Chapter 12 The Glaucomas
The glaucomas are a diverse group of diseases united only by the fact that intraocular pressure (IOP) is too high to permit the optic nerve and, in some species, the retina to function normally. Characteristic changes of glaucoma include disrupted axoplasmic flow in the optic nerve head, death of retinal ganglion cells and their axons, cupping of the optic disc, and visual impairment or blindness.
The production and drainage of aqueous humor are influenced not only by the anatomy of the anterior segment but also by a large number of endogenous compounds, including neurotransmitters, hormones, prostaglandins, proteins, lipids, and proteoglycans. Indeed, so many factors influence the production and drainage of aqueous humor that it is difficult to identify a single pathway or drug that is capable of dramatically lowering IOP in every patient.
Aqueous humor is produced in the ciliary body by both active (selective transport of larger or charged molecules against a concentration gradient) and passive processes (diffusion and ultrafiltration). In diffusion, lipid-soluble substances enter the aqueous humor by passing through the ciliary epithelial cell membrane in proportion to their concentration gradient across the membrane. Ultrafiltration is the passage of water and water-soluble substances (which are generally limited by their size or charge) through theoretical micropores in the cell membrane in response to an osmotic gradient or hydrostatic pressure.
Many substances in the blood pass by ultrafiltration from the ciliary capillaries into the stroma of the ciliary processes before accumulating behind the tight junctions of the nonpigmented ciliary epithelium (the site of the blood-aqueous barrier). Some substances, such as sodium and chloride ions, are then actively pumped across the membrane into the posterior chamber, thereby drawing water passively along this concentration gradient. This process may account for the majority of actively formed aqueous.
Carbonic acid then dissociates, allowing negatively charged bicarbonate ions to pass to the aqueous. Although exactly how this leads to aqueous humor production is unclear, it appears that positively charged sodium ions, and eventually water, follow negatively charged bicarbonate ions into the posterior chamber. Drugs that inhibit carbonic anhydrase therefore decrease aqueous production and reduce IOP.
Aqueous exits the eye via several routes. In the conventional or traditional outflow route aqueous humor passes from the posterior chamber, through the pupil, and into the anterior chamber. Because of temperature differences between the iris and cornea, thermal convection currents occur in the anterior chamber, with aqueous near the iris rising and aqueous near the cornea falling. This is one reason cells and particulate matter in the anterior chamber may settle on the inferior corneal endothelial surface. Aqueous humor then leaves the anterior chamber by passing between the pectinate ligaments to enter the ciliary cleft, which contains the trabecular meshwork (Figure 12-1). After filtering between the beams of the spongelike meshwork, aqueous crosses through the endothelial cell membranes of the meshwork to enter a series of radially oriented, blood-free collecting vessels collectively called the angular aqueous plexus. From there it enters an interconnected set of blood/aqueous-filled vessels (the scleral venous plexus) before draining either anteriorly via the episcleral and conjunctival veins or posteriorly into the vortex venous system and into the systemic venous circulation (Figure 12-2). Contraction of smooth muscle fibers of the ciliary muscle that insert into the trabecular meshwork are probably capable of increasing drainage of aqueous from the eye by enlarging the spaces in the trabecular meshwork. In most species the majority of aqueous humor (about 50% in horses, 85% in dogs, and 97% in cats) leaves the eye via the traditional outflow route.
Figure 12-1 The routes of aqueous drainage from the canine iridocorneal angle. Aqueous humor passes between the beamlike pectinate ligament, then through the trabecular meshwork to enter the angular aqueous plexus and eventually the scleral venous plexus. From there, aqueous humor may drain (1) anteriorly to the episcleral and conjunctival veins, (2) posteriorly into the scleral venous plexus and vortex venous system, or (3) through the ciliary muscle interstitium to the suprachoroid and diffuse through the sclera (uveoscleral flow).
(Modified from Martin CL : Glaucoma, in Slatter D [editor]: Textbook of Small Animal Surgery, 2nd ed. Saunders, Philadelphia.)
Figure 12-2 A, The scleral venous plexus is often visible in normal animals as a series of interwoven blood vessels several millimeters posterior to the limbus. B, Prominent episcleral and, to a lesser extent, conjunctival venous injection in a dog with glaucoma. Increased intraocular pressure compresses the intrascleral blood vessels, which drain posteriorly. This forces more blood through the episcleral and conjunctival veins—one reason the eye appears injected in glaucoma.
