The ophthalmic technician is a critical member of the glaucoma patient management team. Responsibilities integral to the ophthalmic technician’s role in the care of patients with glaucoma include:
Identifying factors that may be indicative of glaucoma when taking a patient’s history
Performing key tests to define the glaucoma patient’s status
Aiding in glaucoma patients’ treatment by teaching them about their condition, demonstrating treatment techniques (such as applying eyedrops), and monitoring their compliance and treatment efficacy in preventing progression
Assisting in the preoperative preparation and especially in the postoperative care of glaucoma surgical patients
Each one of these aspects is essential to the complete care of the glaucoma patient.
An understanding of what glaucoma is, what glaucoma does to the eye, and what we can do about it enables the technician to become a key component of this glaucoma patient management team. It is the ophthalmic technician who has the potential to effect a positive outcome in the prognosis of glaucoma patients. More than 80 million people worldwide are afflicted by glaucoma. There are countless millions in whom glaucoma has not been diagnosed. For every person blinded by glaucoma, there are at least six individuals who have lost useful vision in one eye.
Glaucoma is a localized ocular disease characterized by optic nerve cupping and visual field loss, and is usually associated with elevated intraocular pressure (IOP). The hallmark of glaucoma is a progressive optic neuropathy. Risk factors for glaucoma include:
Family history of glaucoma
People of African or Hispanic ancestry
Trauma to the eye
Glaucoma falls roughly into five classifications ( Table 25.1 ):
Primary open-angle or chronic glaucoma . This condition is thought to arise from a progressive outflow obstruction in the trabecular meshwork of the anterior chamber angle structures, with a subsequent increase in IOP. It is insidious and symptomless, initially causing loss of the peripheral visual field but often undetected until significant irreversible loss has occurred. Most cases of glaucoma fall into this group.
Secondary glaucoma . Secondary glaucoma can be of either the open-angle or the narrow-angle type. The elevated IOP results from a specific disease within the eye, such as iritis, uveitis, venous obstruction in the eye, or tumor, which interferes with aqueous flowing out of the eye. It may occur after trauma or may follow neovascularization in the anterior chamber, as may occur with diabetes. Different types of secondary glaucoma include pigmentary, exfoliative, and uveitic glaucoma.
Angle-closure glaucoma . In this condition, there is a sudden marked increase in IOP caused by mechanical obstruction of angle structures of the eye near the root of the iris. Vision is blurred rapidly, the eye becomes red, and the patient complains of excruciating pain and often halos.
Congenital or infantile glaucoma . This condition is also referred to as buphthalmos (ox eye) because the soft infantile eyeball distends as a result of the elevated IOP and becomes noticeably enlarged ( Fig. 25.1 ).
Normal-tension glaucoma . Patients with this condition have IOP within a normal range but continue to lose field of vision. This condition is often vascular in origin, associated with other vasculopathy and often caused by systemic hypotension while sleeping.
|Primary open angle||Gradual blockage of drainage channel; pressure builds slowly||Gradual loss of side vision; affects side vision first||Progresses very slowly and is a lifelong condition; considered the “thief in the night”|
|Secondary||Injury, infection, tumors, drugs, or inflammation, which causes scar tissue growth, blocking the drainage channel||Gradual loss of side vision; affects side vision first||May progress slowly; similar to chronic open-angle glaucoma|
|Angle-closure glaucoma||Total blockage of drainage channel; sudden increase in pressure||Nausea, blurred vision, severe pain, halos around lights||A medical emergency because permanent blindness occurs rapidly without immediate treatment|
|Congenital (infantile)||Fluid drainage system abnormal at birth||Light sensitivity, excessive tearing, enlarged eyes, cloudy cornea||Must be treated soon after birth if vision is to be saved|
Primary open-angle or chronic glaucoma
Primary open-angle glaucoma (POAG) is a chronic progressive bilateral disease. It most often develops in middle life or later. The onset is gradual and without external signs or symptoms. It has been determined that 3 million Americans have POAG.
The cause of this disorder is obstruction of the outflow of aqueous humor at the trabecular meshwork. Most cases of POAG are caused by an inability of aqueous fluid to leave the eye and not by an overproduction of aqueous fluid ( Fig. 25.2 ).
Because there are often no symptoms until the disease is far progressed, POAG is most often discovered during routine eye examinations or screening examinations, when the patient is found to have elevated IOP or an excavated optic nerve. The diagnosis of this condition usually depends on three objective signs—abnormal cupping of the optic disc ( Figs. 25.3 and 25.4 ), typical changes in the visual field, elevated IOP—and other diagnostic tests ( Box 25.1 ).
