    12. Jonas JB, Gusek GC, Naumann GO. Optic disc, cup and neuroretinal rim size, configuration and correlations in normal eyes [published errata appear in Invest Ophthalmol Vis Sci 1991;32:1893 and 1992;32:474–5]. Invest Ophthalmol Vis Sci 1988;29:1151–8.

    13. Jonas JB, Muller-Bergh JA, Schlotzer-Schrehardt UM, et al. Histomorphometry of the human optic nerve. Invest Ophthalmol Vis Sci 1990;31:736–44.

    14. Jonas JB, Gusek GC, Guggenmoos-Holzmann I, et al. Correlations of the neuroretinal rim area with ocular and general parameters in normal eyes. Ophthalmic Res 1988;20:298–303.

    15. Jonas JB, Schmidt AM, Muller-Bergh JA, S et al. Human optic nerve fiber count and optic disc size. Invest Ophthalmol Vis Sci 1992;33:2012–18.

    16. Montgomery DM. Clinical disc biometry in early glaucoma. Ophthalmology 1993;100:52–6.

    17. Spencer AF, Vernon SA. Optic disc measurement with the Zeiss four mirror contact lens. Br J Ophthalmol 1994;78:775–80.

    18. Garway-Heath DF, Ruben S, Viswanathan AC, et al. Vertical cup/disc ratio in relation to optic disc size: its value in the assessment of the glaucoma suspect. Br J Ophthalmol 1998;82:1118–24.

    19. Varma R, Tielsch JM, Quigley HA, et al. Race-, age-, gender-, and refractive error-related differences in the normal optic disc. Arch Ophthalmol 1994;112:1068–76.

    20. Beck RW, Messner DK, Musch DC, et al. Is there a racial difference in physiologic cup size? Ophthalmology 1985;92:873–6.

    21. Chi T, Ritch R, Stickler D, et al. Racial differences in optic nerve head parameters. Arch Ophthalmol 1989;107:836–9.

    22. Wolfs RC, Borger PH, Ramrattan RS, et al. Changing views on open-angle glaucoma: definitions and prevalences—The Rotterdam Study. Invest Ophthalmol Vis Sci 2000;41:3309–21.

    23. Erie JC, Hodge DO, Gray DT. The incidence of primary angle-closure glaucoma in Olmstead County, Minnesota. Arch Ophthalmol 1997;115:177–81.

    24. Clemmesen V, Alsbirk PH. Primary angle-closure glaucoma (ACG) in Greenland. Acta Ophthalmol 1971;49:47–58.

    25. Alsbirk PH. Anatomical risk factors in primary angle-closure glaucoma. A ten year follow up survey based on limbal and axial anterior chamber depths in a high risk population. Int Ophthalmol 1992;16:265–72.

    26. Johnson CA, Cioffi GA, Drance SM, et al. A multicenter comparison study of the Humphrey field analyzer I and the Humphrey field analyzer II. Ophthalmology 1997;104:1910–17.

    27. Bengtsson B, Heijl A, Olsson J. Evaluation of a new threshold visual field strategy, SITA, in normal subjects. Swedish Interactive Thresholding Algorithm. Acta Ophthalmol Scand 1998;76:165–9.

    28. Henson D, Evans J, Chauhan BC, et al. Influence of fixation accuracy on threshold variability in patients with open angle glaucoma. Invest Ophthalmol Vis Sci 1996;37:444–50.

    29. Vingrys AJ, Demirel S. False-response monitoring during automated perimetry. Optom Vis Sci 1998;75:513–17.

    30. Alsbirk PH. Anterior chamber depth and primary angle-closure glaucoma. I. An epidemiologic study in Greenland Eskimos. Acta Ophthalmol 1975;53:89–104.

    31. Arkell SM, Lightman DA, Sommer A, et al. The prevalence of glaucoma among eskimos of Northwest Alaska. Arch Ophthalmol 1987;105:482–5.

    32. Hu Z, Zhao ZL, Dong FT. [An epidemiological investigation of glaucoma in Beijing and Shun-yi county.] [Chinese] Chung-Hua Yen Ko Tsa Chih [Chinese Journal of Ophthalmology] 1989;25:115–18.

    33. Zhao JL. [An epidemiological survey of primary angle-closure glaucoma (PACG) in Tibet.] [Chinese] Chung-Hua Yen Ko Tsa Chih [Chinese Journal of Ophthalmology] 1990;26:47–50.

    34. Shiose Y, Kitazawa Y, Tsukuhara S, et al. Epidemiology of glaucoma in Japan—a nationwide glaucoma survey. Jpn J Ophthalmol 1991;35:133–55.

    Clinical management outcomes of childhood glaucoma suspects



    To investigate the outcomes of childhood glaucoma suspects.


    Retrospective case series.


    Records of childhood glaucoma suspects were identified using financial claims data; medical history, baseline biometric and exam findings were recorded. Conversion from suspect to glaucoma was determined based on the Childhood Glaucoma Research Network criteria. The study adheres to the tenets of the Declarations of Helsinki.


    214 subjects were enrolled, with median age at initial presentation of 6.37 years (interquartertile range: Q1 = 2.46, Q3 = 8.90). 22 (10.2%) subjects developed glaucoma, 64 (29.9%) had ocular hypertension but no glaucoma, 9 (4.2%) had high-risk condition or syndrome without either ocular hypertension or glaucoma after a mean follow up of 39 +/- 34 months. Neither a family history of glaucoma nor patient gender was significantly different between the groups. 40.2% of subjects (86 of 214) had two or more episodes of intraocular pressure (IOP) > 21 mmHg, among which 25.6% (22 of 86) developed glaucoma after a mean duration of 32.8 +/- 33.5 months.


    Up to 25% of children with 2 or more episodes of elevated IOP may develop glaucoma. In 50% of suspects who converted to glaucoma, elevated IOP was not present at the initial evaluation. There is no significant difference in gender, family history, or baseline central corneal thickness between suspects who developed glaucoma compared to the rest. While suspects who converted to glaucoma had higher average, maximum and minimum IOP measurements, there is no clear cutoff between the groups.

    Citation: Greenberg MB, Osigian CJ, Cavuoto KM, Chang TC (2017) Clinical management outcomes of childhood glaucoma suspects. PLoS ONE 12(9):


    Editor: Paloma B. Liton, Duke University, UNITED STATES

    Received: July 14, 2017; Accepted: September 14, 2017; Published: September 25, 2017

    Copyright: © 2017 Greenberg et al. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

    Data Availability: All relevant data are within the paper.

    Funding: The authors received no specific funding for this work.

    Competing interests: The authors have declared that no competing interests exist.


    Childhood glaucoma is a heterogeneous group of diseases that result in pressure-related damage to the developing ocular structures [1], and accounts for 2–6% of blindness in children world-wide [2]. In 2013, the Ninth World Glaucoma Association Consensus in conjunction with the Childhood Glaucoma Research Network (CGRN) provided formal definitions for childhood glaucoma as well as childhood glaucoma suspect [1]. In clinical practice, pediatric patients are considered glaucoma suspects if they have elevated intraocular pressure (IOP), optic disc appearance or visual field findings suggestive of glaucoma, or anterior segment and/or biometric findings suspicious for glaucoma without meeting the diagnostic criteria for childhood glaucoma. In addition, children may be referred for glaucoma evaluation based on the presence of a high-risk ocular findings, condition or systemic syndrome.

    Overall, childhood glaucoma suspects constitute a significant proportion (approximately 38.5%) of the patients seen in a referral pediatric glaucoma service [3]. The incidence and risk factors of glaucoma conversion in these childhood glaucoma suspects are unknown. In this retrospective study, we investigated the baseline demographic and ocular characteristics as well as the outcomes of childhood glaucoma suspects managed in a tertiary referral center.

