Year : 1960 | Volume
: 8 | Issue : 1 | Page : 16--24
The importance of scleral rigidity in ocular tonometry
Ophthalmological Clinic of the University of Ghent, Belgium
Ophthalmological Clinic of the University of Ghent
|How to cite this article:|
Francois J. The importance of scleral rigidity in ocular tonometry.Indian J Ophthalmol 1960;8:16-24
|How to cite this URL:|
Francois J. The importance of scleral rigidity in ocular tonometry. Indian J Ophthalmol [serial online] 1960 [cited 2020 Jul 6 ];8:16-24
Available from: http://www.ijo.in/text.asp?1960/8/1/16/40691
When the ocular tension is determined with the aid of a SCHIOTZ tonometer the corneal indentation caused by the bar of the apparatus depends on two factors, viz.: the ocular tension on the one hand and the scleral rigidity on the other.
Rigidity and elasticity do not denote the same condition. The rigidity of a body is the resistance which it offers to a change in its shape, while its elasticity is its ability to undergo a change in its shape and to return to its previous shape.
The rigidity of the shell of the eye fundamentally results from physical characteristics of the sclera and, in addition, from corneal and uveal properties.
When a tonometer is applied to the eye, the indentation of the cornea causes displacement of fluid giving rise to scleral distention and a simultaneous increase in ocular tension; the quantity of fluid driven from the eyeball is negligible.
As the weight used is increased, the corneal indentation increases; thus, when ocular tension is determined with the aid of two different weights, two different tonometric readings are obtained.
The greater the difference between these two tonometric readings, the greater the scleral rigidity, as expressed by FRIENDENWALD (1957) in the following equation
in which Pt 1 , and V 1 , represent the tonometric pressure and the volume of the indentation caused by the bar in the determination made with the first weight, whereas Pt 2 and V 2 represent the respective values as obtained with the second weight; K represents the coefficient of ocular rigidity.
Technique of Measuring Scleral Rigidity
If scleral rigidity is to be determined then it is necessary to use FRIEDENWALD's tables of calibration and a perfectly standardized tonometer, ass the least anomaly in the curvature of the bar or in the concavity of its inferior surface produces considerable errors.
To ensure that determination of ocular rigidity be of sufficient exactness it is necessary
1. To compare indentations of sufficiently different volume. The weights used should be 5.5 and 10 g. or, better even if possible, 5.5 and 15 g
2. To make several determinations. In practice it is difficult to make a determination throughout 5-6 consecutive days but it is possible to take the average of three determinations made successively with the two weights; the arithmetical average of the three values of deviations obtained with each weight is then calculated.
The first average value is plotted on the curve of 5.5 g., and the second on the curve of 10 or 15 g, in FRIEDENWALD's monogram [Figure 1]. An oblique line AB is thus obtained, which is subsequently displaced parallel with its original position, by means of a square and a flat ruler until it passes through the intersection of ordinate and abscissa (CD). After this, the ocular rigidity can be read from the arc in the left lower corner of the monogram.
Subsequently, in order to determine the corrected ocular tension, the square is moved upward along the ruler again until it encounters on the 5.5 g. curve, the value of deviation obtained at the first of the three determinations of which the average was taken (line EF). The figure then indicated by the square on the ordinate is that of the ocular tension corrected by the rigidity factor.
Normally, the ocular rigidity varies, between 0.0200 and 0.0250, as shown in the [Table 1].
FRIEDENWALD's tables of calibration have been calculated for an average ocular rigidity of 0.0215, so that rigidities below 0.0215 affect tonometric determinations by an insufficiency error, while rigidities over 0.0215 affect the determinations by an error of excess.
If a glaucoma is suspected, for one reason or another, although ocular tension seems normal (below 22 mm. Hg), and particularly in the case of a tonometric reading above 22 mm. Hg, in the absence of any sign of glaucoma, then ocular rigidity must be determined.
If the coefficient of rigidity is normal, the tonometric readings are correct.