The remainder of the aqueous humor leaves the eye via the uveoscleral pathway (see Figure 12-1). In this route aqueous humor passes through the root of the iris and interstitial spaces of the ciliary muscle to reach the supraciliary space (between the ciliary body and the sclera) or the suprachoroidal space (between the choroid and the sclera). From these locations aqueous humor may pass through the sclera into the orbit either via pores in the sclera where blood vessels and nerves enter the eye or between the scleral collagen fibers themselves. Outflow via this route may substantially increase in certain disease states and in response to certain antiglaucoma drugs, such as the prostaglandin derivatives.
IOP is the result of a delicate balance between production and outflow of aqueous humor (Figure 12-3). In glaucoma both production and outflow are altered. Usually a large percentage of the outflow pathway (perhaps as much as 80% to 90%) needs to be impaired before IOP starts to rise. If the outflow system is impaired to the point that IOP begins to increase, the eye usually attempts to compensate by reducing the passive production of aqueous humor. Active secretion, however, typically continues at a relatively normal rate, perhaps because if it did not, the avascular tissues of the eye that rely on aqueous humor for their nutrition would starve. Because the glaucomatous eye is functioning on a greatly diminished percentage of its normal levels of aqueous humor outflow and production, and because it has exhausted its usual compensatory pathways, pathologic processes or drugs that alter production or outflow only a small amount can have dramatic effects on IOP. This characteristic is one reason that glaucomatous eyes are typically more responsive to antiglaucoma drugs than normotensive eyes, but it also explains why IOP can rapidly rise to very high levels in a matter of 1 to 2 hours in some patients.
Often it is difficult to empirically predict the effect a given drug or its antagonist will have on IOP because many compounds affect both aqueous humor production and outflow—sometimes in complex and contradictory ways. For example, stimulation of β-adrenergic receptors in the ciliary processes increases intracellular cyclic adenosine monophosphate (cAMP), resulting in greater aqueous humor production. β-Adrenergic blocking drugs (e.g., timolol, betaxolol) decrease cAMP, thereby lowering aqueous humor production and ultimately reducing IOP. β-Blockers reduce IOP, however, only if the patient is awake and adrenergic tone is present. This means that although a drug such as timolol can reduce IOP in a cat when it is awake, the agent may not control IOP for the more than 20 hours a day the cat is sleeping.
As expected, β-adrenergic drugs such as epinephrine and its derivative dipivefrin may transiently increase IOP, presumably by increasing aqueous humor production via stimulation of cAMP. A few minutes after application of these drugs, however, IOP begins to decrease, and it stays reduced for several hours. This is because epinephrine also increases aqueous outflow via β2 receptors in the trabecular meshwork, and does so to a greater degree than it increases aqueous humor production. Epinephrine may also lower IOP by (1) reducing blood flow to the ciliary body (thereby lowering aqueous production) and (2) increasing uveoscleral outflow by relaxing the ciliary muscle and recruiting prostaglandins. The latter means, which can be blocked by topical nonsteroidal antiinflammatory drugs, may result in further increases in uveoscleral outflow and additional decreases in aqueous humor production. Complex interactions such as this are but one reason why both β-adrenergic agonists and β-blockers lower IOP in many species. When one considers species and individual differences in the density, distribution, and type of receptors as well as differences in the cause of the glaucoma, it is easy to see why it can be difficult to precisely predict what effect a given drug will have on IOP in a particular patient.
IOP varies slightly with time of day in many species, being the greatest in the morning and gradually declining over the course of the day in dogs and humans. The opposite phenomenon has been suggested to occur in cats, rabbits, and nonhuman primates.
Both production and outflow of aqueous humor tend to decline with age, but production declines at a little faster rate than outflow in most individuals. In humans, aqueous production and IOP tend to decline after 60 years of age, although this tendency varies considerably with ethnic background and the presence of other diseases, such as systemic hypertension and obesity. Similarly, IOP in cats has been shown to decline approximately 1 mm Hg per year after 7 years of age. In a small percentage of humans, and perhaps animals, however, aqueous humor outflow is reduced to a greater degree than aqueous humor production, resulting in increased IOP with age.
Disorders associated with substantially lower blood flow to the eye (e.g., dehydration, hypovolemic shock, cardiogenic shock) tend to result in lower IOP. A dog collar can significantly increase IOP if the dog is pulling against a leash or if the collar is too tight. Dogs with glaucoma probably should be exercised with a harness rather than a collar.