    Materials and methods

    Study population

    A protocol for retrospective review of medical records was approved by the Institutional Review Board (IRB) of the University of Miami. All data were extracted in an anonymized, de-identified fashion and aggregated prior to analysis; the data collection method was reviewed and approved by the IRB. Potential subjects were identified using a financial claims search for International Classification of Diseases 9th and 10th Editions (ICD-9/ICD-10) codes for “glaucoma suspect” or “ocular hypertension” for visits between 2002 and 2012. The subjects were enrolled if they were <18 years of age at the time of the first clinic visit, and if a diagnosis of “ocular hypertension” and/or “glaucoma suspect” was documented in the clinic note. They were excluded if they: 1) met the CGRN criteria for the diagnosis of childhood glaucoma upon initial evaluation, 2) had a history of prior intraocular surgery at the time of the initial visit, 3) had comorbidity that prevents accurate assessment of IOP (e.g. corneal abnormalities), or 4) had less than 6 months of follow up. Baseline patient demographic information and examination findings from each follow up clinic visit were recorded. Baseline automated visual field (Humphrey Field Analyzer, Carl Zeiss Meditec, Dublin, CA; 30–2 or 24–2 protocol, any stimulus size; SITA-standard, SITA-fast or FastPac programs), when available, was graded as “normal,” “abnormal but not glaucomatous,” and “glaucomatous” by a fellowship-trained glaucoma specialist (TCC). If both eyes of a patient were eligible for study, the eye with higher IOP on initial evaluation was included. The decision to initiate treatment was at the discretion of the attending pediatric glaucoma specialist; no criteria or protocol were used in this decision-making.


    Patients were divided into four groups based on the diagnosis of their last visit: Group 1 –glaucoma, Group 2 –ocular hypertension, Group 3 –high-risk condition or syndrome, and Group 4 –other. Group 2 included any subject who had IOP > 21 mmHg on two or more occasions but did not meet the CGRN criteria for glaucoma diagnosis at the end of the follow up period. Any subject with an ocular condition or systemic syndrome associated with an increased risk of developing childhood glaucoma [1] was categorized into Group 2 if they have demonstrated IOP > 21 mmHg on two or more occasions, and was categorized into Group 3 if they had not demonstrated elevated IOP throughout the study period. Subjects without glaucoma, high-risk condition/syndrome or ocular hypertension through the study period who were followed as a glaucoma suspect for other reasons (e.g. family history, increased cup/disc ratio [CDR]) were categorized into Group 4. Conversion from being a glaucoma suspect to manifest glaucoma is declared if two or more of the following findings are present:

    1. A progressive increase in cup-disc ratio or focal rim thinning as documented on serial disc photos not attributed to non-glaucomatous causes;
    2. A progressive thinning of circumpapillary retinal nerve fiber layer (RNFL) of ≥ 10 microns that is not attributed to image acquisition artifacts and non-glaucomatous causes;
    3. Progressive myopic shift coupled with an increase in ocular dimensions out of keeping with normal growth, in the context of elevated IOP > 21 mmHg on two or more occasions;
    4. An acquired visual field defect, or a reproducible deepening and/or expansion of a pre-existing visual field defect that is consistent with glaucomatous optic neuropathy that is not attributed to non-glaucomatous causes.

    Statistical analysis

    The baseline demographic and ocular characteristic between the four groups were compared and analyzed. Categorical variables were compared using Chi-square test, while quantitative variables were compared using one-way analysis of variance. A p-value ≤ 0.05 was considered significant.


    The initial ICD-9/ICD-10 search resulted in 546 entries, of which 214 subjects met the inclusion and exclusion criteria and were enrolled. The median age at initial presentation was 6.37 years (interquartertile range: Q1 = 2.46, Q3 = 8.90) and a mean (+/- standard deviation [SD]) follow up duration of 39 +/- 34 months. At the end of the follow up period, 22 (10.2%) subjects were in Group 1 (glaucoma) based on the CGRN criteria (4 late-onset primary congenital glaucoma, 4 associated with ocular inflammation, 4 juvenile open angle glaucoma; 3 associated with port-wine birthmark, 3 following trauma, one associated with Marfan syndrome, one associated with Axenfeld-Rieger syndrome, one associated with congenital persistent fetal vasculature without prior surgery, and one associated with oculodentodigital dysplasia), 64 (29.9%) were in Group 2 (ocular hypertension), 9 (4.2%) were in Group 3 (high-risk condition or syndrome), and 119 (55.6%) were in Group 4 (other). The follow up duration of each group was not significantly different (mean for Groups 1, 2, 3 and 4 were 32.8 +/- 33.5 months, 43.8 +/- 37.4 months, 33.1 +/- 26.6 months, and 37.7 +/- 32.3 months, respectively; p > 0.10). Neither a family history of glaucoma (Χ2 = 2.7, p = 0.43) nor patient gender (p = 0.40) were significantly different between the groups. Altogether, 40.2% (86 of 214) subjects had two or more episodes of IOP > 21 mmHg. Of these patients, 25.6% (22 of 86) developed glaucoma after a mean follow up of 32.8 +/- 33.5 months. Patient demographics and baseline characteristics are summarized in Table 1. The diagnoses in Group 3 (high-risk condition or syndrome) in this cohort included: uveitis, trauma, Rubinstein-Taybi syndrome, aniridia, microphthalmia, Axenfeld-Rieger syndrome and neurofibromatosis type I.

    On initial evaluation, 50% of suspects who eventually developed glaucoma (Group 1) had baseline IOP < 21 mmHg, with elevated IOP noted on follow up visits. Group 1 had the highest average, maximum and minimum IOP (25.5 +/- 7.1, p<0.01, 34.3 +/- 7.2, p<0.01, and 18.3 +/- 8.5, p<0.01, respectively), and displayed an insignificant trend towards a higher baseline axial length (mean 22.9 +/- 4.0, p = 0.07). Group 3 (high-risk conditions or syndromes without elevated IOP) had a significantly lower baseline cup-disc ratio (CDR; mean 0.39 +/- 0.19, p = 0.02). Group 4 (other) had significantly higher baseline mean circumpapillary RNFL thicknesses (mean 101.3 +/- 11.8, p = 0.02), while Group 1 had the lowest mean thicknesses (mean 87.6 +/- 21.4). There was not a significant difference in baseline visual field findings (Χ2 = 9.7, p = 0.5). In addition, no difference was seen in baseline corneal diameters or central corneal thickness (CCT; p >0.10 for all).


    Although childhood glaucoma suspects constitute the largest proportion of patients seen in a referral pediatric glaucoma service [3], little is known about the clinical course of these patients. To the authors’ knowledge, this is the first study to investigate the incidence and risk factors of glaucoma conversion in childhood glaucoma suspects. Approximately half of our cohort (55.6%) did not demonstrate more than one episode of elevated IOP and did not have high-risk conditions or syndromes for childhood glaucoma. Of the 44.4% of the patients who demonstrated two or more episodes of elevated IOP during the study period, 25.6% converted to glaucoma after a mean follow up of approximately 2.8 years. This suggests that a significant portion of childhood glaucoma suspects, especially those with two or more episodes of IOP > 21 mmHg, do go on to develop glaucoma, and that structural and functional stability on short-term follow up does not rule out the possibility of future glaucoma conversion. Furthermore, since only 50% of those who developed glaucoma presented with baseline IOP > 21 mmHg, the absence of elevated IOP on initial evaluation does not obviate the need for long-term monitoring.

    At the final visit, the subjects with high-risk condition or syndrome but remained without either glaucoma or elevated IOP (Group 3) were significantly younger than the other groups. This is likely an artifact of categorization, as any cohort member who acquired elevated IOP and/or glaucoma over the study period was reassigned to either Group 1 or Group 2. A prior survey showed that glaucoma associated with nonacquired systemic disease, syndrome or ocular anomalies present with a median age of between 0.5 and 2.9 years [3], which suggested that older children with high-risk conditions or syndromes are less likely to remain normotensive or without glaucoma and thus remain in Group 3.

    While the average, maximum and minimum IOP were highest in patients who converted to glaucoma, there were no distinct cutoffs that separated the group that converted to glaucoma from those who remained suspects. We found higher baseline RNFL in normotensive suspects without high-risk conditions or syndromes (Group 4) compared to subjects who developed glaucoma (Group1), which suggests that a thin baseline average RNFL measurement may be associated with an increased risk of glaucoma development in the pediatric cohort.

    The lack of difference in corneal diameter among the four groups was not surprising, as any child with obvious buphthalmos would likely have met the criteria for childhood glaucoma on the initial evaluation and have been excluded. However, the lack of difference in central corneal thickness between the groups is in contrast to prior studies, which showed a significantly increased baseline CCT in glaucoma patients [4–5]. Our finding may be attributed to the fact that many of our patients with ocular hypertension but no glaucoma (Group 2) and high-risk syndromes without glaucoma (Group 3) may have conditions associated with increased CCT, such as microcornea and aniridia [6–8]. Since the role of CCT in childhood tonometry remains uncertain [1], and adjustment of IOP based on central corneal thickness does not improve prediction models for primary open angle glaucoma in adults [9], it would be inappropriate to adjust IOP in childhood glaucoma suspects based on pachymetry.

