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OPHTHALMOLOGY PRACTICE
Year : 1993  |  Volume : 41  |  Issue : 2  |  Page : 91-96

Practical approach to diagnosis and management of primary glaucomas


Schell Eye Hospital, Christian Medical College, Vellore, Tamil Nadu, India

Correspondence Address:
Ravi Thomas
Schell Eye Hospital, Christian Medical College, Vellore - 632 001, Tamil Nadu
India
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Source of Support: None, Conflict of Interest: None


PMID: 8262613

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How to cite this article:
Thomas R, Kuriakose T, Braganza A. Practical approach to diagnosis and management of primary glaucomas. Indian J Ophthalmol 1993;41:91-6

How to cite this URL:
Thomas R, Kuriakose T, Braganza A. Practical approach to diagnosis and management of primary glaucomas. Indian J Ophthalmol [serial online] 1993 [cited 2020 Nov 26];41:91-6. Available from: https://www.ijo.in/text.asp?1993/41/2/91/25612

Primary open angle glaucoma (POAG) and primary angle closure glaucomas (PACG) are commonly encountered by practising ophthalmologists. Several approaches to the evaluation and management of these diseases exist. We present here some practical guidelines based on the experience and management philosophy of our centre, and reflects a very personal approach.


  I. PATIENT WITH RAISED INTRAOCULARPRFSSIJRF (T(lP) Top


On a routine examination a patient's intraocular pressure is found to be high. Alternatively, another ophthalmologist or genefal practitioner has recorded a raised IOP and the patient is seeking a second opinion. The IOP measurement especially by applanation tonometer (or any tonometer) must be a routine in the practice of all ophthalmologists. Let us assume that .the pressure has been recorded as 24 or 26 or even 30 mm Hg.

A single IOP recording of more than 21 mm Hg does not always indicate glaucoma. Such a pressure reading could result from instrument error, faulty recording or simply pure chance. While instruments and other errors can be eliminated by using standard recording techniques, the chance recording of a high IOP is best dealt with by measuring it again. If the second reading is normal, and if gonioscopy, disc examination and the visual field examination are normal, then there is no evidence of glaucoma.

If a repeat IOP is also high, the next step is to determine whether the pressure is raised due to angle closure glaucoma or is associated with open angles. Anytime a high IOP is recorded (including a first meas­urement), a gonioscopy should be done immediately.

It is important to use a gonioscope which will pro­vide an "in situ" or "undisturbed" view of the angle. In order to determine whether the angle closure is the cause of glaucoma, it is inappropriate to use a lens which may artifactually open up the angle, eg the Goldmann 3-mirror lens. The Goldmann single mir­ror or the Zeiss 4 mirror (if used without indentation) are more suitable instruments for this purpose.

If the patient with a raised pressure has a closed angle i.e. trabecular meshwork is not visible, then a diagnosis of angle closure glaucoma is made and the treatment proceeds appropriately as shown in Charts 3 and 4.

If on gonioscopy the central anterior depth is found normal, but the iris has a plateau configuration, the treatment follows the flow chart for angle closure.

Gonioscopy may be, however inconclusive. The angle may look suspicious but not closed, i.e. the raised IOP may (or may not) be due to closure. Angle closure is an absolute phenomenon, and may be intermittent and/or partial. There is inter- and intra­observer variation in gonioscopy, and the situation depicted here is not at all unusual in practice. A repeat gonioscopy out of busy outpatient hours may help to resolve the issue. Alternatively an experienced colleague may be asked to provide an independent and unbiased opinion that may settle the matter. The patient then follows the direction of the flow charts for the management of either POAG or PACG respec­tively. Alternatively the angle may be narrow and closable, but open, in which case this may represent a combined mechanism.

If the IOP is raised and the angles on gonioscopy are open, the patient should be evaluated for POAG, and the patient slots into that flow chart.

