4

The Patient’s History

Symptoms of Glaucoma

Joel S. Schuman, MD, FACS; Rachel L. Anderson, MD; and David L. Epstein, MD, MMM

SYMPTOMS

Blurred Vision With Haloes

When intraocular pressure (IOP) is suddenly elevated from any cause, fluid moves into the cornea, exceeding the capacity of the corneal endothelial pumps to remove it. The resulting corneal epithelial edema can produce symptoms of blurred vision and the perception of colored haloes around lights. (The presence of colored haloes is important because noncolored haloes around lights are a common symptom simply of myopia, astigmatism, and other refractive problems with no IOP implication.) Colored haloes are also common symptoms of patients with nuclear sclerotic lens changes, especially early, without any elevation of IOP. Although such symptoms are more common in various forms of angle-closure glaucoma (especially subacute forms) in which there is rapid elevation of IOP when the iris moves into apposition with the surface of the trabecular meshwork (TM), colored haloes can also be seen in open-angle forms of glaucoma with similarly rapid elevation of IOP, such as with glaucomato-cyclitic crisis, post-cataract surgery, pigmentary glaucoma, and juvenile open-angle glaucoma. However, in primary open-angle glaucoma (POAG), except for cases with very high IOP, there are usually no such symptoms. This is what makes the disease so treacherous. Most patients with POAG are unaware of any symptoms until there is substantial visual field loss, at which time visual function is compromised.

Colored haloes with blurred vision upon arising in the morning is a common symptom in patients with Chandler’s syndrome, an iridocorneal endothelial syndrome variant. It can also be seen in patients with nonglaucomatous primary corneal disease in which edema accumulates in the corneal epithelium overnight because of the lack of helpful evaporation when the eyelids are closed.

Pain

Rapid elevation of IOP can also be accompanied by pain. Although some of this pain may be due to corneal edema or irregularity of the epithelial surface, it characteristically behaves as if it were more global in origin, as perhaps from stretching of the ocular coats. Topical anesthetics typically do not totally alleviate this symptom. With long-standing elevation of IOP, the corneal endothelium may be able to prevent corneal epithelial edema presumably due to the compensatory pumping action of the endothelium. Nevertheless, patients with sustained elevation of IOP to levels of 50 mm Hg or greater often complain of pain even in the absence of corneal edema. Ocular pain may be accompanied by nausea and vomiting.

Blurred Vision (Without Haloes)

In some forms of secondary angle-closure glaucoma, such as malignant glaucoma or uveal effusion syndromes in which there is a forward shift of the crystalline lens, symptoms of myopia can occur. A fascinating entity in this category is myopia due to sensitivity to systemic sulfonamides and other medications, where either forward shift of the crystalline lens and/or lens swelling (or at least increased anterior-posterior lens thickness) can result in temporary myopia.

Sometimes, patients with open-angle glaucoma (eg, POAG, low-tension, and exfoliation) give a very reliable history of a sudden onset of a subjective paracentral scotoma. It makes the clinician contemplate whether some acute mini-event has occurred in the chronic progressive natural history of the open-angle glaucoma, such as some final small vascular event at the level of the optic nerve.1

Subjective Loss of Vision (Acuity)

With high sustained IOP in angle-closure glaucoma and in certain forms of open-angle glaucoma, optic atrophy can develop with accompanying loss of visual acuity and pallor of the optic nerve. These findings may occur in the absence of the contour changes in the disc rim that characterize the cupping that is more commonly seen in chronic glaucoma.

When a patient who has advanced glaucomatous field loss or dense field loss close to fixation complains about subjective loss of acuity, this is a dangerous warning sign. At a minimum, such a presentation indicates the need to advance therapy in order to further reduce IOP. As mentioned earlier, this is often an indication for urgent filtration surgery. In patients with such visual field changes, it is often useful to have the patient test his or her subjective acuity at home between visits by viewing objects on the wall or by using an Amsler grid.

Loss of Color Vision

Subjective loss of color vision is not uncommon in patients with long-standing POAG, and objective measures of color vision often demonstrate abnormalities in such patients. Clinically, it is difficult to relate progression of the disease with measured progressive changes in color vision.

Patient’s Own Sense of (Painless) Pressure in the Eye

Many patients insist that they can sense what the pressure is in their eye. These are notoriously inaccurate except in some patients with acute, intermittent secondary glaucomas with wide fluctuations of IOP. Yet, we have been impressed over the decades by how many questions and comments from patients with glaucoma that were initially quickly dismissed only later proved to have some merit. We should listen to our patients with glaucoma for potential new insights, and although we still may not believe that patients can sense their IOP (except for perhaps the above acute secondary elevations), it is possible that there is some subgroup or some heretofore unappreciated mechanism for this symptom in certain patients.