In addition to the numerous antiglaucoma drugs that alter IOP, other drugs also may affect IOP. Most general anesthetics and tranquilizers cause IOP to fall. Ketamine may temporarily increase IOP, presumably owing to extraocular muscle spasm.
Measurement of and normal values for IOP are discussed in Chapter 5. It is suggested that the reader refer to that discussion before proceeding with this chapter. Despite its disadvantages, the most economical instrument in general veterinary practice is the Schi∅︀tz tonometer with the human conversion tables. Surprisingly, dog-specific conversion tables for the Schi∅︀tz tonometer do not agree as well with the more accurate applanation and rebound tonometers, and dog specific tables should not be used to convert Schi∅︀tz scale readings to IOP estimates in dogs or cats. Two handheld tonometers that are more accurate and easier to use than the Schi∅︀tz instrument are the Tono-Pen applanation tonometer and the TonoVet rebound tonometer. The ability to perform tonometry is essential to every veterinarian engaged in small animal practice. Tonometry minimizes the chances of making an important or even catastrophic error in diagnosis.
Direct and indirect ophthalmoscopy may be used to examine the optic nerve head for cupping of the optic disc, which is the hallmark of glaucoma. The red-free filter (green light) on many of these instruments facilitates examination of the optic nerve and retinal nerve fiber layer.
Gonioscopy is a very useful technique for examining the iridocorneal (filtration) angle and managing glaucoma. It is discussed in detail in Chapter 5. Gonioscopy allows the clinician to differentiate between open-angle and closed-angle glaucoma, to estimate the severity of the obstruction of the iridocorneal angle, and to evaluate the response to therapy (Figure 12-4). It does, however, require considerable practice to recognize the many normal variations and hence gonioscopy tends to be performed almost exclusively by veterinary ophthalmologists. Examples of gonioscopic findings are shown in Figures 12-5 to 12-11.
Figure 12-4 Schematic drawing of a grading system for the width of the iridocorneal angle. The ratio of the width of the anterior opening of the ciliary cleft (A) and the distance from the origin of the pectinate ligaments to the anterior surface of the cornea (B) is estimated. C, Pupil; D, iris; E, pectinate ligament; F, deep pigmented zone; G, superficial pigmented zone; H, cornea.
(From Ekesten, B, Narfström K : Correlation of morphologic features of the iridocorneal angle to intraocular pressure in Samoyeds. Am J Vet Res 52:1875.)
Figure 12-5 Goniophotograph of a normal dog. A, Pupil; B, iris; C, pectinate ligament strands (thin brown lines); D, bluish-white zone of the uveal trabeculae (trabecular meshwork); E, deep pigmented zone; F, superficial pigmented zone; G, cornea.
Figure 12-7 Gonioscopic view of the iridocorneal angle of a dog in which the angle is filled with liberated pigment. The physical width of the angle is normal, but the pigment occludes the trabecular meshwork and prevents readily identifying the pectinate ligament.
Figure 12-8 Gonioscopic view of a closed angle in a dog with secondary glaucoma. The retina was massively detached, resulting in forward shifting of the lens and, ultimately, of the iris into the iridocorneal angle. Note that the pectinate ligament cannot be seen.
Figure 12-10 Marked pectinate ligament dysplasia characterized by large sheets of mesodermal tissue in a 7-year-old Bouvier dog. Although intraocular pressure is still within normal limits, aqueous humor can exit the eye only via a few small “flow holes” in the mesodermal sheets.
The effects of increased IOP on ocular tissues are similar regardless of the cause of the elevation. It is essential to consider whether the lesions and clinical signs observed are associated with or result from the cause of the increased pressure.
Glaucoma is one of the most commonly misdiagnosed eye conditions. Failure of owners to recognize the disease early in its course may prevent effective treatment of the first eye. Failure of clinicians to recognize onset in the second eye may prevent retention of sight.
The clinical signs of glaucoma in the dog are summarized in Figure 12-12. The signs present in a particular animal depend on the duration, intensity, and cause of the pressure elevation. In general the most obvious signs are associated with end-stage disease in which there is no hope of preserving vision. In the very early stages of glaucoma, in which there is a chance of preserving vision, the eye may appear normal and IOP may or may not be elevated. In some patients there is only a history of intermittent episcleral injection (especially in the evening) that spontaneously resolves, and IOP is normal on examination in the office. Glaucoma may be detected in these animals only by performing tonometry when the eye is red or, occasionally, by repeatedly measuring IOP over 24 hours. In other patients the eye may appear to be essentially normal and the only finding is increased IOP on tonometry. In these patients it is essential to differentiate glaucoma from increased IOP measurements associated with an uncooperative patient, technical problems with measuring IOP (excessive tension on the eyelids, a collar that is too tight, compression of the jugular veins during restraint, etc.), and malfunction of the instrument. Specialist assistance may be required to make the diagnosis of glaucoma in its early stages.