If, however, the coefficient of rigidity is increased (over 0.0215), then the tonometric findings show an error of excess. The ocular tension would seem to be exaggerated, which evidently entails the risk of regarding a normal eye as a glaucomatous eye. We are familiar with several instances of this kind, in some of which there was even an operation. Yet it is only necessary to determine scleral rigidity to find that, after correction, ocular tension will have a normal average. The following case reports are elucidative in this respect
Case 1.D).,Cecile, aged 64, was examined for conjunctival irritation. The eyeballs themselves seemed normal; the ocular fundus and the optic disc showed no anomaly.
Yet the Schiotz tonometer (weight 7.5 g.) indicated increased ocular tension, viz.: 31.8 mm. Hg in both eyes, which did not prevent visual acuity from being perfect (0.8 on the right, and 1.0 on the left) and the field of vision from being complete (Goldmann, tests 5/4, 1/4 and 1/3).
In view of these findings, determinations of ocular regidity were resorted to. The average of six determinations in each eye (RE : 3.08 for weight 5.5 g. and 7.16 for weight 10 g.; LE : 2.02 for 5.5 g. and 6.60 for 10 g.) gave a coefficient of 0.033 on the right, and 0.037 on the left. The corrected tension was therefore 19 mm. Hg on the right and 15.5 mm. Hg on the left - values to be considered entirely normal.
Case 2.-C., Jean, aged 54, was examined for progressive loss of vision in the course of 18 months. The examination showed a discrete disturbance in the anterior one-third of the corneal parenchyma and an incipient nuclear cataract. The other refractive media, the ocular fundus and the optic disc., pupil reflexes and motility' were normal. Visual acuity was 3/10 in both eyes.
The ocular tension was increased as determined on the Schiotz tonometer, viz.: 27.3 mm. Hg on the right, and 25.3 mm. Hg on the left.
Tonography, however, yielded a normal result, viz.: on the right R = 4.8 (C - 0.020), and on the left R = 4.2 (C = 0.021). The field of vision was likewise normal in various tests.
Determination of scleral rigidity (average of 6 determinations) gave a coefficient of 0.038 on the right, and 0.043 on the left, i.e. a markedly increased coefficient, so that the corrected ocular tension was actually 15.5 mm. Hg on the right, and 10 mm. Hg on the left. The increased ocular tension was therefore only apparent.
Whereas an increased rigidity may give rise to a pseudo increase in ocular tension, a low rigidity, on the other hand can mask, a genuine hypertension. In such a case an apparencly normal ocular tension can prove -- after correction - to be increased.
This is particularly frequent in cases of myopia and endocrine exophthalmos.
In marked myopia (exceeding 5 D), there is a considerable diminution of scleral rigidity due to thinning of the sclera. This fact, first observed by FRIEDENWALD (1931) and confirmed by GOLDAIANN & SCHA4IDT (1957), was also verified by WEEKERS et al. (in 1957). These authors found an average rigidity of 0.0214 which corresponds with the normal value in 26 subjects suffering from myopia (-1 to -5 D.) In 48 cases of myopia exceeding --5.50 D., however, the average rigidity was no more than 0.0151. This difference is statistically significant.
Determination of scleral rigidity in cases of marked myopia makes it possible to reach the following conclusions
1. Contrary to common belief, the myopic eye is not hypotensive.
2. Ocular hypertension may remain unrecognizable in cases of myopia.
3. In the case of recognizable signs glaucoma in myopic subjects, the condition is sometimes incorrectly referred to as glaucoma "without hypertension".
4. Ocular hypertension as shown by the Schidtz tonometer is as a rule more marked than is indicated by simple tonometric determination.
The following is a report on a case of myopic glaucoma, apparently with hypertension.
Case 3-Mrs. K., Marcel, aged 49, lost the right eye following detachment of the retina. The left eye was examined and showed the following particulars
1. very marked myopic choroiditis with atrophic plaques and Fuchs spot.