Clinicians have an obligation to take the time to talk to all patients with glaucoma, fully explaining their condition and listening to their concerns with particular attention to the ways in which their disease and our treatments affect their quality of life. The glaucomas are one of only a few chronic eye conditions that are usually slowly progressive with time, requiring repetitive visits with generally nonspecific therapies to offer. Most patients with glaucoma bond with their glaucoma practitioner, and such communication is an obligation of our profession. Sometimes, all that can be done for patients is to talk to them and honestly explain their condition. It is humbling how many second opinions are requested by patients with glaucoma, in truth only to find a clinician who will take the time to talk to them.

Blackouts

With high levels of IOP in the 50 mm Hg range or greater, whether due to acute or chronic causes, patients may experience blackouts, presumably because the elevated IOP interferes with vascular perfusion of the optic nerve or retina or because of obstruction of axoplasmic flow. In patients with more moderate elevation of IOP, blackouts should suggest the possibility of underlying carotid disease, where presumably ocular hypoperfusion is being exacerbated by the elevated IOP. Patients with glaucoma with this symptom should have a neuro-ophthalmological evaluation.

There seems to be a connection between blood pressure and POAG, though the exact nature of the relationship is unclear. While some studies have revealed a significant correlation between systemic hypertension and POAG, others have failed to replicate the same, suggesting that confounders may have played a significant role in the positive studies.2–7 The Los Angeles Latino Eye Study revealed a bimodal relationship between vascular pressures and POAG, noting associations between POAG and low diastolic blood pressure as well as low mean, systolic, and diastolic perfusion pressure (where perfusion pressure = blood pressure – IOP). Interestingly, the study also found an association between POAG and high systolic blood pressure and mean arterial pressure.⁸ Given that this study and others suggest that low blood pressure may have a deleterious effect on the optic nerve, some have suggested that using antihypertensives with lower blood pressure goals than otherwise medically necessary may be an unwise treatment strategy.⁶

How might one explain the proposed relationship between systemic hypertension and trabecular and optic nerve pathology in POAG? Perhaps they share aging connective tissue on the one hand but abnormal vascular structures on the other hand. (Schlemm’s canal can be considered a vessel of sorts, perhaps related to venules or lymph channels, with adjacent contractile cells and adventitia.) Others have suggested a possible common pathogenic mechanism in the epithelia of the ciliary body and renal tubules.⁹ The study of the link between blood pressure and POAG is clouded by the effect of antihypertensives on the status of the optic nerve head in patients with glaucoma, as some have been associated with both protective and deleterious effects.^6,9,10

There is evidence that thyroid disease may be associated with POAG^11–13 and anecdotal experience⁵ (that we share) that correction of thyroid status may result in lowering of IOP. The most robust study in this arena relied on self-reported data of “thyroid problems” and thus was unable to further elucidate the link between glaucoma and any particular thyroid disorder.

Diabetes has sometimes been associated with POAG.^14–16 Though the mechanism has not been definitively established, there is evidence that both diseases involve compromised vascular regulation. There is overlap between the risk factors for both diseases, and when both are present, they may influence each other’s progression.¹⁷ While there is evidence that diabetes is associated with a significantly higher risk of open-angle glaucoma,¹⁸ there is still some inconsistency in study results, and further research in this area is warranted.¹⁷ Interestingly, there is evidence that metformin is associated with a reduced risk of developing glaucoma, even when the analysis is controlled for level glycemic control.¹⁹ Other diabetes medications have not been shown to have such an effect.¹⁹

There are no other recognized common systemic diseases that have been unequivocally associated with POAG, but have we performed the appropriate inquiries?

There are many secondary glaucomas that are associated with systemic disease, and they will be detailed in subsequent chapters, for example, increased episcleral venous pressure due to dural shunts or Sturge-Weber syndrome, cortisone-secreting pituitary tumors, various forms of secondary angle closure from tumors, and neovascular glaucomas from diabetes or carotid ischemic disease. One might suspect that formation of pseudoexfoliation material should be part of some systemic disease. In fact, there is evidence of systemic deposition of similar material,^20,21 and the genetics of pseudoexfoliation are still under investigation.^22–27

ACTIVITIES

There is no evidence that patients with POAG or truly any other form of glaucoma should alter their daily life activity. Some patients with pigmentary glaucoma (see Chapter 22) episodically liberate pigment into the anterior chamber, sometimes after vigorous exercise of certain types usually involving head movement. In the absence of more specific management, treatment is given like that for POAG to prevent acute damage to the optic nerve from the transient IOP elevation. It is unclear whether it might even be desirable to shed this pigment earlier and acutely rather than later and more chronically.

