The Effect of Posture and Corneal Thickness on the Measurement of the Intraocular Pressure

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A major difference in the clinical uses of Schiøtz and Goldmann tonometers is the Schiøtz tonometer, which was designed for use on supine patients while the Goldmann tonometer was designed for use on seated subjects. Consequently, the question arose whether measurements of intraocular pressure (IOP) on individual subjects with the two systems agreed. It rapidly became clear that this was not so, and led to intense efforts to make the two systems conform.⁶ This problem was further complicated by recognition that IOP of the undisturbed eye increases when the subject was supine. Despite knowledge of the substantial effect of posture on the central blood pressure, the assumption was made that the postural response on the IOP did not exceed 1 mmHg, based on the measured increment in pressure in the episcleral veins when lying down.^7,8 Confirmation of this conclusion and the consequent agreement of the two systems for the measurement of the IOP was accepted by the Committee for Tonometer Standardization.^9–12

However, paired measurements using the Goldmann and the Schiøtz tonometers on the same subjects by investigators continued to show a significant disagreement. For example, in a series of 45 normal and 45 glaucomatous eyes, the mean difference in IOPs measured with the Goldmann and Schiøtz tonometers was 3.12 ± 1.98 mmHg.⁶

The difficulty in bringing conformity to the two tonometers was aggravated by the pulsatile nature of the IOP. The plunger of the Schiøtz tonometer induces an indentation of the cornea, which is measured by a needle moving across a curved scale in proportion to the magnitude of the indentation. This needle moves to and fro with the pulsations of the IOP and the final reading is taken as the mean of the IOP readings associated with the fluctuations. In this respect, the excursion of the needle represents approximately 2–4 mmHg in healthy subjects.

The procedure for recording the IOP reading with the Goldmann tonometer differs from that of the Schiøtz tonometer in that the operator seeks the applied pressure at which the two half circles of the applanation prism are just in alignment.¹³ This reading corresponds to the minimal point of the IOP pulse wave and is not the average of the minimal and maximal values of the IOP pulse. In Goldmann tonometry, fluctuation of the rings due to the pulsation of the IOP may be observed, but the system provides no way for measurements of either the maximal IOP of the IOP wave, or the magnitude of the pulse amplitude.

The assumption that the postural effect on IOP is small and not greater than 1–2 mmHg for both healthy and diseased eyes was seriously questioned by several investigators and shown to be erroneous based on measurements using modified Goldmann applanation tonometers that could be used in both supine and seated positions.^14–16 The results of these studies revealed the postural effect to vary from a mean of 2.5 mmHg in normal eyes to much higher values in glaucomatous eyes (Fig. 12.1 ).

Figure 12.1.

The influence of posture on the arterial and venous blood pressures below and above the heart

More recently, using the Langham pneumatic objective recording tonometer (see later) that may be used on both supine and seated subjects, a mean IOP postural increase of 2.5 ± 0.2 mmHg (supine − seated) was reported in the eyes of 77 healthy adult subjects, and a mean postural response of 3.5 ± 2.8 mmHg (supine − seated) in the eyes of 45 glaucoma patients (Fig. 12.2 ). A similar abnormal postural response on the IOP was found in patients with low-tension glaucoma (Fig. 12.3 ).

Figure 12.2.

The response of the IOP to posture in eyes of 45 glaucoma patients. The abscissa is the IOP measured in the seated position. The ordinate shows the change in IOP in individual eyes when the subject changed from the seated to the supine positions (From Kreiglstein and Langham.¹⁷ Reprinted from Ophthalmologica. Used with permission from S. Karger AG, Basel.)

Figure 12.3.

The postural response on the IOPs in six patients with low-tension glaucoma. The interval between readings in each position was, on the average, 7 min (From Kreiglstein and Langham.¹⁷ Reprinted from Ophthalmologica. Used with permission from S. Karger AG, Basel.)

The parameters that determine the postural effects on systemic blood pressure and IOP are gravity and vascular autoregulation. On standing, the eye and the brain are above the level of the heart and, because the vascular resistance in the cervical arteries and the brain is relatively low, the arterial pressures feeding the eye and the brain are exposed to the full hydrostatic action of gravity, namely a pressure change of approximately 35–40 mmHg. The brain is an open system, and the hydrostatic effects on the arterial and venous pressures are equal, and consequently the cerebral perfusion is affected only by the change in the cervical arterial response to posture. By contrast, the eye is a closed system, and the venous pressure within the eye must always exceed the IOP, albeit if only by a small amount, to maintain a continuous flow of blood through the eye.