It may be appropriate to consider here why 21 mm Hg is considered as a cut-off point for a normal IOP. The IOP is distributed in the normal population in a Gaussian (or "bell shaped") manner. If one looks at [Figure - 1], the mean IOP is approximately 16 mm Hg. As with any range of values, an upper limit is s7et which will include most of the normals. Two stan­dard deviations above the mean will include 95% of the normal population. Two standard deviations above the mean is 21 mm Hg. The statistical definition of 21 mm Hg as normal simply implies that 95% of normals have an IOP of 21 mm Hg or less. By definition, therefore, it follows that 5% of normals will have IOP above 21 mm Hg. One could as well use a cut-off of 3 standard deviations above the mean or an IOP of 24 mm Hg. In this situation only 1 % of the normal population would have a pressure of more that 24 mm Hg. It should be noted, however, that even a pressure above 24 mm Hg can still be normal for some (1% of the population). In the same way, a pressure of 30 mm Hg may still be normal but is even more unlikely than 21 or 24. It becomes clear therefore, that higher cut-off levels of intraocular pressure are increasingly unlikely to be normal and are more likely to be abnormal.

This detailed explanation is provided here to drive home the fact that a raised IOP may be normal for that individual person. Such a person needs further evaluation (flow chart for POAG suspect) before a diagnosis of POAG is made. A statistical cut-off point of 21 or 24 does not mean that all the patients above the cut-off should be started on treatment or, even worse, operated.

So how did a cut-off of 21 or 24 mm Hg come to be? As is well known, the incidence of glaucomatous damage is more common with higher IOP's. Adapt­ing a cut-off point of 21 or 24 mm Hg provided a screening strategy to detect glaucoma. In other words, it was not selected because it represented the "nor­mal", condition, but because it made screening for glaucoma damage more efficient.


  II. PATIENT WITH A SHALLOW ANTERIORCHAMBER (AC) & NORMAL IOP Top


This is another common problem encountered in a clinic. The shallow AC may be suspected on a "flashlight" test, and/or on the slit lamp (van Herick test). The IOP is normal. The question is "Is this eye susceptible to ACG, ie, is the angle capable of clo­sure?". It will be assumed that secondary causes for the shallow AC have been excluded.

A gonioscopy is done. As mentioned in the last section, the gonioscope used should be one that produces minimal artifacts. If the angle is open, the patient is no longer an ACG suspect. A shallow AC suspected on flashlight or (less commonly) van-Her­ick test can quite often be totally open on gonioscopy and virtually incapable of closure.

If the angle is totally closed or if the trabecular meshwork cannot be visualized, Indentation Gonioscopy is done to look for the presence of peripheral anterior synechiae (PAS). The ideal instru­ment for indentation gonioscopy is a special lens (Zeiss or Sussmann 4 mirror lens), and the idea is to open up the angle as much as possible and look in the re­cesses for synechia. This maneuvre is akin to looking in the angle for a foreign body, and the aim is to open up the angle entirely. It is quite different from trying to assess the "in situ" state of the angle to judge whether it is capable of closure, which was discussed earlier. A good view of the angle can also be obtained (most of the time) with the standard single mirror gonioscope by asking the patient to look in the direction of the mirror, and .also by pressing backwards towards the cornea with the gonioscope. For this purpose, the 3 mirror lens which usually produces artifacts may actually be useful. It is better to have the special indentation lens, learn to use it, and pick up many more synechiae, but single mirror lens can do a job similar to an indentation gonioscope provided we understand and accept the compromises. The inden­tation gonioscope is better, and we ourselves use one in this situation, but also understand that not every­body can own both.

If PAS are found, and evidence of past angle clo­sure is seen, one is justified in proceeding with a peripheral iridectomy (laser or surgical). Following this, it is necessary to reassess the angle, as well as check the IOP before and after dilatation.

If there are no synechiae, a provocative test can be considered. Many such tests are available, the easiest being measurement of the IOP in the mid dilated position during routine examination. As there are other causes for a rise of IOP after dilatation, all "positive" provocative tests must have confirmation of angle closure by gonioscopy. If a formal provocative test is to be done, the Mapstone's test is usually used. The description and justification for this is beyond the scope of this article. If a provocative test is positive, a PI is done. If negative, the patient can be followed up. If during follow up, the IOP rises on routine dilata­tion, or a provocative test becomes positive (with the angles closed in either situation), or synechiae develop, a PI is done. Following this, it is necessary to reas­sess the angle, as well as check the IOP before and after dilatation.