2. The optic disc was pale and seemed a little excavated.
3. The ocular tension according to the Schiotz method was normal, viz.: 18.5 mm Hg.
4. The visual acuity was 0.4 (6/15) after correction (-17 D. sph. -0.5 D. cyl. axis at 172º).
5. The field of vision showed a nasal deficiency, characteristic of glaucoma [Figure 2].
6. Determination of scleral rigidity yielded a coefficient of 0.012, so that the corrected tension was -24 mm. Hg (i.e. considerably- higher than it appeared to be at tonometry).
The diagnosis of glaucoma was therefore obvious.
Since the introduction of determination of scleral rigidity, glaucomata without hypertension have become exceptional. Yet they do exist, as demonstrated by the following observation:
Case 4.-B., P almyre, aged 57, complained of visual difficulties over a two year period.
Objective examination of the eyes only revealed a hollow disc, slightly atrophic, in both eyes.
The visual acuity was 10/10 in both eyes. The field of vision showed the nasal deficiencies characteristic of glaucoma [Figure 3].
In no case did the ocular tension exceed 21.8 mm.. Hg in either eye throughout a year of observations; it always varied between 14.3 and 21.8 mm. Hg.
Tonographic results were variable right eye R = 4-10, left eye R= 4.5 -10.
Gonioscopy showed an iridocorneal angle which was open and normal in both eyes.
Scleral rigidity was normal: 0.020 on the right and 0.021 on the left; the corrected tension was therefore 15 mm. Hg on the right, and 13.5 mm. Hg on the left.
This, therefore, was a genuine case of glaucoma "without hypertension".
II. Endocrine exophthalmos.
Distinction is made between two types of endocrine exophthalmos, viz. thyrotoxic or hyperthyroid exophthalmos, and thyrotropic or ophthalmoplegic, oedematous exophthalmos.
A. Thyrotoxic exophthalmos. This is the exophthalmos seen in Graves disease. It is associated with retraction of the superior palpebra by a spasm of the palpebral levator muscle. This spasm explains all the other changes usually seen, and particularly the Von Graefe sign, characterized by failure of the superior palpebra to follow a downward movement of the eyeball.
These manifestations, which would seem to depend on an increase in tonus of the sympathetic system, are not associated with either chemosis or diplopia, although heterophoria or a deficiency in convergence are not uncommon.
B. Thyrotropic exophtalmos . This exophthalmos is seen either in hyperthyroids treated by medication or surgery, or spontaneously in subjects apparently free of any thyroid symptom.
This exophthalmos, which may be very marked and give rise to lagophthalmos, is associated with ocular paresis and more oz less marked chemosis.
It has been attributed to pituitary secretion of an exophthalmic substance related to thyrotropic hormone and producing an increase in the water concentration of various tissues (WYBAR, 1957).
ALBERT (1945) was able to induce exophthalmos in a minnow by injecting an anterior pituitary extract. DOBYNS and WILSON (1954) demonstrated that injection of serum from subjects suffering from thyrotropic exophthalmos produced exophthalmos in goldfish, whereas serum from normal subjects had no such effect.
The two types of exophthalmos can be combined, and it is not uncommon to find that a thyrotoxic exophthalmos, when treated, becomes a thyrotropic exophthalmos.
Differential diagnosis between these two forms of exophthalmos can be based on an injection of the patient's serum into a goldfish; it is far more simple, however, to differentiate by determining the ocular rigidity.
WEEKERS & LAVERGNE (1958) have demonstrated that scleral rigidity is normal in thyrotoxic exophthalmos, whereas it is considerably diminished in thyrotropic exophthalmos. We have been able to confirm this.
In 26 cases of thyrotoxic exophthalmos, WEEKERS & LAVERGNE (1958) found an average rigidity of 0.0226. In all our cases we likewise obtained a normal rigidity value.