    This study has several imitations. The retrospective design in a tertiary care setting may introduce selection bias. Childhood glaucoma suspects who are thought to have a very low risk of glaucomatous conversion, i.e. a child referred for a family history of adult-onset glaucoma, may have been followed elsewhere after an initial consultation at our institution, and was thus excluded from the analyses. This would concentrate the pool of high-risk glaucoma suspects in our cohort and thus yield a higher conversion rate. On the other hand, the initial medical record search was designed to catch those diagnosed with “ocular hypertension” or “glaucoma suspect,” which may have missed patients with high-risk conditions or syndromes (e.g. chronic steroid usage, Lowe syndrome, etc.) but were not coded as suspects. Our exclusion of Peters anomaly (due to the presence of corneal abnormalities and inability to obtain accurate IOP measurements) and patients with prior intraocular surgery may limit the generalizability of our findings. Our protocol precluded subgroup analyses of glaucoma conversion risk based on initial categorization, which may further limit the data’s application in prognosticating glaucoma in high-risk children.

    In summary, childhood glaucoma suspects require periodic monitoring, with special vigilance paid to those with two or more episodes of elevated IOP, as up to 25% may convert to glaucoma. The potential benefit of initiating prophylactic IOP-lowering therapy should be weighed against the risk and burden of topical therapy, especially in young children with minimally elevated IOP and no other risk factors. Since 50% of suspects who eventually converted to glaucoma did not present with elevated IOP, normal IOP on presentation does not preclude the need for monitoring. There was no significant difference in gender, family history, or baseline CCT between suspects who developed glaucoma compared to those who did not. While suspects who converted to glaucoma had higher average, maximum and minimum IOP measurements, there was no clear cutoff between the groups. Future efforts should focus on elucidating the amount of risk reduction per increment of IOP reduction in pediatric ocular hypertension patients.


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      Kong L, Fry M, Al-Samarraie M, Gilbert CE, Steinkuller PG. An update on progress and the changing epidemiology of causes of childhood blindness worldwide. J aapos, 2012. 16(6): p. 501–7. pmid:23237744
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      Hoguet A., Grajewski A, Hodapp E, Chang TC. A retrospective survey of childhood glaucoma prevalence according to Childhood Glaucoma Research Network classification. Indian Journal of Ophthalmology, 2016. 64(2): p. 118–123. pmid:27050345
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      Lopes JE, Wilson RR, Alvim HS, Shields CL, Shields JA, Calhoun J, et al. Central corneal thickness in pediatric glaucoma. J Pediatr Ophthalmol Strabismus. 2007 Mar-Apr;44(2):112–7. pmid:17410963
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      Lopez JP, Freedman SF, Muir K, Duncan L, Stephens D, Atenafu E, et al. Central corneal thickness in children and adolescents with pediatric glaucoma and eye disorders at risk of developing glaucoma. J Pediatr Ophthalmol Strabismus. 2011 Mar-Apr;48(2):108–16. pmid:20506965
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      Bayoumi NH, El Shakankiri NM. Central Corneal Thickness in Aphakic Children With Microcornea-Microphthalmia. J Glaucoma. 2016 Jun;25(6):497–500. pmid:27253817
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      Brandt JD, Gordon MO, Gao F, Beiser JA, Miller JP, Kass MA; Ocular Hypertension Treatment Study Group. Adjusting intraocular pressure for central corneal thickness does not improve prediction models for primary open-angle glaucoma. Ophthalmology. 2012 Mar;119(3):437–42. pmid:21705084

    Glaucoma – Conejo-Simi Eye Medical Group

    What is Glaucoma?

    Glaucoma is a leading cause of blindness. At least 3 million Americans suffer from glaucoma. Glaucoma is a disease of the optic nerve. The optic nerve is the cable that carries the information about the images we see from the eye to the brain. Many glaucoma cases are associated with elevation of eye pressure. Glaucoma optic nerve damage without high eye pressure is referred to as “low tension glaucoma” or “normal pressure glaucoma.” Glaucoma treatment, whether it is medication, laser, or surgery, aims to reduce eye pressure in order to protect the optic nerve and prevent vision loss.

    Visual loss from glaucoma results from damage to the optic nerve which leads to progressive loss of the field of vision. Usually people do not notice these blind areas until much of the optic nerve damage has already occurred. If the entire nerve is destroyed, blindness results. Early detection and treatment are the keys to preventing optic nerve damage and blindness from glaucoma.

    Who is at risk for Glaucoma?

    High eye pressure alone does not mean that you have glaucoma. A qualified ophthalmologist takes many kinds of information into account to determine your risk for developing the disease.

    Several important risk factors include but are not limited to:
    • Age
    • African ancestry
    • A family history of glaucoma
    • Past injuries to the eyes

    Your doctor will weigh all of these factors before deciding whether you need treatment for glaucoma or whether you should be monitored closely as a glaucoma suspect. If you are labeled as glaucoma suspect, it means that your risk of developing glaucoma is higher than normal and that you require more extensive monitoring.

    Types of Glaucoma

    Primary Open Angle Glaucoma

    The vast majority of glaucoma patients have primary open angle glaucoma (POAG). The rise in eye pressure associated with open angle glaucoma has to do with a cell problem at the drain (trabecular meshwork) that increases resistance in the drain.

    Closed Angle Glaucoma

    This is a process in which the drain (trabecular meshwork) is blocked by the iris, leading to high pressure. Acute angle closure glaucoma is a medical emergency of high eye pressure that can lead to sudden and permanent blindness. This attack of glaucoma occurs when the drain is suddenly blocked, and is associated with severe eye pain, blurring of vision, colored halos around lights, nausea and vomiting. Chronic angle closure glaucoma occurs when scar tissue slowly clogs the drain and leads to high eye pressure and optic nerve damage.

    Other Types of Glaucoma

    There are other types of glaucoma, such as glaucoma associated with trauma or inflammation, pseudoexfoliative glaucoma, pigmentary glaucoma, or neovascular (new blood vessel) glaucoma. Congenital glaucoma refers to a glaucoma someone is born with and is associated with abnormal eye anatomy.

    How is Glaucoma Detected?

    Regular eye examinations are the best way to detect glaucoma. During a complete and painless eye exam for glaucoma, your doctor will:

    • Check your vision
    • Measure your intraocular pressure (tonometry)
    • Examine the external anatomy of the eye
    • Evaluate the optic nerve appearance (ophthalmoscopy)

    If there is concern for glaucoma, additional testing may be performed. This can include:

    • Gonioscopy (exam of the internal drains of the eye)
    • Imaging of the optic nerve
    • Visual field testing to detect peripheral (or side) vision loss

    How often should a person with glaucoma see an ophthalmologist?

    After the initial examination and diagnosis, glaucoma patients are managed like other patients with chronic disease, requiring regular visits to assess disease severity and response to therapy. Most patients will need periodic medical examinations, diagnostic testing and individualized management with drugs or procedures. Once the diagnosis and treatment regimen are established, the average patient needs to be seen 3-4 times yearly. Frequency of visits and testing depends upon risk of progressive damage and severity of glaucoma.

    Eye drops for Glaucoma

    If you are diagnosed with glaucoma, eye drops may be prescribed to control pressure in your eye. Eye drops lower eye pressure, either by decreasing the amount of fluid produced within the eye or by improving the drainage of fluid from the eye.

    Glaucoma medications can preserve your vision, but they may also produce side effects. You should notify your ophthalmologist if you think you may be experiencing side effects.

    Lasers Treatments

    Laser treatment of Anatomical Narrow Angles or Angle Closure Glaucoma

    Angle closure involves the lens coming too close to the iris and blocking the passage of fluid into the front of the eye. Relief of this block allows the iris to move away from the drain and the drainage angle to open, allowing escape of fluid and lowering of the eye pressure. This is now commonly and simply done by making a small hole in the iris with laser (laser iridotomy), which provides another route for fluid to enter the front of the eye. For additional information, ask your doctor about the laser iridotomy procedure.