It must be emphasized that eyes with positive provocative tests may never develop angle closure, and eyes with negative tests may go into closure. A negative test does not eliminate the need for follow up, espe­cially if the clinician is very suspicious and/or the patient has symptoms suggestive of closure.

If on gonioscopy one is not sure whether the angle can close one should proceed as follows. If on iden­tation gonioscopy we find that the patient has synechia, a PI is done. If there are no synechiae, but the patient complains of symptoms suggestive of closure (not tension headaches) a formal and/or informal provoca­tive test is used and proceed according to the result.

The point that there is no study to show that go­nioscopy is able to predict which eyes will go into closure needs emphasis. Indentation gonioscopy, however, provides valuable information on which treatment can be based.

The alert and practical reader will ask the obvious question: why not a laser PI for all shallow AC's? The fact is that eyes with "occludable" angles actually develop ACG. Laser PI is certainly non invasive compared to surgery, but is not without risks. The decision must therefore be made differently on a community policy basis, and differently for the indi­vidual patient. As a policy in a developing country, even if 10% of "shallow" AC's go into closure, it may be worthwhile to overtreat 90% with a relatively in­nocuous laser.

The individual patient in our hospital is told about the disease, explained the pros and cons, the fact that the diagnosis is not certain, that he or she may never develop the disease, and that one can wait and pick up early signs (synechia or provocation) but that laser treatment is relatively innocuous. The patient partici­pates in the decision making process. If the patient is illiterate, of poor socioeconomic status, of doubtful compliance and cannot understand the situation, we proceed to a laser PI.


  III. RAISED IOP WITH CLOSED ANGLES & ACUTE SYMPTOMS Top


Acute symptoms : If the angles are closed, and the patient has painful red eyes, shallow anterior chamber with corneal edema and a dilated pupil, this represents an acute angle closure glaucoma which needs to be dealt with as emergency.

1. A Gonioscopy is performed if possible to confirm that there is angle closure glaucoma.

2. Other possible stimulating conditions are ruled out, eg. neovascular glaucoma.

3. The IOP is lowered with Timolol, Diamox and if necessary IV Mannitol and oral glycerol.

4. Pilocarpine 2% is instilled once the IOP begins to decrease. Note that intensive pilocarpine therapy as advised in older texts is not advisable. With a markedly raised IOP, pilocarpine will not pene­trate well through the cornea, and unless the pressure is lowered, neither will the ischemic iris sphincter respond. Therefore once the IOP has started decreasing, we instill pilocarpine 3 to 4 times over one to two hours. The objective of therapy is to control the acute attack.

Once this is achieved, the patient is assessed to deter mine whether he requires peripheral iridectomy or a trabeculectomy. The basis for this decision can be found in standard texts.

One must remember an important principle. In an acute PACG, once the acute attack is controlled, the emergency is over; it is best to try and stabilise that eye, decrease the congestion, and allow acqueous dynamics return to normal before further evaluating the patient or attempting an invasive surgery like trabeculectomy. It may be necessary to do a laser PI to control the attack. During the acute attack, even a YAG laser PI may be difficult and in such situations, an argon laser pupilloplasty and gonioplasty can be helpful. We have not done an emergency trabeculec­tomy for acute PACG in a long time.

If a PI is performed, the patient is reevaluated. The IOP is checked in the mid dilated position. If the IOP does not rise, the angles are open without any PAS, there are no signs of disc damage, and enough time has elapsed for the ciliary body to recover (this may take 3 to 6 months), the patient can be seen on a routine basis at yearly intervals. This will enable us to detect a raised IOP due to subclinical trabecular damage caused by the closure. If the IOP is not controlled, medical treatment may be required, and if this fails, the patient may need a trabeculectomy.

If initial evaluation suggests that a patient needs a trabeculectomy, then this is done electively.