Figure 12-12 Clinical signs of canine glaucoma: 1, Descemet’s streaks (advanced cases); 2, aphakic crescent; 3, luxated lens (some cases); 4, corneal edema; 5, iris atrophy; 6, enlarged episcleral vessels; 7, fixed, dilated pupil; 9, shallow anterior chamber; 11, cupping of the optic disc; 12, retinal atrophy and vascular attenuation; 13, buphthalmos. Not shown: 8, increased intraocular pressure; 10, partial or complete loss of vision; 14, ocular pain; 15, loss of corneal sensitivity.
IOP values exceeding 25 mm Hg in dogs and 27 mm Hg in cats in conjunction with compatible clinical signs are sufficient for a presumptive diagnosis of glaucoma. IOP values greater than 20 mm Hg are suspicious for glaucoma if other clinical signs, especially anterior uveitis, are present or if the patient is being treated for glaucoma. Often IOP exceeds 40 mm Hg by the time the owner notices changes in the eye. Frequent measurement of IOP is an integral part of diagnosis and treatment of the patient with glaucoma.
An acute increase in IOP to 50 to 60 mm Hg or more is typically described by a human as “the worst headache of my life.” It is likely that animals experience a comparable degree of pain with pressures in this range. If the IOP rise is acute, the dog may be blepharospastic, depressed, less active, timid, or, in rare cases, more aggressive. Some sleep more, eat less, vomit, and are less interested in play. On occasion they rub at the eye, but this behavior is an unreliable sign of glaucoma. Application of pressure to the affected eye through the upper lid or to the surrounding area may cause severe pain. If the condition is not treated, severe pain and blepharospasm are replaced by signs of chronic pain that many owners may not properly recognize as being attributable to glaucoma. Frequently the owner believes that the pet is simply “getting old” and this is why it is less active, sleeps more, and is less playful. A surgical procedure that alleviates the increased pressure (and accompanying pain) almost invariably results in a comment from the owner that the pet “acts like a new dog.”
Engorgement of episcleral veins (see Figure 12-2, B) is one of the more common signs of increased IOP. Episcleral engorgement arises because the increased IOP reduces flow through the ciliary body to the vortex veins, and increased flow passes forward via anastomosing episcleral veins at the limbus (see Figure 12-1). Conjunctival capillaries may also be engorged, but usually to a lesser degree. Episcleral vascular engorgement is a sign of intraocular disease (anterior uveitis or glaucoma) and may be differentiated from superficial conjunctival vessel engorgement (which indicates ocular surface disease) by the following features:
Increased IOP impairs the function of the corneal endothelium, resulting in corneal edema. Typically the entire cornea is diffusely edematous in glaucoma, and the edema can be quite dramatic in acute glaucoma when IOP is very high (Figure 12-13). In advanced cases subepithelial bullae may form, which can lead to corneal ulceration if they rupture. In chronic glaucoma both superficial and deep vascularization, scarring, and pigmentation are common.
Chronic increases in IOP results in stretching of the cornea and sclera and enlargement of the globe (buphthalmos; Figure 12-14). Buphthalmos may be especially pronounced in young animals and in shar-peis, who have a more easily distended cornea and sclera than most adult dogs. Buphthalmic eyes are almost invariably blind, although limited vision may be retained for a while in some puppies and shar-peis. Buphthalmos is irreversible even if the pressure is later reduced, although a variety of surgical procedures are available to restore a cosmetically acceptable appearance.
By the time severe stretching has occurred, atrophy of the ciliary body may have reduced the IOP to normal and pain may be lessened. As the cornea stretches, linear ruptures in Descemet’s membrane, called Descemet’s streaks (Haab’s striae), may occur (Figure 12-15).