    Laser treatment of open angle Glaucoma

    Laser trabeculoplasty is a simple office procedure that has gained wide acceptance in the treatment of open angle glaucoma. The newer laser surgical option for treatment of open-angle glaucoma is called selective laser trabeculoplasty, or S.L.T. During the S.L.T. procedure, your doctor directs a low frequency laser beam into the trabecular meshwork, which is the primary drainage region of the eye. The S.L.T. laser selectively treats specific cells leaving untreated portions of the trabecular meshwork intact. The procedure increases drainage of fluid out of the eye, resulting in lowered pressure in the eye. For more information, ask your doctor about the S.L.T. procedure.

    Surgical Treatment of Glaucoma

    There are many surgical options available to treat glaucoma. Filtering procedures have been developed to shunt the fluid from the inside of the eye to a reservoir under the conjunctiva on the surface of the eye to bring down eye pressure. Trabeculectomy is a common operation for the control of elevated intraocular pressure in adult glaucoma. Glaucoma drainage devices, such as the Ahmed valve or the Baerveldt drainage implant, are another excellent option to control eye pressure. Cataract surgery can help to lower eye pressure and has the benefit of improving vision at the same time. A variety of minimally invasive glaucoma surgeries may be performed as stand-alone procedures or in conjunction with cataract surgery to lower eye pressure. Research is ongoing and there are many novel and exciting glaucoma procedures. For more information about surgical treatment of glaucoma, and whether one of these procedures may be right for you, consult with your doctor.

    Source: American Academy of Ophthalmology and American Glaucoma Society

    Dr. Shayna Mangers is a fellowship trained glaucoma specialist and a member of the American Glaucoma Society. She will work with you to create a glaucoma treatment plan customized for you, taking into account your medical conditions, lifestyle, and personal preferences.

    For more information, including frequently asked questions, please visit the American Glaucoma Society website.

    Glaucoma Surgery FAQs

    Signs of eye glaucoma, symptoms and treatment

    Glaucoma is a whole group of diseases in which damage to the optic nerve occurs, which leads to decreased vision up to the onset of blindness. As a rule, the development of pathology is caused by an increase in intraocular pressure. Most often, the disease occurs in elderly people, but in general, no one is immune from glaucoma, since the exact causes and mechanisms of the development of this pathological condition have not yet been identified.

    Glaucoma is diagnosed and treated by an ophthalmologist.

    Risk factors for the development of glaucoma


    If we are talking about congenital glaucoma, then its development is caused by impaired formation of the organs of vision in the prenatal period. Often this happens due to various intrauterine infections, such as rubella, mumps, toxpolasmosis, etc.

    Severe external factors, for example, radioactive radiation, poisoning of a pregnant woman with chemicals, etc., can also affect the development of the disease.


    Acquired glaucoma can be primary or secondary . Risk factors for its development include:

    • age over fifty years
    • increased intraocular pressure
    • race – in people of the black race, the disease is diagnosed several times more often
    • eye injuries
    • chronic eye diseases
    • general diseases of the body (obesity, diabetes mellitus, etc.)
    • chronic stress
    • hereditary predisposition
    • long-term use of certain medications (antihistamines, antidepressants, etc.).

    Types of glaucoma

    In medicine, it is customary to distinguish several types of glaucoma:

    • open-angle glaucoma – the most frequently diagnosed form of the disease. An increase in intraocular pressure is caused by a very slow outflow of intraocular fluid through the open corner of the anterior chamber, which is designed to act as a filter
    • angle-closure glaucoma – the angle of the anterior chamber closes, which leads to blocking the outflow of intraocular fluid.The disease is diagnosed only when certain changes in the fundus of the eye are detected
    • congenital glaucoma – diagnosed in newborns and one-year-old children, its development is associated with a congenital eye pathology that impedes the outflow of fluid
    • normotensive glaucoma – a poorly understood type of ocular pathology in which damage of the optic nerve occurs when the intraocular pressure is normal
    • pigmentary glaucoma – a rare form of the disease in which pigment is deposited on the iris, clogging the filtering corner and preventing the outflow of intraocular fluid.The drainage system can be damaged due to the developed inflammation in the blocked corner of the anterior chamber of the eye
    • secondary glaucoma – a disease that develops against the background of another eye pathology or prolonged use of drugs from the group of corticosteroids
    • neovascular glaucoma – pathological vascular growth occurs on the iris, which block the outflow of fluid
    • pseudoexfoliative glaucoma – on the back of the cornea, as well as on the iris and in the anterior corner of the eye, there are layers that look like flakes
    • Iridocorneal endothelial syndrome – the rarest type of disease in which only one is affected eye.The development of pathology is caused by the growth of cells from the posterior surface of the cornea into the anterior filtering corner.

    Signs and symptoms of glaucoma

    With open-angle glaucoma, you may not feel any pathological symptoms at the initial stages of the development of pathology. Only sometimes is it possible for a kind of rainbow circles to appear before the eyes. As the development of irreversible changes, the following clinical signs appear:

    • gradual deterioration in visual acuity
    • mild headaches
    • deterioration in peripheral vision, when you can see perfectly straight ahead, but objects from the side do not fall into the field of vision
    • impaired adaptation of vision when moving from a bright room to a dark one.

    In an acute attack of angle-closure glaucoma, the clinical picture is usually more noticeable. Pathological symptoms can occur after prolonged visual stress and disappear after rest:

    • eye pain
    • blurred vision
    • light sensitivity
    • appearance of rainbow circles when looking at light
    • nausea and subsequent vomiting
    • heart rhythm disturbances.

    Chronic angle-closure glaucoma is characterized by persistent pain in the eye and gradual deterioration of vision.

    Diagnostics in our clinic

    If you suspect glaucoma, the doctors of our clinic will prescribe you a comprehensive examination, which will include special ophthalmological and general examinations. Ophthalmological examinations include:

    • tonometry – checking intraocular pressure
    • visometry
    • computer perimetry to detect changes in the field of vision
    • campimetry to study a blind spot, that is, an area that you cannot see
    • ophthalmoscopy to detect damage to the optic nerve
    • computed tomography of the retina
    • assessment of the thickness of the cornea of ​​the eye
    • stress tests used in the diagnosis of angle-closure glaucoma.

    You also have to undergo a general examination, which includes clinical and biochemical blood tests, as well as consultations of narrow specialists. This is very important in order to identify background pathology that can lead to severe complications.

    Glaucoma treatment

    The doctor develops the tactics of glaucoma treatment individually, taking into account the type and stage of development of the disease, as well as its causes.

    Conservative treatment consists in the use of special eye drops to reduce intraocular pressure.The duration of the course of treatment is always individual. It is very important that you strictly follow the prescriptions of your doctor and do not stop therapy at the first sign of improvement.

    Sometimes, with glaucoma, surgery may be indicated, the main purpose of which is to normalize the outflow of intraocular fluid through the angle of the anterior chamber. The doctor, if necessary, can refer to the following types of operations:

    • laser trabeculoplasty – often used for open-angle glaucoma;
    • Laser iridotomy is an effective method of treating angle-closure glaucoma.With the help of a laser, a small hole is made in the iris, which ensures the normal outflow of fluid;
    • peripheral iridotomy – removal of some part of the iris provides the intraocular fluid with access to the drainage system;
    • trabeculectomy – formation of a valve from the sclera of the eye.

    In a number of situations, patients with glaucoma may be indicated for treatment with bypass surgery. A shunt is a special valve or small tube that is implanted into the eye and acts as a drainage system.

    Preventive measures

    To avoid many ophthalmic diseases, including glaucoma, you can follow simple preventive rules:

    1. Avoid eye strain by giving them rest while reading, working at the computer or writing.
    2. Perform special eye exercises every day, standing in front of a mirror.
    3. Massage the 90,004 eyelids and eyes.
    4. Limit the time at the computer, and if this is not possible, then use special protective glasses and make sure that the monitor is located at least sixty centimeters from your eyes.
    5. Correctly and rationally Eat so that your body receives all the necessary trace elements and vitamins.

    If you really care about the health of your own eyes, do not forget about regular examinations with an ophthalmologist, which will help identify any pathologies at the earliest stages of development.

    See also : Fitting glasses and lenses, Inflammatory eye diseases.


    Glaucoma is a fairly common disease.It affects mainly people over 40 years old. But this ailment can affect young and even newborns. Today ophthalmology knows only one way to prevent blindness in glaucoma – timely recognition and correct treatment. DETAILS

    Thanks to modern methods of treatment, most patients manage to preserve their eyesight and the joy of perception of the world around them.