In 8 cases of thyrotropic exophthalmos, however, ocular rigidity was considerably diminished (3 cases by WEEKERS & LAVERGNE, and 5 personal observations) ; the average coefficient for 16 eyes was 0.0106, with a minimum of 0.0080 and a maximum of 0.0155. [Table 2]
Of these 8 patients, 6 were hyperthyroid and under treatment (radioactive iodine, antithyroid substances) ; the other two showed no goitre or any sign of Graves' disease; they were not treated.
The diminution in scleral rigidity would seem to be in accordance with imbibition of the sclera by water, which alters its physical properties. This change is clinically revealed by more or less marked chemosis which accompanies thyrotropic exophthalmos.
The diminution in scleral rigidity seen in thyrotropic exophthalmos is not only a diagnostic aid but also makes ii possible to demonstrate ocular hypertension, which is relatively frequent: 4 patients out of 8 showed an increased ocular tension. Yet this hypertension may well remain unrecognized if ocular tension is not corrected by means of rigidity values.
It is true that this hypertension is as a rule hardly marked; it can, however, give rise to changes in the field of vision (WEEKERS & LEVERGNE, 1958). It is not associated with any change in the iridocorneal angle. Its development parallels that of the exophthalmos and it disappears as the exophthalmos disappears. It is undoubtedly because of its short standing at the time of the first examinations that its functional symptoms are not as a rule very marked.
The hypertension is favourably influenced by any therapy which reduces the secretion of aqueous humour (diamox, neptazane, adrenalin). Myotics, however, hardly affect it.
In exceptional cases there may be an acute crisis, with closure of the iridocorneal angle (' WEEKERS & LAVERGNE, 1958) ; medication is then, insufficient, and an operation must be resorted to.
It is still impossible to decide whether ocular hypertension in thyrotropic exophthalmos is due to an increaed resistance or to increased secretion of aqueous humour: the diminution in scleral rigidity makes it impossible to interpret the tonographic curves. It seems, however, that an increase in resistance following an increase in intrascleral venous tension is involved.
It must be pointed out once again that the ocular tension is normal in thyrotoxic exophthalmos.
A few remarks on non-inflammatory exophthalmos are appropriate here. It is generally understood that an orbital tumor is suggested by unilateral exophthalmos, whereas bilateral exophthalmos indicates hyperthyroidism. The problem, however, is not quite so simple. The following facts must be taken into account:
1. The exophthalmos can be only apparently unilateral. Generally speaking, the apex of the cornea is localized about 12 mm. in front of the temporal orbital margin. There are, however, a great many exceptions to this rule. And an exophthalmos of 18 mm. is therefore not necessarily pathological.
On the other hand, the impression may be that the exophthalmos is unilateral whereas in fact it is bilateral, although more marked on one side than on the other (e.g. 24 mm. on the right, and 20 mm. on the left).
2. Another important fact is that even a unilateral exophthalmos can be due to hyperthyroidism, pituitary hyperfunction or chronic orbital myositis.
In an attempt at differential diagnosis, let us first consider the symptoms of an orbital tumour :
1. The chief symptoms - exophthalmos - is progressive and irreducible.
2. There is often more or less marked ptosis with paresis of one or several ocular muscles. The internal muscles (pupillary sphincter and ciliary muscle) are hardly ever affected.
3. According to the localization, there is sometimes papilloedema or atrophy of the optic disc, which obviously involves functional disturbances.
4. Corneal sensitivity may be diminished.
The clinical diagnosis can then be confirmed by the following examinations :
1. Radiography or, better even, tomography of the orbit.
2. Radiography after :
a) Injection of air, which does not penetrate the tumour mass and therefore clearly delimits the growth.
b) Injection of a contrast medium, which fills the free spaces and outlines their contours.
4. A biopsy.
I. It has been pointed out that unilateral exophthalmos may be due to orbital myositis. The following case is an example
Case 5. - The patient was a man aged :12 who underwent a sympathectomy for arteritis 4 years previously. In September 1956 the right eye became exophthalmic. An orbitotomy revealed no tumour. The patient was examined in March 1957, when he showed the following symptoms :
1. Exophthalmos, marked on the right (27.5 mm.) and less marked on the left (22.5 mm).
2. In repose, the gaze was directed straight ahead but the right eyeball turned down.
3. On the right there seemed to be complete paralysis of the superior rectus muscle, and paresis of the internal and the external rectus muscle; the inferior rectus muscle retained its normal function.