Intraocular pressure: tonometry
Central corneal thickness
Structural: optic nerve
Stereo disc photography
Nerve fiber layer thickness (optical coherence tomography [OCT])
Ultrasound biomicroscopy (UBM)
Confocal scanning ophthalmoscopy (Heidelberg retina tomograph)
Retinal nerve fiber layer assessment (GDx VCC)
Functional: visual fields (see Ch. 18 )
Standard automated perimetry (SAP; white on white)
Short-wave automated perimetry (SWAP; blue on yellow)
Frequency doubling technology (FDT)
In contrast to POAG, some people have high IOP but do not show any changes in their optic discs or visual fields. These are individuals whose nerve can tolerate higher than normal IOPs without apparent damage. Some ophthalmologists believe they may be preglaucomatous or “glaucoma suspects.” However, ophthalmic personnel label this condition ocular hypertension to avoid using terms that might needlessly upset and worry patients. The term ocular hypertension creates a convenient category, without a gloomy label, for keeping patients under close observation. Actually, most of these people will live most of their lives without needing therapy. However, they must remain under observation because some individuals in this group are at greater risk of developing preventable glaucomatous changes in their optic disc and field. Topical ocular hypotensive medication is effective in delaying or preventing the onset of POAG in individuals with elevated IOP. Clinicians should consider initiating treatment for individuals with ocular hypertension who are at moderate or high risk for developing POAG.
At one time, people older than 40 years with pressures greater than 21 mm Hg were considered to have glaucoma and were treated on the basis that field loss would inevitably follow. However, clinical evidence has shown that whereas an estimated 10 million Americans older than age 40 years have pressures greater than 21 mm Hg, only 0.3% of the same population have detectable visual impairment. Of those with ocular hypertension, 10% have field loss and another 4% will develop field loss during the 5- to 10-year follow-up.
Therapy for those with ocular hypertension is not without risk. Therapy may restrict a healthy person to a schedule requiring medication 1 to 3 times daily, limiting the patient’s ability to manage daily activities or interfering with systemic medication or systemic conditions. For these reasons, the decision to treat this group of patients with elevated IOP is a judgment call dependent on the perceived threat to vision. Thus ocular hypertension is often treated by watchful waiting.
Secondary glaucoma occurs as a result of an additional pathology within the eye. Because in essence there are two diseases in the eye—the precipitating cause and the glaucoma—the condition is often more difficult to treat. Secondary glaucomas include secondary open angle, reviewed in this section and secondary angle closure, reviewed under Angle-Closure Glaucoma, in the following text.
Causes of secondary open-angle glaucoma include pigment or protein accumulation in the drainage structures, iritis, cyclitis, and trauma and rarely invasion of the trabecular meshwork by tumors of the iris, ciliary body, and choroid.
Pseudoexfoliative (or exfoliative) glaucoma
Exfoliative glaucoma is caused by the accumulation of an insoluble protein in the drainage channels or other structures of the eye resulting in higher pressures than in patients with other types of glaucoma. The abnormal protein is often found in the lens epithelium, trabecular meshwork, iris, ciliary processes, conjunctiva, and periocular tissue. This condition is common among those of Scandinavian descent and seems to be related to a gene abnormality. It rarely occurs in patients younger than age 50 years.
Traditional IOP-lowering medications may be less effective in patients with exfoliative glaucoma, thus requiring additional therapy such as argon laser trabeculoplasty (ALT) or selective laser trabeculoplasty (SLT).
Pigmentary glaucoma occurs when iris pigment granules flake into the aqueous humor or other structures, such as the trabecular meshwork, and clog the drainage channels of the eye. This condition tends to occur at a younger age, usually in the 20 s or 30 s, and in near-sighted patients. It is more common in men than in women.
Patients are often treated with drops, such as a prostaglandin or a beta blocker, because these drops have a relatively low incidence of side effects and are well tolerated in younger patients. Miotics can be used to treat pigmentary glaucoma because it causes the pupil to constrict and prevents the iris from rubbing against the lens, thereby preventing release of pigment onto the surrounding structures. However, miotics often cause blurred vision and require more frequent dosing, thus limiting their use. Other options include laser iridotomy and ALT or SLT.
Neovascular glaucoma is a severe form of secondary glaucoma. It is associated with the proliferation of vessels in the anterior chamber angle. The blood vessels generated through neovascular glaucoma are abnormal, and when new blood vessels form in the anterior chamber angle, the aqueous outflow can be compromised. Typically, the three most common conditions responsible for neovascular glaucoma are diabetic retinopathy, central retinal vein occlusion, and carotid artery obstructive disease.
Neovascular glaucoma is often treated with panretinal photocoagulation, which has been shown to reduce anterior segment neovascularization. Traditional IOP-lowering medications also can be used to lower the pressure, as well as trabeculectomy and aqueous drain implants.
Traumatic glaucoma refers to any injuries to the eye that result in glaucoma. Blunt trauma, such as a direct injury to the eye or a blow to the head, usually as a result of sports, can cause an accumulation of blood and debris that clogs the drainage channels. In this case, glaucoma medications can be used to control eye pressure, and surgery may be necessary. In most cases, the elevated eye pressure is temporary.
When a penetrating eye injury occurs, such as by a sharp instrument, it can cause the eye to become swollen and bleed, leading to elevated eye pressure. In addition, drainage channels can be blocked by damaged tissue and scarring. Ocular trauma is often treated by topical corticosteroid therapy as an initial treatment to minimize permanent tissue damage and scarring.