    Heredity plays an important role in the occurrence of glaucoma.If your relatives have had glaucoma, you need to be especially vigilant and regularly see an ophthalmologist. We draw your attention to the fact that people suffering from diabetes mellitus, hypertension and asterosclerosis are more likely to suffer from glaucoma. Therefore, in addition to regularly visiting a therapist or endocrinologist, they should be examined by an ophthalmologist at least twice a year.

    Remember! Every person needs to be examined by an ophthalmologist at least once a year.


    With glaucoma, patients need systematic and long-term treatment, always under the supervision of a doctor. As a rule, treatment begins with the use of drugs: drops are instilled into the eyes, which reduce intraocular pressure; take pills that improve the nutrition of the optic nerve and retina. In some, unfortunately, rare cases, with this treatment, intraocular pressure becomes normal, and the condition of the optic nerve does not worsen.In such a situation, drug treatment is sufficient, however, the drugs will have to be used for life.

    Therefore, experts have developed qualitatively new methods of treating glaucoma: effective, safe and less traumatic. These include laser surgery and surgery.

    In the first case, the laser beam, freely entering the eye, acts on the drainage system and improves the outflow of intraocular fluid. Laser treatment is painless, short-term, performed on an outpatient basis.Its significant advantage is that the eyeball is not exposed to surgery.

    Unfortunately, the laser beam can not help all glaucoma patients. Such treatment can be effective only in the initial stages of the disease, when the intraocular pressure is slightly increased, as well as in the attacks of glaucoma described earlier. For the vast majority of those suffering from this ailment, surgery is the most effective treatment.

    According to experts, glaucoma should be diagnosed and treated surgically much earlier than it is done now.It has been proven that the use of traditional medicines often not only does not help, but also has a negative effect on the eye. The most common drugs that lower intraocular pressure decrease the production of intraocular fluid. This leads to a malnutrition of all structures of the eye, intensifies dystrophic changes in the optic nerve and retina. Surgical operation to create a new outflow pathway for intraocular fluid, performed as early as possible, will ensure the preservation of vision in patients with glaucoma.

    This operation was called “non-penetrating deep sclerectomy”. It can be successfully used in any form of open-angle glaucoma. The most important advantage of the operation is that it is performed without opening the eyeball. This eliminates the possibility of infection, significantly reduces the risk of complications during the operation.

    Non-penetrating deep sclerectomy is performed under local anesthesia, instillation of drops with the obligatory participation of anesthesiologists who will prepare you for surgery and help relieve nervous tension.For its implementation, an excimer laser, special microsurgical instruments with blades made of diamond, sapphire and other high-strength materials are used. The duration of the operation is on average 15-20 minutes.

    The operation is performed for various types of primary, congenital and secondary glaucoma in eyes with preserved visual functions (presence of visual fields) The total treatment time for one eye is 10 days (preoperative examination 2-3 days, on the 4th day – surgery).

    In addition to non-penetrating deep sclerectomy, other types of antiglaucomatous operations, developed in the leading ophthalmological clinics of the world and widely used in the Eye Microsurgery MNTK, are also used according to indications.

    If, in addition to glaucoma, cataracts are found in you, then you need surgical treatment, which consists in carrying out a non-penetrating deep sclerectomy and removing the cataract with the replacement of the clouded lens with an artificial, reliable and perfect one.Depending on the indications, the intervention is performed alternately or simultaneously.

    After the operation, you will need to instill anti-inflammatory drops, so you need to purchase them in advance, following the doctor’s recommendations.

    After 9-14 days, if the appointments are performed correctly, the redness of the operated eye will disappear. You will be able to calmly look at the light, watery eyes and the sensation of a foreign body in the eye will not bother you.

    If the operation is done in a timely manner, it normalizes intraocular pressure and preserves vision.

    In the future, we recommend that you regularly, 2-3 times a year, visit an ophthalmologist to check visual acuity and control intraocular pressure, since the progression of disorders in the vascular and drainage systems of the eye, as well as excessive scarring in the area of ​​the antiglaucomatous operation performed can again lead to an increase IOP in a small percentage of cases (1.5-2.2%). The reason for the lack of effectiveness of the operation can be determined by an ophthalmologist and the necessary treatment can be carried out.

    A number of innovative treatments have been developed, also aimed at preserving the vision of patients with glaucoma.These include: magnetic and laser stimulation of the optic nerve, which improves vision, especially in advanced glaucoma, as well as vasoreconstructive surgery. This operation is performed strictly according to the indications of patients with impaired blood supply to the eye, which, unfortunately, often happens even with normal intraocular pressure. As a result of a simple surgical procedure, more blood will flow to the eye, carrying nutrients.

    Laser treatment of glaucoma

    The widespread use of the laser to combat glaucoma began in the 70s of the last century.Currently, laser treatment of glaucoma has rightfully established itself all over the world as the most effective and safe method. In this case, laser treatment of glaucoma can be performed as an independent method of treating glaucoma, and in combination with microsurgical antiglaucoma surgery.

    Benefits of laser glaucoma treatment:

    • restoration of the outflow of intraocular fluid from the eye along natural pathways;
    • high efficiency of intraocular pressure reduction;
    • minimal risk of complications;
    • laser interventions are painless, carried out under local anesthesia by instilling anesthetic drops;
    • laser treatment for a short time, carried out on an outpatient basis;
    • short, short period of recovery (rehabilitation).

    Laser treatment of glaucoma is most effective in the early stages of the disease.

    Depending on the type of glaucoma – open-angle or closed-angle, the nature of changes in the drainage apparatus of the eye, various types of laser interventions (operations) are used.
    Laser treatment is carried out using the most modern original technologies developed at the Eye Microsurgery MNTK and advanced, innovative techniques used in world practice.Our specialists use the most modern equipment, the latest laser installations, which allow us to carry out the entire wide range of laser interventions for the effective treatment of glaucoma.

    Specialists of MNTK “Eye Microsurgery” will select the optimal method of glaucoma treatment for you, which will preserve your eyesight and restore the joy of life.

    Patient Memo

    Your doctors

    Glaucoma: description of the disease, causes, symptoms, cost of treatment in Moscow

    A disease that affects the visual organs is called glaucoma.The main reason for the development of glaucoma is increased intraocular pressure, as a result of which intraocular fluid circulates poorly. Necrosis of the optic nerve begins, a person’s visual function worsens, and complete blindness may occur. To prevent such consequences, it is necessary to contact an ophthalmologist in a timely manner, who will prescribe treatment for glaucoma. To do this, you should recognize the symptoms in time. Depending on the type of disease, the symptoms will be slightly different.

    Varieties and characteristics

    With open-angle glaucoma, which is more common than other forms of the disease, excess fluid accumulates, resulting in increased eye pressure.The reason for this is the lack of outflow of the accumulated liquid. In most cases, the doctor prescribes a drug that works to lower intraocular pressure. There are situations when such a drug does not bring the desired result, so the patient may be prescribed surgery.

    Open-angle glaucoma, and especially the early stage, may not show any symptoms. There is no increase in intraocular pressure, but the structure of the eye is still affected.It is possible to suspect this form of glaucoma already when the last stage comes. The danger is that preventing vision loss is no longer possible.

    The first dangerous signal that an eye disease is developing is bright circles around objects. A feature of this border is the transfusion of different colors. In addition, a person may experience headache and eye pain. Glaucoma is characterized by blurred vision and blurred objects.

    A person may not assume that it is glaucoma that develops, and make himself a false diagnosis. In such a situation, precious time is wasted, since only a qualified doctor can make a diagnosis. He examines the patient with a special device.

    With age, the risk of glaucoma increases, therefore, for preventive purposes, people over forty years old are recommended to come to an appointment with an ophthalmologist once a year.This is important even in the absence of any dangerous symptoms.

    With angle-closure glaucoma, when the anterior part of the eyeball is disturbed, a person complains of the occurrence of strong painful sensations in this place. In addition, the space between the cornea and the iris narrows, there is no possibility of the accumulated excess fluid outflow. As a result, there is an increase in intraocular pressure. Among the symptoms of this form of glaucoma, one can distinguish the appearance of nausea, vomiting, redness of the eye, rainbow circles in front of it.In an acute attack of glaucoma, which is an urgent condition, the patient needs immediate treatment. Otherwise, the person’s vision may disappear for a while.

    There are a number of difficulties that a person with this form of glaucoma will have to face. Namely:

    • Prohibition of tilting the head down. If you do not follow this rule, the risk of negative health effects increases.

    • Do not work in a very hot and unventilated area.