4. The conjunctival and episcleral veins of the right eye were dilated, but there was no chemosis properly speaking.
General examination was negative. There was no sign of hyperthyroidism, emaciation, tachycardia or asthenia. The BAIR was normal (+3%)
The thyroid was slightly hypertrophic. Absorption of radioactive iodine was accelerated. These two signs indicated overstimulation.
The question may be raised whether this case was one of thyrotropic exophthaloms.
Verification of the passive movements of the eyeball, however, showed that it was impossible to displace the eye in upward direction. This excluded paralysis of the superior rectus muscle and indicated myositis of the inferior rectus muscle. This diagnosis was confirmed by the fact that the eyeball, even in repose, was turned down.
The cause of this myositis was probably hypophyseal, as the exophthalmos was bilateral, and as the metabolism was not increased.
This case (and other similar cases) shows that the following measures should be taken in the case of exophthalmos :
1. Verification of the position of the eyeball, recording its possible deviation in one direction or another.
2. Verification of the passive mobility of the eyeball; when it is impossible to displace the eye within the region of action of an apparently paralysed muscle it must be concluded that there is a lesion of the antagonist muscle (which cannot be extended due to myositis); the diagnosis of paralysis should then be rejected.
II. Exophthalmos, even when unilateral, may be of endocrine origin, in which case:
1. The exophthalmos is only apparently unilateral (it is simply more marked on one side than on the other).
2. There is retraction of the superior palpebra, which does not follow the eyeball in its downward movement.
3. There is often white chemosis with dilation of episcleral veins and orbital myositis.
It has thus been shown how a differential diagnosis can be made between thyrotoxic exophthalmos and thyrotropic exophthalmos.
The technique of measuring scleral rigidity is described in detail.
The importance of measuring scleral rigidity in arriving at the true tension state in an eye is discussed. Apparently high but normo-tensive and apparently hypo-tensive but really glaucomatous cases can be unmasked. This is illustrated by 3 cases.
One case is described of glancoma with low-tension even after correction for rigidity.
The role of myopia and thyrotropic states in lowering scleral rigidity are discussed.
A differential diagnosis between thyrotropic and thyrotoxic exophthalmos is fully discussed.
|1||ALBERT A.-Endocrinology, 37, 389, 1945.|
|2||DOBYNS B. M. et WILSON L. A.-J. Clin. Endocr., 14, 393, 1954.|
|3||FRANCOIS J.-Belgisch Tijdschr. Geneesk., n° 12, 590, 1958.|
|4||FRIEDENWALD J. S.-Amer. J. Ophth. 20, 985. 1937.|
|5||FRIEDENWALD J. S.-Trans. Amer. Acad Ophth. Otolaryng. 61, 108, 1957.|
|6||GOLDMANN H. et SCIIMIDT T.-Ophthalmologica, 133, 330, 1957.|
|7||LAVERGNE G., PRIJOT E. et WEEKERS R.-Arch. Opht. Paris, 17, 256, 1957.|
|8||LAVERGNE G., WEEKERS R. et PRIJOT E.-Bull. Soc. Beige Opht., 116, 298, 1957.|
|9||SCHMIDT T.-Klin. Mbl. Augenh., 129, 196, 1956.|
|10||WEEKERS R. et LAVERGNE G.-Brit. J. Ophth. 42, 680, 1958.|
|11||WEEKERS R. et coll.-Le diagnostic precoce du glauconle debutant. Bull. Soc. Beige Opht., 121 1-209, 1959.|
|12||WEEKERS R. et LAVERGNE G.-Ophthalmologica, 134, 276, 1957.|
|13||WYBAK K.-Fortschr. Augenh., 7, 119, 1957.|