Glaucomatocyclitic crisis is a condition with self-limited recurrent episodes of markedly elevated IOP with mild idiopathic anterior chamber inflammation. It is most often classified as secondary inflammatory glaucoma.
In 1948 Posner and Schlossman first recognized glaucomatocyclitic crisis and described the features of this syndrome. For this reason, the entity is often termed Posner–Schlossman syndrome (PSS).
Most commonly, a “crisis” presents with slight discomfort. The patient may be pain-free even though the IOP is quite elevated. The patient may report blurred vision or halo vision if the IOP is high. A history of attacks of blurred vision lasting several days, which recur monthly or yearly, is usual. IOP is usually elevated in the range of 40 to 60 mm Hg.
The favored initial treatment for PSS is a combined regimen of a topical nonsteroidal antiinflammatory drug (NSAID; e.g., diclofenac) and an antiglaucoma drug, such as timolol or dorzolamide. Prostaglandins are often avoided initially. Surgery is never indicated.
Primary angle-closure glaucoma
Angle-closure glaucoma may be primary or secondary. Primary angle-closure glaucoma constitutes approximately 10% of all glaucoma cases and occurs in about 5% to 10% of the older adult population. In the general population, a higher incidence of angle-closure glaucoma occurs in association with shallower anterior chambers. Angle-closure glaucoma shows increased incidence among people of Asian and Inuit descent and is less common among people of African ancestry.
Patients with this disorder have essentially normal but often short (hyperopic) eyes with a shallow anterior chamber and a narrow entrance into the angle. Such crowding of the angle structure tends to occur more often in hyperopia and increases as the patient becomes older. The narrowing is mainly caused by the increased size of the crystalline lens as a cataract forms, which tends to push the entire iris diaphragm forward, narrowing the endocorneal angle of the anterior chamber to less than 20 degrees, thus enabling the term narrow angle .
A common trigger mechanism that brings about closure of a critically narrowed angle is dilation of the pupil. Pupil dilation relaxes the iris and causes its tissue to bunch up toward the base of the iris, thereby effectively blocking the angle outflow structures. Also dilation of the pupil may relax the periphery of the iris sufficiently so that the pressure in the posterior chamber exceeds that in the anterior chamber, resulting in further forward displacement of the iris and crowding of the angle structures. If the pupillary border of the iris is bound down (as a result of inflammation) to the anterior lens capsule, or if the pupil is blocked by a prolapsed vitreous body, a pupillary block mechanism exists. This may lead to bowing of the iris, or iris bombé ( Fig. 25.5 ). In this situation, the pupil is blocked so that the aqueous pressure from the posterior chamber bows the iris forward, thus blocking the angle of the anterior chamber and preventing fluid outflow.
An attack of acute angle-closure glaucoma can become fully developed within 30 to 60 minutes. The abruptness of the onset is so characteristic that a presumptive diagnosis of acute angle-closure glaucoma can virtually be made over the telephone. The attack commonly begins under conditions that lead to pupillary dilation, for example, conditions of dark adaptation (movie theaters), fear, or emotional arousal. Such attacks are often precipitated by dilation during an eye examination.
The pain can vary from a feeling of discomfort and fullness around the eyes to a severe, referred pain that can radiate to the back of the head or down toward the teeth. With severe pain, the patient may be prostrate and nauseated and may even vomit. Vision is usually reduced and patients often report seeing halos as the result of a cloudy edematous cornea.
Certain drugs can also precipitate an attack, the most common being cyclopentolate and tropicamide. Other often used medications that can precipitate an attack are epinephrine derivatives. These drugs are frequently agents in common hay fever remedies, and the package insert indicates their contraindication in glaucoma; however, the phenylephrine derivative drugs are usually safe in open-angle glaucoma.
Examination reveals that the eyelids and conjunctiva are edematous and congested, especially around the limbus. The cornea appears steamy and hazy because of epithelial edema, which results from aggregations of tiny water droplets in the superficial layers of the cornea. The iris itself appears dull, gray, and patternless because of the edema. The pupil is typically middilated and may be oval. It does not respond normally to light. The IOP is often extremely high, in the range of 40 to 60 mm Hg or higher.
This type of ocular catastrophe is preceded in nearly half of cases by premonitory self-limiting episodes of aching blur, lasting a few hours each time and occurring with increasing frequency before an acute attack. Also the patient may report seeing halos or rainbows around lights, which are caused by the slight edema of the cornea in these premonitory periods. These halos, although not pathognomonic of glaucoma, are most significantly related to this disease and are caused by dispersion of light by the epithelial edema. They are typically composed of two colored rings: an inner blue-violet ring and an outer yellow-red ring ( Fig. 25.6 ). Between attacks, little or no abnormality may be noted.
The halos caused by subacute attacks can be distinguished from the permanent halos caused by lens opacities by placing a stenopeic slit across the line of vision. A glaucoma halo remains intact but with diminished intensity behind the slit, whereas a lenticular halo is broken up into segments that revolve as the slit is moved. The halos that are sometimes caused by conjunctival debris can be swept away by movements of the lid.
Secondary angle-closure glaucoma occurs as a result of an underlying pathologic etiology.