The eye is a unique system in respect that the increase in hydrostatic pressure while lying supine would substantially modify the ocular perfusion pressure and the steady state IOP, unless compensatory physiological mechanisms acted to minimize the postural effect. In the systemic vascular circulation these compensatory mechanisms are located in the cervical arteries. An increase of blood pressure in the internal carotid artery due to lying down activates vascular reflexes, including the baroreceptor sensory nerve located in the carotid sinus at the bifurcation of the internal and common carotid arteries. The sensory receptors connect by afferent nerves to neural centers in the medulla, which send inhibitory efferent pulses via the vagus nerve to the heart, to decrease cardiac ejection and peripheral resistance. In normal healthy subjects, this autoregulation of the arterial circulation from the carotid receptors reduces the anticipated postural increase of 35–40 mmHg in the ophthalmic arterial pressure to 10–12 mmHg. Should the baroreceptors be impaired, such as that occurs when the cervical sympathetic nerve is denervated or modulated by hypotensive drugs, the fall in arterial pressure on standing may be sufficient to cause syncope and induce a major change in the ocular perfusion pressure with transient visual loss.

The physiological significance of the compensatory vascular reflexes is seen in the relatively small effect of posture on the IOP in healthy subjects, namely, a mean of 2.4 mmHg (supine minus seated values). This limited effect of posture on the IOP in healthy subjects contrasts with the abnormally high effect of posture on the IOP in patients with certain ocular diseases including open angle glaucoma. The cause of this abnormally large impairment of the postural response on the IOP in clinical disease remains to be clarified but suggests that the autoregulation in the cervical arterial circulation is impaired. The postural effect is not a transient volumetric response but is a change in the steady state IOP and consequently has to be associated with change in either or both the rate of formation of the aqueous humor and the outflow resistance in the drainage channels.

The Effect of Corneal Thickness on Tonometric Measurement of the IOP

Goldmann recognized that the thickness of the cornea would influence the readings made with his tonometer and advised that the accuracy was confined to corneas of normal thickness (i.e., 540 μm). In 1961, Goldmann and Schmidt reported that the error was 7 mmHg in measurements of IOP in rabbit eyes having a mean corneal thickness 100 μm thinner than normal human corneas in man (namely a true IOP of 20 mmHg gave a Goldmann IOP reading of 13 mmHg).¹⁸ Errors of this magnitude were confirmed in manometric studies on human eyes about to undergo cataract surgery by Ehlers et al.¹⁹ These investigators found a strong correlation between corneal thickness and the disparity between the actual IOP and the Goldmann reading. Analysis of the corneal thickness revealed that thin corneas gave an underestimate of the IOP and thick corneas gave an overestimate of the IOP. Ehlers calculated that a cornea of 460-mm thickness yielded an underestimate of the IOP of 5.2 mmHg; namely, an IOP reading of 14.8 mmHg was really 20.0 mmHg.

The importance of corneal thickness in the measurement of the IOP has been underlined by subjects who have undergone LASIK corneal refractive surgery. In this procedure, the refractive character of the cornea is modified by a reshaping, which causes a substantial decrease (average approximately 100 μm) in corneal thickness, from the normal mean thickness of 540 μm in healthy eyes, to a mean of approximately 440 μm. On the basis of the observations of Goldmann, this thinning of the cornea would mean an underestimate of approximately 4–6 mmHg in IOP. This potential error of Goldman applanation IOP in measurement of abnormally thin corneas has been confirmed in patients who underwent LASIK refractive surgery. Langham and O’Brien, using the Langham pneumatic tonometer that is essentially unaffected by changes in corneal thickness (see later), studied ten subjects prior to LASIK surgery and reported the mean IOP measured by the Goldmann and the Langham tonometers to agree well (16.7 ± 1.2 and 16.2 ± 0.9 mmHg, respectively); the mean difference between the IOP readings made with the two tonometers in individual eyes was 0.5 ± 0.3 mmHg. In the same patients, 3–58 weeks after LASIK refractive surgery, the mean IOPs were 13.1 ± 1.5 mmHg in the operated eyes and 16.9 ± 1.4 mmHg in the unoperated eyes, measured by the Goldmann and Langham tonometers, respectively; the difference of the IOPs measured with the two tonometers in individual eyes was 3.8 ± 0.4 mmHg (Langham − Goldmann). Thus, the IOP measured with the Langham tonometer showed LASIK refractive surgery to have no significant effect on the IOP whereas the Goldmann readings indicated that surgery induced a substantial decrease of IOP. The mean corneal thickness in these patients was 535 ± 10 and 425 ± 23 μm prior to and following surgery, respectively.²⁰