Depth of the anterior chamber (distance between cornea and iris) is evaluated with an oblique focal source of light or, better yet, by biomicroscopy. Decreased depth of the anterior chamber is often associated with impediments to outflow through the pupil (because the lens and iris are in greater contact) and the iridocorneal angle (because the anterior chamber is more crowded). A shallow anterior chamber is an especially prominent sign in cats in which aqueous humor is misdirected into the vitreal cavity (resulting in a forward displacement of the lens and iris) and in any animal in which the lens is anteriorly luxated or subluxated. Therefore a shallow anterior chamber should alert the clinician to the possibility of glaucoma. Glaucoma may also be associated with an abnormally deep anterior chamber in animals with posterior lens luxation or in buphthalmic eyes.
As IOP rises, the pupillary constrictor muscle becomes ischemic and the pupil dilates to midrange or larger (Figure 12-16). A dilated pupil, along with episcleral injection and pain, may be among the first signs noticed by the owner. Mydriasis is not an invariable sign of glaucoma— the pupil may be normal in mild IOP elevations, and miosis may be present in uveitis-induced glaucoma. In these latter cases, a careful examination is necessary to distinguish glaucoma from uveitis, and it is possible for both to be present in the same eye. In chronic glaucoma, or when IOP is acutely markedly elevated, the direct and consensual pupillary light reflexes are usually greatly impaired or absent. The longer glaucoma remains unresolved, the greater the chance that peripheral anterior synechiae will form and permanently block the drainage angle by fixing the peripheral iris in position.
Figure 12-16 Mydriasis (and anisocoria) in a Shiba Inu dog with primary angle-closure glaucoma. A dilated pupil may be the result of ischemia of the iris sphincter muscle or interference with the function of the optic or ciliary nerves.
If a luxated lens enters the anterior chamber and touches the corneal endothelium, a focal area of corneal edema may result. This opacity is frequently permanent, even if the lens is later removed. The continuous presence of a luxated lens in the anterior chamber damages the endothelium over a wider area and lowers the probability of successful surgical removal of the lens.
The recognition of how the final state was reached is important in determining which combination of therapeutic methods is required. History and signalment are critical factors in differentiating between these various possibilities. In all three pathways the lens may be displaced anteriorly or posteriorly or may be in the plane of the iris (either superiorly or inferiorly). An aphakic crescent is formed when the lens zonules have broken for a portion of the circumference of the lens, and it is possible to visualize the tapetal reflex through a crescent-shaped space between the lens equator and the pupillary border (Figure 12-17). After luxation the lens frequently, but not invariably, becomes cataractous.
Figure 12-17 Chronic glaucoma in a basset hound resulting in buphthalmos and secondary tearing of lens zonules. The equator of the lens is visible superonasally that creates an aphakic crescent in this region.
Primary lens luxation, as occurs in terriers and certain other breeds (Box 12-1), may result in pupillary block with acute elevations in IOP. The presence of vitreous strands in the anterior chamber in the absence of buphthalmos suggests primary lens luxation. In these animals the lens may be completely luxated or only partially luxated (subluxation), and usually the lens is not cataractous until it becomes luxated (Figures 12-18 and 12-19).
Modified from Gelatt KN, Brooks DE (1999): The canine glaucomas, in Gelatt KN (editor): Veterinary Ophthalmology, 3rd ed. Lippincott Williams & Wilkins, Philadelphia.
Figure 12-18 Lens subluxation in an 8-year-old wirehaired fox terrier. Notice that the anterior chamber is deeper superiorly than inferiorly, indicating that the lens has shifted position. The iris and lens also “trembled” when the eye moved (iridodonesis and phacodonesis).
Primary glaucoma tends to occur in middle-aged to somewhat older dogs of certain breeds (Box 12-2), and the lens subluxation or luxation does not occur until the globe has become buphthalmic and the lens zonules are stretched beyond the breaking point (secondary luxation). Similarly, primary cataract formation in a wide variety of breeds is frequently followed by lens luxation and glaucoma. Lens-induced uveitis from a secondarily luxated lens that has become cataractous from elevated IOP, and decreased IOP from the uveitis further complicate diagnosis and treatment. Thus the combination of glaucoma, cataract, and lens luxation in any particular eye may occur through several mechanisms and may be associated with a variety of IOP values at any given moment.
From Miller PE (1995): Glaucoma, in Bonagura JD (editor): Kirk’s Current Veterinary Therapy XII: Small Animal Practice. Saunders, Philadelphia. Breeds are listed in descending order of frequency as recorded by the Veterinary Medical Data Base over a 20-year period.