The conditions that can lead to secondary angle-closure glaucoma are:
Iritis or uveitis
Scar tissue or peripheral anterior synechiae between the iris and the trabecular meshwork
Posterior synechiae to the lens
Blockage of drainage channels by the accumulation of “flaky” protein or iris pigment
The most common cause of anterior synechiae is chronic angle-closure glaucoma and the most common cause of posterior synechiae is chronic, severe iritis.
Congenital glaucoma is an extremely uncommon disease. It is estimated that an average ophthalmologist is unlikely to see more than one new case of congenital glaucoma in 5 years of practice. Despite its rarity, the signs and symptoms of the disease are so characteristic that a diagnosis should not be missed.
Often the parents are aware that their baby has something wrong with the eye in the first few weeks or months of life. The child appears extremely sensitive to light and tears profusely. Many infants even keep their eyelids tightly closed most of the day to avoid the light. However, it is the corneal haziness caused by the corneal edema that makes most parents suspect that something is wrong with the child’s eyes. Because the eyeball tissue is distensible in early infancy, the increased IOP causes progressive enlargement of the infant’s eye and cornea. Most infant corneas measure less than 10.5 mm in horizontal diameter. A measurement greater than 12 mm is considered diagnostic of congenital glaucoma. These eyes, hazy and enlarged, appear so abnormal that the term buphthalmos has been commonly applied to designate this condition (see Fig. 25.1 ).
It is important that any child with a symptom of tearing is seen immediately because the earlier glaucoma is diagnosed and brought under control, the better is the prognosis. In most cases, tearing is caused by a blocked tear duct, but the ophthalmic assistant should always be aware of the possibility of congenital glaucoma.
Screening and aids in diagnosis
Screening for glaucoma
A comprehensive screening program consisting of tonometry, optic disc examination, and screening perimetry, although costly, helps detect and initiate early treatment to prevent vision loss. Screening programs that involve a single tonometer reading are inadequate because they miss many glaucoma patients. The overreferral rate of screening by pressure measurement alone is enormous, ranging from 10% to 30%, which means that large groups of patients undergo costly follow-up examinations. Also some glaucoma cases are missed: low-tension glaucoma, diurnal variations in which higher pressures are not found during office visits, and angle-closure glaucoma in which the pressure may be normal between attacks. Usually, the IOP criterion for a glaucoma referral is 21 mm Hg. Because structural damage precedes functional change, screening test results are vastly improved if one includes an inspection of the optic disc. This usually requires the services of an ophthalmologist or well-trained technician.
In suspected cases of open-angle glaucoma in which the pressure is borderline and the disc is equivocal in appearance, the ophthalmologist may resort to provocative tests to determine the presence or absence of glaucoma.
Normally the IOP is greatest in the early morning and lowest during the day. This diurnal variation in the IOP seldom exceeds 3 or 4 mm Hg. However, in a glaucomatous patient, it may exceed 7 to 8 mm Hg. In this test, ocular tension measurements are taken throughout the day and sometimes during the night, noting times when the IOP is found to be highest. A drawback is that it is costly and time-consuming because the patient must be hospitalized for a full 24-hour diurnal test to be performed. Often checking a patient’s pressures over the course of a day is adequate to find fluctuation, or bringing the patient back for pressure checks at various times in the day on subsequent visits can assist in determining large diurnal IOP variations.
Observation over time is the most widely used method of following glaucoma. In suspected cases, patients usually are told that they have borderline glaucoma or that glaucoma is suspected and they are asked to return to the office on three or four occasions during the year. On these occasions the pressures are measured, the optic discs are examined, and the visual fields are tested. The ophthalmologist basically looks for an alteration in any one of these three parameters to confirm the diagnosis or determine the adequacy of control. The patient may show a pattern of gradually increasing pressures, increase in cupping of the disc, or an early glaucomatous field defect, which is an indication of the need to initiate or increase treatment.
The shallow-chambered, narrow-angled eye should be identified by a routine eye examination. The observer can easily see the convex iris diaphragm by illuminating the limbal area with a flashlight and noting the proximity of the iris periphery to the cornea. If there is any doubt as to whether the angle is narrowed, mydriatic drops, such as cyclopentolate (Cyclogyl) or homatropine should not be used because they can, in such an eye, induce an attack of acute angle-closure glaucoma. It must also be emphasized that the finding of normal pressure by tonometry before dilation is no guarantee that this type of glaucoma will not ensue. The only method of assessing such an eye is by examination of the angles themselves with the use of the gonioscope.
Many tests provoke an angle-closure attack and therefore confirm the diagnosis of angle-closure glaucoma. The dark room provocative test is the time-honored method of revealing this condition. In this test, the patient is kept in a dark room for 60 to 90 minutes, and the ocular pressure is subsequently measured. A rise of 8 mm Hg or more is considered a positive reaction. Unfortunately, this test is not specific for predicting future angle-closure attacks and, although useful, is not relied on as much as the mydriatic test.