Both acute²⁸ and chronic²⁹ exercise may actually lower IOP in POAG patients. One should be aware that vigorous exercise just prior to ophthalmologic visits should be discouraged to avoid spuriously low IOP readings.

Recent research into the influence of sleep characteristics on glaucoma yielded interesting results. Patients who slept 10 hours or more per night had significantly increased odds of having glaucoma as defined by disc parameters. Visual field defects were most likely in patients who slept 3 hours or less or 10 hours or more per night. Further, patients who reported daytime dysfunction due to sleepiness had greater odds of visual field dysfunction. It is unclear whether these abnormalities in sleep parameters are a cause or consequence of glaucoma.³⁰

Some claim that a supine position at night results in spikes of IOP elevation and optic nerve damage. It is true that in both normal patients and patients with glaucoma, the IOP is slightly higher (1 to 2 mm Hg) in the supine position.³¹ This likely relates to changes in venous pressure influencing the eye pressure. There are likely compensatory vascular responses. While this area, like most in glaucoma, deserves further evaluation, it seems premature to instruct patients to significantly alter their lifestyle or sleeping postures, without a firm understanding of the implications of this normal postural change in IOP. It is clear, however, that IOP does rise at night and that this is indeed associated with the supine position.32 One study³³ demonstrated elevated IOP to substantially high levels in patients sleeping prone with firm eye pressure against a pillow. This finding warrants further evaluation before any change in recommended sleep habits for patients with glaucoma would be appropriate.

A question in all these studies is how long the elevation in IOP is sustained. For example, if one pushes on one’s own eye, one can substantially elevate IOP initially, but then changes in ocular vascular volume and enhanced outflow from the eye as in tonography may or may not provide compensation. One might imagine that sustained levels of high IOP might induce pain or some discomfort to either awaken the patient or change head position (which is likely changing spontaneously regardless).

Reading and close work, if anything, by increasing mechanical traction on the scleral spur and TM from contraction of the ciliary muscle, similar to pilocarpine, would be expected to lower IOP in patients with open-angle glaucoma.

Theoretically, close work might be thought to potentially increase relative pupillary block in a patient with a predisposed narrow angle, but if ever a factor, it would be in those patients who had not yet been diagnosed. Those with known angle-closure glaucoma who have had an iridectomy would not be at risk. (Spontaneous angle-closure attacks precipitated by close work must be very rare, perhaps for the same reason that very weak concentrations of pilocarpine similarly do not precipitate such attacks, and more commonly can actually be used to treat an attack—see Chapter 23 for a discussion of vectors involved in acute angle-closure glaucoma due to pupillary block.)

EMOTIONS

Many patients with POAG will inquire whether their emotions affect their IOP, and rarely a patient is encountered whose IOP seems better controlled when tranquilizers are prescribed. (Some patients get apprehensive having their IOP measured, especially at the slit lamp, and may hold their breath or contract their eye muscles to give spurious readings—see subsequent chapters for techniques to avoid such artifacts, including using the Perkins handheld applanation tonometer, iCare rebound tonometer, Tonopen, or pneumatonometry). Yet, there still is a rare patient in whom tranquilizers seem to cause modest, though real, IOP lowering. Except for this rare occurrence, there is no known relationship between IOP in POAG and emotion. One hopes that time will not prove this to be a premature incorrect answer based on insufficient data, similar to past patient queries about such conditions as systemic hypertension.

In contrast, in patients with unsuspected narrow angles, emotion (presumably from sympathetic discharge resulting in pupillary dilation) can precipitate an attack of angle-closure glaucoma. Numerous cases have been observed where emotion was believed to have been involved. Of course, patients with known angle closure who have had iridectomies will not be at risk (except perhaps for some rare cases of plateau iris; see Chapter 27). A common situation where emotion-induced glaucoma may occur is in the fellow eye of an eye with acute angle-closure glaucoma (which often from the acute pain, etc, has much emotional effect on the patient), as well as strong emotional events such as death of a close relative or severe physical injury or illness.

FOOD AND DRINK

In the patient’s diet, we know of no food that influences glaucoma one way or another, although some transient osmotic influences might be detectable. Large volumes of water consumed rapidly do cause a transient rise in pressure in many glaucomatous eyes, and this is the basis of the so-called water drinking test. However, the fluid intake in ordinary living, if it has any deleterious effect on glaucoma at all, must be so insignificant in the overall picture that it has not seemed to us necessary to advise a patient with glaucoma to change his or her usual intake of fluid in any way. In the case of tea and coffee, we think the same advice generally applies.