ALL CASES UNDERGO A LASER OR SURGICAL PI FOR THE FELLOW EYE.


  IV. ANGLE CLOSURE - NO ACUTE SYMPTOMS Top


If a patient is occasionally symptomatic with raised IOP and closed angles, a PI is required for this pro­dromal phase of the disease.

If the patient does or does not have symptoms and the angles are closed with a raised IOP, the patient has chronic ACG. An indentation gonioscopy is performed to determine if the closure is appositional or synechial. If the closure is synechial, the patient is assessed on standard textbook criteria, and undergoes a PI or a trabeculectomy. If the IOP is uncontrolled after a PI, filtering surgery may be necessary. Appositional closure requires a PI, followed if neces­sary by medical therapy to control the IOP. If the pressure is uncontrolled, a trabeculectomy may be nec­essary according to indications. If the patient's socio­economic status is low, and his compliance and understanding suspect, we prefer a trabeculectomy.

If following a PI, gonioscopy reveals a plateau like configuration, and the IOP rises (with closure) on dilatation, we diagnose a plateau iris syndrome and treat the patient with long term pilocarpine, or go­nioplasty. Trabeculectomy may be necessary. A word of warning. A laser PI should be at least 150 microns in size and peripheral in location.

Occasionally, even before a PI, the angle may appear plateau like. With the ophthalmologist's penchant for hair splitting, this is called plateau iris configuration as opposed to the syndrome we just discussed. The treatment is the same: PI to eliminate any element of pupillary block, followed by long term pilocarpine or gonioplasty.

ALL CASES UNDERGO FULL EVALUATION AND TREATMENT FOR THE FELLOW EYE ALSO.


  V. POAG SUSPECT Top


The patient may be a suspect because of a raised IOP, suspicious discs, or occassionally on the basis of suspicious fields alone.

If the IOP is high, the patient's disc and visual fields are evaluated. If these show glaucomatous changes, the patient has POAG. If the disc and fields are normal, and the IOP is raised, the patient fits into the "ocular hypertensive" category. Without going into the controversies surrounding this term, we prefer to call them glaucoma suspects. The reason for this can be deduced from our discussion of the distribu­tion of the "normal" TOP.

If the IOP is normal and the patient is a glaucoma suspect for whatever reason, a diurnal variation of IOP (DVT) is recorded. If this shows a high peak or a large variation, the patient's disc and fields need evaluation. If the DVT is negative, the patient was probably a suspect due to disc and field criteria, and these need to be critically reevaluated.

A patient with normal TOP may be a POAG sus­pect due to the appearance of his discs and/or visual fields. A DVT, therefore, is desirable. If the discs and fields show characteristic changes of POAG, and the TOP is normal, the diagnosis is "normotensive" glaucoma (the inverted commas indicate our reserva­tions about this term.) The reason is again the distri­bution of the normal TOP. (Sommer 1989) Subse­quent DVT may reveal a raised TOP, which confirms POAG. If, with a normal TOP, the disc and field show no glaucomatous changes, the diagnosis of POAG can be excluded.

As usual we come to our equivocal category - the disc and the visual field look suspicious, but we are not convinced. In this instance, the disc and field examination are repeated and if the same indecision prevails, additional information is needed. If the patient has risk factors for POAG, the patient is followed up and the entire work up is repeated. If we are suspi­cious enough we may decide to follow up those without risk factors also.


  VI. SCHEME FOR MANAGEMENT OF POAG Top


It should be obvious by now that a raised TOP is not synonymous with glaucoma. TOP is a risk factor, and is a causal risk factor for glauccma. There are other risk factors for POAG, such as increasing age, a family history of POAG, and high myopia. How­ever, there is no way we can decrease the risk from age, or family history; and even if someone were to perform a radial keratotomy and eliminate the high myopia, it would not decrease the risk of glaucoma in any way. In other words, all these other risk factors are non-causal. The fact is that at the moment the TOP is the only risk factor we can manipulate to therapeutic advantage.