    • Stress of vision (darkness, twilight, poor lighting) can aggravate the course of the disease.

    • Strict control of the amount of liquid that a person drinks throughout the day.

    • Any drug that can cause dilated pupils or increased intraocular pressure is prohibited.

    The onset of angle-closure glaucoma is characterized by the following symptoms:

    1. Vision deteriorates, objects become blurry.

    2. Painful sensations, localization of which are eyebrows and eyes. Such pain is characterized by a certain frequency.

    3. A bright rainbow rim appears around any light source, as well as around an ordinary object.

    4. Acute periods of the disease are replaced by lulls. If there are no symptoms, this does not indicate that the progression of glaucoma has stopped. During such periods, visual function continues to deteriorate.

    5. The angle of the anterior chamber of the eye narrows and closes. If the intraocular pressure rises significantly, there is a strong reddening of the protein, corneal edema. Such a symptom is noticeable even to an ordinary person who does not have a medical education.

    With the development of mixed glaucoma, the outflow of the accumulated excessive amount of fluid becomes difficult, the angle of the anterior chamber of the eye is blocked.

    The occurrence of secondary glaucoma is associated with an inflammatory process, trauma, surgery, diabetes mellitus, malignant or benign formation, and the intake of certain medications.

    The presence of congenital glaucoma is a consequence of intrauterine malformation.In most cases, such a disease is diagnosed in a child. It is possible to eliminate this form of eye disease only with the help of an operation.

    Who is at risk

    There is a category of people who are at risk of developing the disease.

    • Active smokers, alcoholics. Due to the excessive consumption of alcoholic beverages, intracranial pressure will constantly increase.

    • Failure to comply with the correct power supply.

    • Those who self-medicate prescribe medication for themselves.

    It is necessary to warn the doctor about concomitant diseases. It happens that blindness appears as a result of understatement. For example, if a person has hypertension or bronchial asthma, and an attack occurs, the administration of aminophylline is necessary. Because of this drug, glaucoma will worsen, a person may lose sight. This means that to inform the doctor about a particular disease before starting treatment.

    How does the disease manifest

    If we talk about the first symptoms of glaucoma, the following can be distinguished:

    1. The appearance of rainbow circles. The appearance of such circles occurs when looking at the light. The subject in question is dark and the halo is rainbow-colored. According to doctors, this symptom occurs earlier than others. Rainbow circles are a consequence of increased intraocular pressure that occurs due to corneal edema.Also, circles can signal that the lens is pathologically changed or conjunctivitis develops.

    2. Blurred vision. Sometimes glaucoma is the cause of the fog before the eyes. As a result, a person is unable to see the details of surrounding objects. It will appear that there is a slight haze around the objects. In some cases, a person is unable to determine the border of the object in question and its color. This sign will be present for a long time (from 10 minutes to 5-6 hours).

    3. Headache and eye pain. The development of glaucoma is accompanied by a headache. The intensity of the pain increases if the disease affects both eyes. The localization of painful sensations is the temple on the side where the disease develops. The pain is pulsating.

    4. Excessive lacrimation. The presence of glaucoma of the eye provokes a violation of the outflow and inflow of fluid that is inside the eye. In addition, intraocular pressure rises.Lacrimal fluid is produced in large quantities. If such a symptom appears, you should not contact the ophthalmologist of the medical center.

    5. Falsely moisturizes the eye. With glaucoma, a person feels as if the eye is filled with tears. As he tries to wipe away his tears, he realizes that tears are missing. This phenomenon is directly related to increased intraocular pressure.

    If you find one or more warning signs of an eye disease, you should immediately visit a doctor.

    Features of treatment methods

    To get rid of intraocular pressure, eye drops are prescribed to the patient. They normalize the outflow of excess fluid from the eye. Glaucoma is treated with the following drops:

    1. Drops containing prostaglandins. Thanks to such drugs, intraocular pressure is reduced. After the first use, a person may notice that the mucous membranes of the eyes turn red, tingling appears, the iris has darkened, and vision has deteriorated.In some cases, the color of the eyelashes may change.

    2. Use of beta blockers. This medication prevents excessive fluid production in the eye. Before use, it is necessary to take into account all concomitant diseases, since the drug has side effects. This includes hypotension, slow heartbeat, decreased potency, increased fatigue.

    3. Use of carbonic anhydrase inhibitors. Such drops are rarely prescribed to a person with glaucoma.The action of such a drug is aimed at reducing the production of intraocular fluid. However, there may be a metal taste in the mouth cavity, urination frequency, tingling sensation in the extremities.

    4. Use of alpha-adrenergic receptor agonists. After applying such drops, the production of fluid in the eyes decreases, and its outflow improves.

    Surgical intervention is indicated for those patients who are diagnosed with primary open-angle glaucoma.Medicines are not able to eliminate such a pathology. Local anesthesia is administered before the operation. Linear trabeculoplasty is often used. To perform surgery, you need a gonioline lens.

    In addition, deep and non-penetrating sclerectomy may be prescribed to treat angular glaucoma. Thanks to this procedure, it is possible to reduce intraocular pressure by thinning the area of ​​the peripheral cornea. Better permeation of eye fluid through the membrane will occur.Collagen drainage is required to prevent scarring.

    The surgical intervention that is necessary to get rid of glaucoma is not as dangerous as it seems. The duration of the operation is approximately 20-30 minutes. The patient does not need to stay at the clinic. When the operation is over, you should be under the supervision of a specialist for some time. Then the person can go home. The next appointment is scheduled in three to four days. At home, drops should be instilled into the operated eye.Only a doctor chooses drops.

    Varieties of surgical intervention

    A patient who has an acute attack of glaucoma needs hospitalization. Therapeutic measures can be based on taking medications, or on surgical intervention. During each attack, intraocular pressure rises significantly, and complete blindness can occur. Further restoration of vision after this is impossible.

    With timely assistance to the patient, the function of the eye can be fully restored.There are several types of surgeries that are used to correct glaucoma:

    • Non-penetrating sclerectomy is used to treat open-angle disease. Intraocular pressure decreases after the operation. This is due to the fact that a limited area of ​​the peripheral cornea has become thinner.

    • Conducting trabeculectomy. This is a penetrating surgical intervention.

    • Carrying out cyclocoagulation.This operation helps to reduce the production of eye fluid.

    • After iridectomy or iridocycloretraction, the intraocular fluid will function normally.

    • Carrying out iStent. It is a minimally invasive innovative technique for eliminating glaucoma. The procedure is performed using a special device. Thanks to this method, the outflow of excessively accumulated fluid is normalized, the pressure inside the eyes decreases.

    Prevention of glaucoma – Rossiyskaya Gazeta

    About glaucoma – a disease due to which hundreds of thousands of people go blind every year in Russia, I know firsthand. My grandfather, who went through the Patriotic War, has not seen anything from his long, almost 90-year life for the last ten years. Three of his sisters suffered from glaucoma, and also became blind in old age. That is why the seminar on glaucoma, which was organized by the experts of the Russian Glaucoma Society and the Society of Ophthalmologists of Russia, became an excellent opportunity for me to ask the questions of our best glaucoma specialists that concern me.The main conclusion: the onset of blindness can be postponed for many years, but this will require a lot of effort and follow certain rules.

    Rule 1. Do not ignore the prophylactic medical examination – visit an ophthalmologist

    Glaucoma is incurable yet. It affects both children and adolescents, and adults, but still, in most cases, the disease overtakes at an advanced age. Doctors still do not know exactly why the retina and optic nerve begin to die off and a person gradually loses the ability to see.Perhaps genetics is to blame (my ancestors are a serious argument in favor of this opinion). Other reasons are also possible – a heavy load on the eyes, vascular diseases. At the same time, there is good news: drugs have been created that slow the progression of the disease. Therefore, if the diagnosis is made on time and treatment begins, the darkness can win back a dozen years, or even more.

    The insidiousness of the disease (as is the case with many other ailments) is that glaucoma does not hurt. And until vision begins to fall and a person does not turn to an ophthalmologist “just” for glasses, he will not even suspect that he is at risk of going blind.

    What to do? Well, of course, make sure to check your eyesight regularly – and not at the pharmacy to buy glasses faster, but at the ophthalmologist, who will look at the fundus and measure the intraocular pressure.