Loss of some or all vision is a common sequela of glaucoma. In the early stages peripheral vision may be lost (Figure 12-20), and it is difficult, if not impossible, to detect these changes in most animals. Complete vision loss can occur in a very short period (hours to a day) if the increase in IOP is very high, or over a period of weeks to months if the pressure increase is more insidious. Preservation of vision depends on control of IOP.
Cupping, or posterior bowing of the optic disc through the lamina cribrosa, is the hallmark of glaucoma. Retinal nerve fibers run parallel to the surface of the retina and then turn 90 degrees to enter the multilayered, fenestrated meshwork of the lamina cribrosa before exiting the eye. Glial cells, blood vessels, and collagen beams form variably sized pores through which the optic nerve fibers pass. When IOP rises the scleral lamina cribrosa bows posteriorly, distorting the alignment of the pores and compressing the optic nerve fibers. Although this change may initially be so subtle as to not be detected ophthalmoscopically, it is sufficient to mechanically interfere with axonal axoplasmic flow and also probably with blood supply to the optic nerve head. Very large increases in IOP may also interfere with blood flow to the choroid and produce vision loss through ischemic damage to the photoreceptors and outer retinal layers. In acute glaucoma the optic disc may appear swollen in response to ischemia. Within a day or two the increased pressure may cause the disc to appear pale and compressed. As ganglion cell axons die, optic nerve head tissue is lost and pressure forces the lamina cribrosa outward (Figures 12-21 to 12-23). This change indicates irreversible damage to the optic nerve. Wallerian degeneration of the optic nerve follows (Figure 12-24).
(From Slatter D : Textbook of Small Animal Surgery, 3rd ed. Saunders, Philadelphia.)
Figure 12-22 The scleral lamina cribrosa in normal and glaucomatous eyes. A, Normal (upper) and glaucomatous (lower) eye pore arrangement. From the normal pores in the normal eye, glaucoma causes pore misalignment and posterior movement or cupping of the lamina cribrosa. B, Trypsin digestion and scanning electron microscopy of a normal dog optic nerve head demonstrates the three-dimensional architecture of the scleral lamina cribrosa (original magnification, ×60). C, Trypsin digestion and scanning electron microscopy of a primary open-angle glaucomatous optic nerve head shows posterior displacement and loss of pore arrangement, which may impair axoplasmic and local capillary blood flow (original magnification, ×60).
(From Brooks DE, et al. : Morphologic changes in the lamina cribrosa of beagles with primary open-angle glaucoma. Am J Vet Res 50:936.)
Figure 12-23 Optic disc cupping. Most retinal vessels disappear at the disc edge. The center of the disc is in focus below the level of the retinal surface and is grayish. There also is a peripapillary ring of altered retinal reflectivity.
(Courtesy Dr. Christopher J. Murphy.)
In advanced glaucoma, profound retinal atrophy with increased tapetal reflectivity occurs together with attenuation or complete loss of retinal vessels, atrophy of the pigment epithelium in the nontapetal fundus, and optic atrophy (grayish-white appearance; Figure 12-25). These findings are also present in advanced progressive retinal degeneration (progressive retinal atrophy). In progressive retinal degeneration the other signs of glaucoma are lacking, the disease is usually bilateral, the optic disc is not cupped, and differential diagnosis may be determined by the breed of dog and lack of other clinical signs of glaucoma. Ophthalmoscopically visible retinal and optic nerve lesions of glaucoma are irreversible.
Figure 12-25 Retinal changes in acute primary angle-closure glaucoma. A, The retinal cells, which stain brown in this immunohistochemically stained section, are undergoing apoptosis. B, Histologic section of a retina showing segmental loss of nuclei in the photoreceptor layer (*).
(Courtesy Dr. Richard R. Dubielzig.)
Elevation of IOP decreases blood flow in the choroid, resulting in ischemia. This ischemia can be demonstrated functionally by depressed electroretinograms, and in some patients it is possible to visualize wedge-shaped defects in the retina that correspond to pressure-induced infarction of the choroidal blood supply (Figure 12-26). Early in glaucoma, if the pressure elevation is acute and very large, the photoreceptors in the retina undergo necrosis. In the next few days they begin to die by apoptosis as well. Ophthalmoscopically the cell death is seen as increased tapetal reflectivity. As in any other severe retinal atrophy, the condition is irreversible.
Figure 12-26 Postenucleation specimen from a dog with acute primary angle-closure glaucoma. Light-colored, roughly wedge-shaped regions of retinal necrosis, presumably secondary to impaired choroidal circulation, are apparent.
(Courtesy Dr. Richard R. Dubielzig.)