The mydriatic test for angle-closure glaucoma consists of instilling one or two drops of a weak-acting mydriatic agent, such as phenylephrine (Neo-Synephrine) 2.5%, into the conjunctival sac. Again, an 8 mm Hg rise in pressure by the end of 1 hour is considered a positive reaction in which gonioscopy confirms that the angle has narrowed and possibly closed during the period of pressure elevation.
Measuring IOP, or tonometry , is an essential part of all eye examinations for adults and children. The reason is simple: routine tonometry can assist in detecting undiagnosed glaucoma. Glaucoma affects an estimated 3.5% of adults between the ages of 40 and 80 years, and the prevalence increases in individuals older than age 70 years; in fact, some investigations have found elevated IOP (>21 mm Hg) in as many as 6.5% of normal individuals and 80% of untreated glaucoma patients.
Because eye pressure measurement is such an important parameter to record, most ophthalmologists instruct their personnel to perform tonometry. It therefore behooves the ophthalmic assistant to understand the basic techniques and underlying physiologic principles of tonometry and to become comfortable, competent, and knowledgeable with it.
Eye pressure is not measured directly. It is simply not practical or safe to place a needle in the eye and record the actual IOP. Instead, the pressure is determined noninvasively. Noninvasive devices work via either an indentation or an applanation principle. Each method has advantages, as well as limitations, which are outlined in the following text.
The accuracy of either technique is limited by the physical properties of the cornea. During the actual measuring process, an indenting apparatus deforms the cornea more than an applanating one. Therefore more aqueous fluid, normally in the anterior chamber of the eye between the cornea and the iris, is displaced by indentation. The displaced aqueous ultimately distends the other structures inside the eye. These intraocular structures have an inherent elastic property that resists distension; that is, the eye does not expand like a balloon, but rather its natural elastic qualities maintain a constant volume. Because the volume does not change, the pressure inside the eye must change. Thus the IOP as measured by indentation is “falsely” elevated. This phenomenon is well known, and calibration charts formulated to compensate for this abnormal false elevation of pressure are readily available.
The applanation technique differs from the indenting technique by displacing a lesser amount of fluid. Therefore applanation tonometer-induced IOP elevation is a less significant concern but becomes a significant concern when corneal thickness is greater or lesser than the average for which the applanating device is calibrated. This is the major reason that many ophthalmologists believe applanation techniques are more accurate than the indentation procedure.
In applanation tonometry, the cornea is flattened and the flattened area is measured, or a specific known area is flattened and the amount of force needed to flatten this area is measured. (The word applanation originates from the Latin planare or ad planare , meaning “to flatten.”) The higher the IOP (the harder the eye), the smaller the flattened area is, assuming that the same pressure is used for flattening each time tonometry is performed.
Applanation tonometry eliminates some of the errors inherent in indentation tonometry. Indentation tonometry creates pressure forces in the indented ocular wall and these forces act against the plunger of the tonometer. In addition during indentation tonometry, the considerable weight of the tonometer itself artificially raises the IOP. However, in applanation tonometry, the pressure forces that are created in the applanated ocular wall are lying in the plane of applanation and oppose each other; thus they cancel each other for all practical purposes. Also in applanation tonometry, the artificial increase of the IOP during tonometry caused by the weight of the tonometer is minimal. Another common source of error of indentation tonometry is underestimation of the IOP in eyes that have low “ocular rigidity,” such as the eyes of myopes. Applanation minimizes this error.
Goldmann applanation tonometer
The Goldmann applanation tonometer, the most commonly used tonometer, enables a reliable measurement of IOP to within ± 0.5 mm Hg. This tonometer, because it flattens or applanates the cornea and does not indent it, gives accurate information about the pressure in the undisturbed eye. Scleral rigidity can be disregarded because less than 0.5 mm of volume is displaced. It also causes little increase in pressure, so that minimal massage effect is produced by repeated measurements that might lower the pressure. A plastic tip is attached to a sensitive balance mounted on the slit lamp ( Fig. 25.7 ). This small tip is designed to minimize both the “inward” pull from the liquid tear film on the cornea and the “outward” push from the elastic cornea. The volume of displaced fluid inside the eye is so small that any variation in ocular rigidity can be ignored. When the circular tip with a 3.06-mm diameter is used to applanate the cornea, no significant elevation of eye pressure is created.
One disadvantage of the Goldmann applanation tonometer is its lack of portability. However, handheld applanation tonometers have been devised. Other disadvantages are that the technique requires training for successful use. In addition, corneal distortion associated with conditions, such as scarring or high astigmatism, creates difficulty in obtaining reliable endpoint measurements. Corneal abrasions are always a potential hazard if the assistant is too aggressive during the pressure reading or if any underlying corneal problem is present. Infection is a potential risk as well, thus cleaning the tip or single-use tips are necessary.
The method of applanation tonometry is as follows: a drop of a local anesthetic solution is placed into the lower conjunctival sac. Then a drop of fluorescein from a fluorescein strip (small strips of filter paper impregnated with fluorescein) is instilled into the eye. Combination drops, which include both an anesthetic and fluorescein, are available. After the drop is instilled, the patient’s head is positioned at the slit-lamp microscope with the chin on the chin rest and forehead pressed firmly against the headrest.