    “In 20 percent of cases, a patient with glaucoma comes to blindness,” said the President of the Russian Geographical Society, Professor Evgeny Egorov. …Today, 90% of patients have a different type of disease – open-angle glaucoma, which has been asymptomatic for a long time. ” that it does not manifest itself until the onset of blindness, patients come to doctors dramatically late.Moreover, the loss of visual fields occurs fragmentarily, and often the second eye compensates for that part of the “picture” that is no longer accessible to the affected eye – the person continues to see and does not understand that, in fact, is already going blind.

    “Most often the patient comes to the appointment to pick up his glasses, because he began to see worse, and when he closes one eye, he says:” Oh, why did you turn off the light? I don’t see anything! “That is, one eye has already gone blind, but the person has not even noticed it,” says Professor Yegorov.

    Rule 2. Measure intraocular pressure

    This is one of the most important procedures at an appointment with an ophthalmologist. Because if the pressure is high, this is one of the signs of glaucoma. “The level of pressure is the main factor that we can have a therapeutic effect on glaucoma.It happens, in rare cases, the disease goes away with normal blood pressure; there are individual deviations from the norm, for example, in patients with vascular diseases or with high myopia. But even in such cases, the doctor may see an increase in pressure. ” intraocular pressure only once every three years and only for people 60 and older.We had to make a lot of efforts to change the standards – after all, the disease is getting younger, and at the age of 60 it is already difficult to stop the development of glaucoma, – explained Professor Yegorov. – It’s good that the order has been changed: now every Russian over 40 can come and be examined once a year. And if the disease is detected at an early stage, in time, start delaying the onset of blindness therapy. “

    Rule 3. Do not be lazy and get treated

    Ophthalmologists are encouraging: the initial stage responds well to treatment in 98% of cases.If a developed degree of glaucoma is diagnosed, drug therapy helps 67% of patients. Launched glaucoma is treatable, alas, in less than a third of patients.

    “Today, an effective, so-called preservative-free therapy has appeared,” explains Aleksandr Kuroyedov, professor of the Department of Ophthalmology at the Pirogov Russian National Research Medical University.And in many cases, patients simply stopped treatment. “

    But compliance (adherence to treatment) is one of the most important conditions for effective therapy, emphasizes Professor Kuroyedov. If a patient does not follow a doctor’s appointment regularly or even more so stops treatment, the progression of glaucoma is inevitable.

    ” Po According to our data, at least 70% of patients on standard therapy eventually stop fulfilling their prescriptions, such “fatigue” occurs on average six months after the start of treatment, and it is very important that the doctor supports the patient and insists on continuing therapy.With the advent of preservative-free drugs that do not give side effects, it has become easier to achieve adherence to treatment in our patients, “says Alexander Kuroyedov.

    RG reference

    According to expert estimates, glaucoma affects 20 to 60 million people in the world Every minute 1 adult becomes blind from it, and every 10 minutes – 1 child.Glaucoma (a disease leading to the gradual death of the retina and optic nerve) is congenital, childhood, adolescent, young age, but still the risk of its development increases significantly over the years …If at the age of 60 2.5 people out of 1000 get sick, then at 80 it is already 17.5. The number of people with such a diagnosis is growing by 3-4% per year: in 2006 there were slightly more than a million in Russia, in 2018 – almost 1.4 million. At the same time, according to experts, at least another 0.5 million cases have not yet been diagnosed. In two out of three people, glaucoma is found in advanced stages.

    Medical, laser and surgical treatment of glaucoma

    Fasting of admiration and gratitude.Or … If we all worked like this … It began with an unpleasant one. I suspected the need for surgical treatment of the dog’s eye.

    The gynecologist’s suspicion requires confirmation by an ophthalmologist. And we trudged to the doctors. Not that they were given to the first comer, they visited status places, but there was still no readiness to put the pet on the operating table. We turned to our favorite word of mouth. And it sent us to the Clinic of Dr. Shilkin.To say that I am delighted, and especially in such a situation, is to say nothing. Only a couple of very cool “human” ophthalmological clinics have such equipment in the operating room, as there is. The level of education of doctors and equipment of offices is simply off scale. Care … Well, at least the fact that the examination carried out by the doctor with all kinds of “scopes” is observed by the assistant and the owner of the animal, and on different monitors located at the right angle, it is worth a lot. Everything seen is commented on.Moreover, even the “banal” microscope, with the help of which the smear is viewed, has additional monitors. Communication … I think if all the “human” doctors talked like that, we would not have any lawsuits. First, you need to hear it. This kind of empathy is not common. And secondly, for example … “After the operation … complications are possible. To reduce their risk, we will prescribe … But these drugs have side effects …. Most often they appear on …. day. But if you notice … earlier, call – write – come.”Everything is spoken clearly first by the doctor, then by the assistant and written down in the recommendations. By the way, they quickly” figured out “me. In the second minute of examining the dog in a monologue mode, the doctor asked what kind of doctor I was. Apparently, it is written on the forehead. The empathy, which I wrote about above, is not related to the fact that I am “my own.” It so happened that I had to observe different animals, their owners, doctors and other employees of the clinic for a very long time and carefully, so I can state it.P. S. After 8 months the operated eye “liked” the doctor even more than the second, absolutely healthy. Not advertising. The dog was operated on by D.A. Rotanov.

    Eye drops for glaucoma | Taufon

    Glaucoma is a multifactorial disease that is always accompanied by an increase in intraocular pressure. The disease has several stages, in the absence of treatment and untimely seeking help, glaucoma leads to an irreversible decrease in visual acuity, and subsequently to blindness.

    Causes of glaucoma development

    In a healthy eye, constant intraocular pressure is maintained due to the balance between production and the outflow of aqueous humor (intraocular fluid). With glaucoma, this process is disrupted, as a result of which there is a constant or periodic increase in intraocular pressure. With long-term preservation of high pressure figures, atrophy of the optic nerve head develops, which leads to a narrowing of the visual fields, and in the future – to complete blindness.

    Glaucoma symptoms

    In the early stages, glaucoma, as a rule, does not have pronounced symptoms of the disease. Sometimes patients may notice the appearance of rainbow circles in front of their eyes. As the disease progresses, peripheral vision deteriorates due to narrowing of the visual fields. Unfortunately, patients may not always notice these symptoms on their own. And only when the central visual zone is already suffering (a dark spot may appear), most patients go to the doctor.

    Diagnostics of glaucoma

    At an early stage of the disease, the main problem of its diagnosis is the absence of visible symptoms. That is why it is important to undergo scheduled examinations annually in order to identify the disease in time and avoid serious consequences. If glaucoma is suspected, the doctor measures intraocular pressure and assesses the condition of the anterior segment of the eye (examines the angle of the anterior chamber of the eye) using a mirrored lens. Also, the diagnostics must necessarily include:

    • examination of visual fields in both eyes,
    • measurement of refraction and determination of visual acuity.

    Treatment of glaucoma with eye drops

    If the disease is detected in time at an early stage, then its course can be controlled and loss of vision can be prevented. The main goal of glaucoma treatment is to normalize intraocular pressure. This is achieved by reducing the production of intraocular fluid or improving its outflow. In the initial stages, glaucoma treatment involves the use of eye drops, which lower intraocular pressure. In addition to special drugs that reduce intraocular pressure, the doctor can also prescribe vitamins, drugs that improve metabolism in the tissues of the eye, for example, Taufon® eye drops, and also refer the patient to other specialists, for example, to a therapist, in order to normalize arterial pressure.Therapy can also include laser and / or conventional surgery. Treatment tactics depend on the severity and type of the disease, as well as the reasons for its development. Eye drops for glaucoma, as well as for cataracts, as part of complex therapy can be prescribed both before and after surgery to ensure rapid tissue recovery. However, the result can be achieved only with strict observance of all the recommendations of the attending physician and the systematic regular use of anti-glaucomatous drugs.It must be remembered that self-medication for this disease can only worsen its course and accelerate vision loss.

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    90,000 Glaucoma diagnosis


    Glaucoma is an eye disease associated with the accumulation of intraocular fluid. The accumulation of fluid increases pressure inside the eye and can damage the nerve that carries visual information to the brain (called the “optic nerve”).As a result, vision is impaired.


    In a normal, healthy eye, fluid is constantly formed (the so-called “aqueous humor”). The fluid washes the structures of the eye, delivering nutrients to the cornea and lens. The fluid change takes place thanks to the small holes (forming the trabecular meshwork). Thus, the constant formation and drainage of fluid keeps the eye moist and healthy.