Rarely, very high levels of caffeine intake in patients with POAG have been associated with some IOP elevation, but attempts to study this systematically in POAG patients have commonly yielded negative results.^34,35 Therefore, it seems that this must be a very rare phenomenon. Regardless, patients with POAG under poor control with vastly excessive caffeine intake (usually from coffee) should prudently be counseled to try to decrease intake for general medical health reasons, if not also for some possible beneficial effect on IOP.

Argemone oil has been an occasional toxic contaminant of edible cooking oils. It has been of interest for many years, principally in India, because it has been suspected of causing epidemic dropsy glaucoma. This glaucoma is described as a reversible, noninflammatory, open-angle glaucoma occurring in epidemics of toxic dropsy. The IOP is raised, and in the most severe cases, there is glaucomatous damage to the optic nerve. The elevation of IOP is spontaneously reversible, but the damage to the optic nerve is not. Alkaloids that are found in argemone oil, particularly sanguinarine and dihydrosanguinarine, have been suspected to be the active toxic components of argemone oil. A more detailed review of observations on argemone oil was made in 1993 by Grant and Schuman.³⁶

There does not seem to be an association between alcohol consumption and risk of POAG.³⁷ Alcoholic beverages need not be avoided by glaucomatous patients. In fact, the IOP is nearly always temporarily lowered by strong alcoholic drinks, and it may be lowered even by wine and beer.38,39 Patients, however, should be asked not to imbibe on the day of an office visit simply because it may result in a falsely low IOP level that is not sustained. Lowering of pressure by alcohol is slight in normal eyes, but in glaucomatous eyes, it is occasionally sufficient to cause a transitory decrease from pressure levels of 30 or 40 mm Hg to normal. When the equivalent of 50 mL of ethyl alcohol is consumed rapidly, the IOP may be lowered for several hours, returning to its previous level in 4 or 5 hours. The condition of the IOP in a so-called hangover has not been investigated. In exceptional instances, before the prolonged lowering of IOP, there has been a brief rise of a few millimeters of IOP a few minutes after drinking whiskey.

The duration of lowering of pressure is longer than we would expect from the theoretical osmotic action of ethyl alcohol, which is known to pass from blood to aqueous humor only a little less rapidly than water. In general, it has been found that alcohol taken in a dilute form, such as beer, can induce essentially the same changes in IOP as an equal amount of alcohol in concentrated form, such as whiskey.

It is most intriguing that the duration of diuresis induced by alcohol is similar to the duration of effect on IOP. Because alcohol is believed to induce diuresis principally through suppression of release of antidiuretic hormone from the hypophysis, it would be interesting to learn whether the change in concentration of the hormone in the circulation is involved in the lowering of IOP.

SYSTEMIC MEDICATIONS

Atropine and many drugs having anticholinergic, atropine-like properties are reputed to be dangerous for patients who have glaucoma. For this reason, a considerable proportion of drugs that have been introduced in recent years, including many psychopharmacologic agents, antihistamines, antispasmodics, and medications for parkinsonism, have been labeled with warnings against their use in the presence of glaucoma. Actually, only in eyes that are anatomically predisposed to angle-closure glaucoma do atropine-like drugs present a significant hazard, and these eyes constitute a small proportion of all glaucomatous eyes in the Western hemisphere. In eyes that have the anatomic peculiarity of a very shallow anterior chamber with precarious narrowing in the periphery, the angle can be caused to close, and an attack of acute angle-closure glaucoma can be provoked by dilation of the pupil with atropine-like medicines given systemically. Eyes of this special type are subject to angle-closure glaucoma from many other influences, including sympathomimetic agents and mydriasis in response to darkness.

Ironically, patients who have precariously narrowed angles, in whom an acute attack of angle-closure glaucoma may be precipitated by an atropine-like drug, are rarely aware of any threat of imminent glaucoma in their eyes. Conversely, patients in whom chronic open-angle glaucoma has been diagnosed and who are under proper treatment stand in little or no danger from systemic use of drugs having atropine-like effects. In other words, the atropine-like drugs pose a threat to people who are unaware of the possibility of glaucoma, whereas these drugs present little or no problem to people in whom glaucoma is already diagnosed and under proper treatment. On the warning labels of drugs having atropine-like effects, it is appropriate to advise that one should be alert to the possibility of precipitating acute glaucoma in patients who have abnormally shallow anterior chambers.

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