Once the cornea is in focus, the appropriate blue filter is used and the slit diaphragm is opened completely. In the beam, the whole surface of the patient’s eye should glow (fluoresce) in a bright greenish yellow. The blue light should be approximately 45 to 60 degrees to the side of the tonometer and should illuminate the front end of the prism head. The low magnification is used on the slit-lamp microscope. The patient’s lids must be open and unblinking. It is necessary to avoid any contact between the tonometer and the lid margin or lashes because this contact only induces further blinking. The patient is instructed to look straight ahead or at some target device attached to the slit lamp or the examiner’s ear to ensure fixation. Once the patient is ready, the tonometer, with the measuring drum set at 1 g (1 on the dial), is brought forward by the joystick of the slit lamp until it comes into contact with the center of the cornea.
Looking through one eyepiece of the microscope, the examiner sees, at the moment of contact, a bright yellow-green spot that quickly separates into two bright yellow-green semicircular arcs as the tonometer is moved slightly farther forward. These arcs should be in sharp focus and of equal circumference both above and below the horizontal dividing line. Any necessary correction should be made by the control lever or the height adjustment control on the slit lamp. The calibrated drum on the side of the tonometer is then turned toward higher numbers corresponding to increasing force of applanation. As this occurs, the two semicircular arcs move until they overlap, the inner edge of the upper semicircle becoming aligned with the inner edge of the lower semicircle ( Fig. 25.8 ). This is the desired endpoint at which the reading is taken from the drum.
The reading obtained is multiplied by 10 to convert the number to equivalent millimeters of mercury of IOP. Therefore 1 on the drum is equal to 10 mm Hg. It is best to take at least two readings from each eye to obtain an average value. If the values obtained on two successive readings are approximately the same, the technique is probably adequate.
Checking the calibration of the Goldmann applanation tonometer
Applanation tonometers should be calibrated for accuracy by the use of a central weight regularly. For the Goldmann tonometer, a short rod of measured weight is attached to the balancing arm of the tonometer and the rod set at 0, 2, and 6 respectively. At each measure, the measuring drum should be placed at the corresponding stop. At each stop, the tonometer head should move only ± 0.05 g (0.5 mm Hg) of these settings ( Fig. 25.9 ).
The applanation tonometer consists of a plastic removable tip that contains a prism. This tip has a flat anterior surface, which is brought into contact with a fluorescein-stained tear film of the cornea, which it displaces to the periphery of the contact zone until a surface of known and constant size, 3.06 mm, is flattened. The prism within the tip splits the image of this 3.06 mm circle into two semicircles. The inner border of the semicircles, when they are touching, represents the line of demarcation between the cornea flattened by applanation and the cornea not flattened. Thus this is the endpoint of the measurement of an applanation circle of 3.06 mm. This tip is connected to a spring device that allows measurement of the amount of pressure needed to flatten the cornea and is regulated by a knob on the side that has markings of this amount of pressure. The knob can regulate the spring tension to produce a force that is between 0 and 8 g. Once the inner semicircles are touching following turning the knob to apply adequate pressure to flatten the cornea, this number is read from the knob’s outer ring.
Errors in Goldmann tonometry
If the fluorescein ring is too wide ( Fig. 25.10 ), too much fluorescein may have been instilled. In this case, a small tissue can be used to absorb excess fluorescein and the procedure repeated. Alternatively, the measuring prism may not have been cleaned of previous fluorescein. A wide band results in an erroneous high reading.
If the fluorescein band is too narrow ( Fig. 25.11 ), evaporation of the stained tear layer during protracted measurement has occurred. The reading on the drum will be lower than normal. The patient should be told to blink several times and the measurement repeated.
The two semicircles may not be on the middle field ( Fig. 25.12 ). The patient may have moved slightly or the chin rest may not be properly adjusted; thus the fluorescein rings are not two exact semicircles because of incorrect centering of the tonometer head. This produces a considerably elevated IOP. The slit lamp should be adjusted up or down to obtain two exact semicircles.
If the patient’s head is not pressed firmly against the forehead bar, there may be intermittent contact of the prism with the cornea, resulting in apparent pulsations of the fluorescein rings. However, note that the normal cardiac cycle pulsation can be seen as pulsation of the rings.
With a spherical or near-spherical cornea, measurement can be made in any meridian. However, if astigmatism greater than 3.00 diopters exists, the flattened area becomes elliptical rather than circular. In this instance, the tonometer prism head should be set with the axis corresponding to the axis of the minus cylinder.
Standard applanation tonometry with fluorescein cannot be used over a soft contact lens. The MacKay-Marg tonometer, a pneumatic tonometer, or an electronic tonometer may be used in this situation.
Breath-holding or a tight collar can create a false high reading.
If it is necessary to hold the lids apart with the fingers and thumb, care must be taken to avoid pressing on the globe; this will falsely raise the IOP.
Evaluating the pressures
If the pressure is found to be more than 21 mm Hg with the Goldmann applanation tonometer measurements, the eye is considered abnormal. A pressure of 21 mm Hg should be regarded as borderline. Pressures between 18 and 21 mm Hg are generally normal, but the patient should be seen for repeated examinations. This reading may be unsafe in corneas that are thin.