    With glaucoma, more fluid is produced in the eye than is excreted.this leads to a buildup of fluid that increases pressure inside the eye (intraocular pressure). Increased pressure affects all structures of the eye, but most often the optic nerve is damaged.


    Glaucoma affects the width of view, that is, the ability to see objects outside of the fixed point, or the so-called “peripheral vision”. The development of the disease occurs gradually, so many patients do not notice such visual impairments.As glaucoma progresses, blind spots appear in peripheral vision and the patient sees less and less clearly than before. Delayed detection of glaucoma, as well as the lack of adequate treatment for the disease can lead to blindness. Fortunately, today, thanks to modern technology and the alertness of doctors, this happens extremely rarely.


    Although the damage to vision cannot be repaired, the good news is that with continued and adequate treatment (such as eye drops), further narrowing of peripheral vision can be stopped.In addition, in some cases perform operation . We will consider detailed information on treatment options below.


    There are two types of glaucoma: open-angle and closed-angle. Open-angle glaucoma is a common chronic condition (that is, the disease has a long duration). This type of glaucoma is associated with blockage of the drainage system and is often detected during routine eye examinations. Angle-closure glaucoma, or excessive fluid formation, is less common and acute (that is, it manifests itself in short-term, but severe and acute attacks).Blindness can develop very quickly without treatment. This type of glaucoma develops when the angle of entry into the drainage system is closed, which leads to fluid filling.

    Glaucoma can be caused by other disorders that affect the structure or function of the eye. This is the so-called “secondary glaucoma”. Secondary, chronic glaucoma can be caused by swelling or swelling of the eye. An acute attack of secondary glaucoma can occur with diabetes mellitus, cataracts, with prolonged treatment with corticosteroids; however, this rarely happens.


    Early detection and diagnosis of glaucoma is the basis for preserving vision. During the examination, the ophthalmologist with a routine examination can detect early signs of illness that the patient may not be aware of.


    The measurement of pressure inside the eye is called tonometry. A tonometer is a device for measuring intraocular pressure.


    The eye doctor examines the fundus with an instrument called an ophthalmoscope.This procedure allows you to see and evaluate the slightest changes in the optic nerve.


    Changes in the visual fields can also be detected by visiting an eye doctor. The visual field is examined in various ways. Regular examinations can detect the slightest irregularities that are difficult to notice on your own.


    Regardless of whether glaucoma is chronic or presents with a severe, painful attack, delay in treatment can lead to serious problems.



    The main treatment is the use of eye drops, which reduce the formation of fluid in the eye or increase its excretion. Some drops do both at the same time.


    • Beta Blockers
    • Carbonic anhydrase inhibitors
    • Prostaglandins
    • Adrenergic drugs
    • Cholinergic drugs

    Operation for glaucoma is performed when conventional treatment is ineffective or when the disease progresses rapidly, even if the eye pressure was brought back to normal.



    For an acute attack of glaucoma, your eye doctor will do two things. First, he will prescribe one of the treatment options listed above to relieve pain and reduce blood pressure. Secondly, it will perform a laser operation to open the angle of the drainage system and increase the outflow of fluid.


    Continuous treatment can slow the progression of the disease and preserve vision.



    HOW TO USE EYE DROPS (These instructions apply both to the preparations in the vial and to the drops in the single dose vial. Please read the following recommendations carefully before using the eye drops)


    • Use eye drops according to your doctor’s recommendations and directions for use.
    • If using more than one type of drops, read the instructions for use.
    • Wash your hands before using drops.
    • Do not touch the eye with the tip of the drop bottle.
    • Like all medicines, eye drops should be kept out of the reach of children.

    STEP 1

    Tilt your head back and pull the lower eyelid of the eye into which you want to drop the drops with your index finger so that a pocket is formed.

    STEP 2

    Turn the bottle upside down with the dispenser. Press lightly on the bottle.

    STEP 3

    Put the number of drops recommended by your doctor into the pocket formed by the lower eyelid. Close your eyes for 1 or 2 minutes to absorb the drops.


    • The contents of one bottle of drops are usually enough for one month after opening.
    • After this period, it is necessary to start a new bottle instead of the old one, even if the old one is not fully used.
    • A vial with a single dose of the drug can be used only once, an opened vial cannot be stored.
    • If you have problems using the eye drops, write them down and consult your doctor. Treatment may need to be changed.


    You are, of course, concerned about the diagnosis of glaucoma. After all, glaucoma is a serious disease that, if left untreated, can lead to blindness.However, you can lead a normal life, which practically does not differ from the lifestyle of healthy people, subject to the course of treatment and regular consultations with an ophthalmologist.

    Inside the eye, intraocular fluid is constantly produced, which provides nourishment and oxygen to the internal structures of the eye, and also frees them from metabolic products. Intraocular fluid is excreted into the blood vessels through the complex drainage system of the eye. In the eye of a healthy person, the process of production and outflow of intraocular fluid is well balanced.When outflow is disturbed, intraocular fluid accumulates in the eye and causes an increase in intraocular pressure.

    Maintaining intraocular pressure at a good level is the main goal of treatment. With a normal value of intraocular pressure, the risk of damage to the optic nerve decreases, and the likelihood of preserving vision increases.

    For most people, normal blood pressure is considered a level of 16-26 mm Hg.

    For each patient with glaucoma, the level of normal pressure is individual, depending on the stage of the disease.

    Once glaucoma is diagnosed, it is necessary to reduce the intraocular pressure by any of the three main methods:

    • medicated
    • laser
    • surgical.

    In most cases, eye drops are prescribed to reduce intraocular pressure. The main condition for the treatment of glaucoma is compliance with the daily regimen of instillation of the prescribed drops (usually 2 times a day at 8 and 20 hours).

    An important sign of glaucoma is changes in the visual field and the appearance of defects in the visual field.Changing the visual field serves to assess the course of the disease and the effectiveness of treatment.

    The field of vision is the space that is simultaneously perceived by the motionless eye. If you fix your gaze at any point, in addition to it, you can see objects to the right and left, up and down from it.

    Glaucoma is a dangerous and insidious ailment: the patient begins to notice changes in the visual fields only when the disease is already in its advanced stage.

    Unfortunately, there is currently no cure for glaucoma.However, with early diagnosis of the disease and proper treatment, it is possible to stop the progression of the disease. This can be assessed by the level of intraocular pressure and the absence of an increase in visual field defects.


    In addition to maintaining normal intraocular pressure, it is necessary to receive courses of conservative treatment 1-2 times a year, including the use of drugs and physiotherapy methods.

    Medicines improve eye nutrition, normalize general and local hemodynamics.

    Physiotherapy treatments include magnetotherapy, low-energy laser irradiation, and electrical stimulation of the optic nerve and retina.


    • Work as long as your age and general health allow, do not strain. Avoid physical and nervous strain. The maximum weight that can be lifted is 10 kg.
    • Even weeding the beds can be an overload for you if you are working on a slope.Adapt some kind of bench, chair and do not bend over. Whatever you do, read, draw, knit, do not sit with your head tilted and in poor lighting.
    • You can watch TV, but also in good lighting (not in the dark!) And in the correct posture so that your head is neither tilted nor tilted back.
    • When reading and other strenuous visual work, take small breaks of 10-15 minutes every hour.
    • Eat rationally according to age, prefer vegetable dishes, fish, raw vegetables and fruits, limit animal fats and sugar.
    • The liquid, if there are no other indications for this, can not be particularly limited, but you cannot immediately drink more than a glass. Tea is even useful, as the caffeine it contains improves blood circulation in the tissues of the eyes, and increases intraocular pressure in rare cases. A cup of coffee is also not forbidden, but to be sure, it is better to do a caffeine test: measure the intraocular pressure before drinking coffee, and 1-1.5 hours after that.
    • If you are a smoker – quit smoking immediately! Nicotine is bad for your eyes.
    • Do not wear tight collars, ties – anything that impedes blood circulation in the head and neck area.
    • Good sleep is very important to you. Introduce evening walks into your daily routine; if you can’t sleep – take 2-3 teaspoons of honey at night, washed down with warm water, do warm foot baths.
    • Follow the prescribed drip regime exactly. If you have to leave home for a long time, do not forget to take them with you.
    • In case of angle-closure glaucoma, a sharp change in illumination is difficult for the eyes.Give pilocarpine a drop of pilocarpine before going to a movie theater or other darkened area to prevent pupil dilation.
    • See your doctor regularly. Even with stabilization of intraocular pressure, a follow-up examination is recommended every 3 months.