Our practical management of POAG is based on the concept of the Target IOP. Earlier we discussed how 21 mm Hg was statistically (for screening pur­poses) defined as the "normal" IOP. Unfortunately, this statistical cut-off has crept into clinical practice, and most surgeons aim for lowering of IOP to 21 mm Hg in all cases. What needs to be done is determine a Target IOP for each individual patient that will prevent progression of the glaucomatous damage. This Tar­get pressure is determined by considering the amount of existing glaucomatous damage (based on the disc and field examination,) and the baseline TOP at which this damage has occurred. That is, the target pres­sure is determined by correlating the existing damage to the current TOP and the risk factors. For instance, a patient with advanced field damage a cup to disc ratio of 0.9:1 and baseline TOP of 24 mm Hg probably needs a pressure (Target TOP) of 15 mm Hg or less to prevent progression. On the other hand, in a patient with early field changes, a cup/disc ratio of 0.4:1 and baseline TOP of 30 mm Hg, the disease would proba­bly not progress with an IOP of 21 mm Hg (Target TOP). The Target TOP is therefore not fixed. During the course of the follow up, it may need to be reset at a different level.

In the flow chart we chose a cut-off of 16 mm Hg for two reasons. First it has been shown that in most patients, the glaucoma does not progress if the TOP is brought down to 16 or below. Second, we find it easier to achieve IOP's of 16 or less with surgical treatment.

If it is felt that an individual requires a target of TOP greater than 16 mm Hg, the patient is started (after a unilateral therapeutic trial) on medical treat­ment. Additional drugs are added to achieve the target. In selected cases an argon laser trabeculoplasty is performed to reach the target, aided by medications if required. If with this treatment the disc and fields are stable, and the DVT is within the target specified, the patient is followed up. If the Target TOP is achieved and the patient is well controlled, but is on a drug that is not well tolerated, the target can be reset to a higher value and attempt to withdraw the offending drug. The patient is followed up. If there is no progression, all is well. If there is progression, the Target TOP needs to be reset to a lower level and steps taken to achieve this. If the Target IOP cannot be achieved with medication and ALT, or if the damage progresses despite this, the patient probably needs filtering surgery.

We must emphasise that progression is determined on the basis of a change demonstrable on at least two reliable fields performed under similar conditions without other cause to account for it.

The Target IOP is 16 mm Hg or below, which usu­ally cannot be achieved with medical treatment. Hence we advise surgery for these patients. Following surgery the patients are evaluated for characteristics of disc, fields and their DVT. If the disease is not controlled, medical treatment is added to achieve control. If despite the addition of medical treatment the field progresses, the patient undergoes another trabeculectomy with an­timitotics (our current preference is mitomycin). We sometimes consider mitomycin for the first trabeculec­tomy. Such cases include amongst others, those with a very low Target IOP and patients whose compli­ance is suspect. If the field progresses despite this and the addition of medications, we consider a seton like the molteno implant.

We would like to emphasise that this practical approach is just a guideline to managing patients. There will be some who do not fit in well, and some who will perhaps not fit at all. The guidelines should not be considered sacrosanct and should be modified as per the practioner's own criteria and as knowledge improves.

To conclude we cannot resist paraphrasing Paul Koch (in the preface to his book), "If you can under­stand the approach, and begin to use it, modifying it as you go along, we've done our job. If not, that's your problem." As was stated in the beginning, it is a very personal approach.


  Suggested reading Top


1. Sommer A. Intraocular pressure and glaucoma. Am J Ophthalmol. 107:186-88, 1989 (editorial).

2. Anderson DR. Glaucoma. The Damage Caused by Pressure.XLVI Edward Jackson Memorial Lecture. Am J Ophthalmol. 108:485-95, 1989.

3. Wilensky JT, Kaufmann PL, Frolichstein D, Gieser DK, Kass MA, Ritch R and Anderson R. Follow up of Angle Closure Glaucoma Suspects. Am J Ophthalmol. 115:338-46, 1993.


    Figures

  [Figure - 1], [Figure - 2], [Figure - 3], [Figure - 4], [Figure - 5], [Figure - 6], [Figure - 7]



 

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