The pressure normally varies in an eye at different times of day. It is highest in most people in the morning and lowest during the waking hours, the time when ophthalmologists conduct their clinics. It is because of this diurnal variation that the tension may be borderline or less than borderline and the patient may still have glaucoma. In addition to the diurnal variation, there are other low-tension glaucomatous states in which the pressure recordings may be normal or even below normal and the patient may still have clinical evidence of the disease. Although applanation tonometry is the best method of discovering the most characteristic risk factor for glaucoma, it is not an infallible test, for the reasons mentioned.
As mentioned, elevated IOP without demonstrable damage to the optic nerve and without visual field changes is called ocular hypertension . These cases require relentless and meticulous repeated observations.
The monitoring of glaucoma requires an ongoing evaluation of pressure, optic disc assessment, and visual field change.
Hints for tonometry use
Educate the patient . Less anxiety is created if the examiner tells the patient that the tonometer tip will touch the tear film instead of saying the tip will actually touch the eye.
Instill topical anesthetic . Again, tell the patient what to expect: “This drop may feel cold or may even sting for a few seconds.” Tell the patient to dab the eye with tissue paper, and to avoid rubbing or wiping the eye. After the anesthetic is given, touch the conjunctiva with a strip of fluorescein-impregnated paper. A drop of a combination topical anesthetic–fluorescein mixture, such as Fluress can be used.
Alignment . Place the patient’s chin on the rest and press the forehead against the headband. The patient’s eyes should be open. Ask the patient to stare straight ahead and not at the blue slit light.
Slit lamp and tonometer alignment . Set the magnification on low (this is much easier to use). Position the tonometer with the plastic tip centered and position the light so that the tonometer tip is as brightly illuminated as possible—usually a 45-degree angle between the light and tip. Do not forget to use the blue filter! Remember, if corneal astigmatism is greater than 3.00 diopters, set the tip corresponding to the axis of the minus cylinder of the astigmatism ( Fig. 25.13 ).
Move the slit lamp toward the patient, with the joystick held back. Once 3 to 5 mm away from the cornea, slowly advance the slit lamp forward with the joystick. At this point, the examiner can look through the left eyepiece and begin to see a faint purple semicircle created by the reflected corneal image of the prism tip. These arcs will touch each other just before the tip actually touches the cornea.
Align tonometer mires . Just as the tip touches the cornea, two bright green semicircles appear. If this does not happen, pull the joystick back, recheck both patient and tonometer alignment, wipe the tip, and start again. If the semicircles are slightly out of line, alignment can be adjusted without repositioning the slit lamp.
Proper measurement depends on the two arcs being sharply focused, symmetric, and bright. Rotate the dial on the tonometer scale until the inner edges of the two arcs exactly align ( Fig. 25.14 ). To calculate the IOP, multiply the scale reading × 10. Pulsatile movements of the mires can be frustrating as the examiner tries to carefully touch the two inner edges together. A setting halfway between the two extreme pulse pressures will provide the truest pressure measurements.
Perkins handheld applanation tonometer
The principle of this instrument is the same as that of the Goldmann applanation tonometer, in that an applanating surface is placed in contact with the cornea and that force applied is varied until a fixed diameter of applanation is achieved. In the handheld instrument, the Goldmann doubling prism tip is mounted on a counterbalanced arm and the change in force is obtained by rotation of a spiral spring. The instrument operates on two AA batteries, and a tiny light bulb underneath the doubling prism gives off a cobalt blue glow. The instrument can be used in any position and need not be held vertically. The patient can be sitting or lying flat.
The method of use is as follows: the eye is anesthetized with one drop of a fluorescein solution (Fluress). The tonometer should be held so that the thumb rests on the thumb wheel, controlling the spring. The light is switched on by turning the thumb wheel until the scale reading is above 0 and the filter holder is adjusted to illuminate the end of the doubling prism, when the latter is at approximately its midpoint of travel, which is the position used for measurement.
The instrument has a forehead rest that can be used when the tonometer is positioned on the patient’s cornea. It is easier to hold the tonometer obliquely, with the handle slanted away from the patient’s nose. Care should be taken that the prism is not touching the lids, in which case the readings obtained will be invalid.
The doubling prism is applied to the center of the patient’s cornea, with the scale reading 1. Semicircles of fluorescein should now be visible through the viewing lens; force is adjusted by turning the thumb wheel until the inner margins of the semicircles coincide. The tonometer is then removed from the eye and the reading noted. The reading is multiplied by 10 to give the tension in millimeters of mercury. The usual method is to repeat the reading for each eye twice and, if elevated, to take three readings.
If the semicircles appear large and are not reduced by altering the force of the spring, the tonometer has been pushed too close to the eye. Withdrawing it slightly will bring the prism within the range of free movement.
Electronic applanation tonometer
Electronics represents the final adaptation of the applanation principle and is best represented by the MacKay-Marg tonometer or the Electro Medical Technology tonometer. With this technique, as the tip is applied to the eye, the pressure flexes an ultrathin membrane. This pressure is indirectly transmitted to a force transducer. The pressure waveform is converted into electrical impulses proportional to the applied pressure and recorded on a graph with a thermal stylus. This original device is no longer available, but several miniaturized versions that function on similar principles have been developed and appear accurate and reliable.
Other applanation tonometers
Several lightweight, portable, handheld tonometers are available. One of them, the Tono-Pen ( Fig. 25.15 ), is a pen-like instrument that permits repeated accurate reading by applanation. It is a very useful instrument that incorporates its own battery power supply and digital readout and provides both an IOP reading and an indicator of the reliability of the value. The results correlate well with the Goldmann tonometer, although it slightly overestimates low IOPs and underestimates high IOPs. It can take measurements in an eye with an irregular or edematous cornea or through a soft contact lens in a variety of clinical settings because the area of applanation is much smaller than with the Goldmann applanation tonometer. Also available are applanation tonometers that can measure the IOPs through the use of an operating room microscope. This operating room device allows the surgeon to estimate whether the IOP is high, medium, or low at the end of intraocular surgery. Another is the AccuPen, a handheld tonometer that uses high-resolution, real-time waveform analysis to provide accurate IOP measurements. It uses gravity offset technology, which requires less calibration compared with other handheld tonometers. The user enters the central corneal thickness and the AccuPen creates an adjusted IOP.
The Icare® rebound tonometer uses a tiny plastic-tipped, single-use probe surrounded by a magnetic field. A magnetic coil “fires” the probe forward onto the cornea, creating a very small applanation region. The time it takes the probe to return to its resting position is indicative of the IOP. There is no air puff involved like other noncontact tonometers and the contact time is so brief that often no anesthetic need be used. The first version of the rebound tonometer is the Icare TA01i. The disadvantage of this tonometer is that the probe fell out of the tonometer if it was faced downward.
The Icare PRO adds a sensor that allows for IOP measurements in the supine position. In addition, the probe does not fall out if the tonometer is not in the upright position and there is greater accuracy when measuring IOP.
The Icare HOME tonometer is easy to use for patients who need to monitor their IOP consistently. It can automatically identify which eye is being measured and the patient only has to place the tonometer in front of their face without tilting the device and wait for a “green” ring signal to measure. If the tonometer is in an incorrect position, the device will display a red signal and the probe is not launched.
The Icare IC100 allows for self IOP measurements and improves on the upright position sensor. The newest generation Icare IC200, allows for 200 degrees of positional freedom so measuring the IOP for patients can be done in various positions.
Dynamic contour tonometer
The dynamic contour tonometer (DCT) is a digital tonometer that provides a direct transcorneal measurement of IOP. This tonometer is based on the principle that, by surrounding and matching the contour of a sphere, the pressure on the outside equals the pressure on the inside. In the DCT, the tip of the probe matches the contour of the cornea. A pressure transducer built into the center of the probe measures the outside pressure, which should equal the inside pressure, and the IOP is recorded digitally. The DCT eliminates the systematic errors inherent in other tonometers, such as the influence of corneal thickness and rigidity.
Indentation tonometry (Schiøtz tonometry)
Although Schiøtz tonometry has been largely replaced by applanation, it remains useful for general practitioners, hospitals, and less affluent countries.
The Schiøtz tonometer has been used historically for the detection and determination of IOP because it is convenient to use, portable, fairly reliable, and low in cost. It is not dependent on batteries, electricity, or a slit-lamp biomicroscope.
When the Schiøtz tonometer is used, the patient is usually placed in a recumbent position and asked to look up at a fixation point directed vertically above ( Fig. 25.16 ). The corneas are anesthetized with a topical anesthetic, such as proparacaine. If the blinking motion is excessive, the examiner may pinion the lids against the margin of the orbit with his or her fingers, taking care not to press on the globe itself. The tonometer is allowed to rest on the patient’s cornea, and the extent to which the plunger of the tonometer indents the cornea is, indirectly, a measure of IOP. The greater the distance the plunger indents the cornea, the softer is the eye or the lower the IOP. This is recorded on a scale on which the reading reflects the excursion distance of the plunger. If the eye is soft, as the Schiøtz tonometer plunger moves, the recording needle moves farther along the scale located at the top of the tonometer. The higher the scale reading, the lower the eye pressure. Conversely, minimal excursion of the plunger suggests that the eye is firm and the IOP high.
The indicator on the tonometer points to the scale readings of the tonometer. Converting from scale readings with Schiøtz tonometry to millimeters of mercury requires a conversion table or graph ( Table 25.2 ). This is usually supplied with the instrument. This chart converts plunger excursion into IOP (mm Hg), which is designated P o, the true eye pressure before the tonometer is placed on the cornea. Once the tonometer rests on the eye, an abnormally high pressure is created and this is often referred to as P 1 .
|Pressure (mm Hg)||Pressure (mm Hg)|
|Tonometer reading||5.5 g||7.5 g||10 g||15 g||Tonometer reading||5.5 g||7.5 g||10 g||15 g|