The canine glaucomas

Glaucomas occur in 1.8% of the canine population in North America. The frequency of bilateral breed-predisposed glaucomas in purebred dogs is the highest of any animal species, except humans. Primary glaucomas are of both open and closed iridocorneal angle types that affect primarily purebred dogs and are thought to be inherited in many breeds. The modes of inheritance have been reported for primary open-angle glaucoma in Beagles (autosomal recessive), and in the Great Dane and Welsh Springer Spaniel (autosomal dominant). Whereas primary open-angle glaucoma occurs as a chronic disease spanning several years, the angle-closure glaucomas typically manifest as acute clinical situations, followed by a chronic cycle of secondary degeneration.

Glaucomas in small animals may be divided by gonioscopy (examination of the iridocorneal anterior chamber angle) and etiology into primary, secondary, and congenital (Box 10.1). Primary glaucomas affect both eyes, although one eye may demonstrate clinical signs of glaucoma several months to years before the opposite eye. Traditionally, the symptoms of primary glaucomas are divided into acute and chronic. However, clinical experience suggests that many of the primary breed-related glaucomas are chronic in their development, with acute elevations in IOP toward the end of the disease that produce overt clinical signs which prompt presentation to the veterinarian. This suggests that treatment for most primary glaucomas in dogs is started with the disease in an already quite advanced state.

The clinical signs of acute and often marked elevated levels of IOP, associated with primary closed-angle glaucoma, are a dilated, fixed, or sluggish pupil, bulbar conjunctival and episcleral venous congestion, and corneal edema, as well as patient discomfort and visual disturbances (Fig. 10.1). With prolonged elevations of IOP, secondary enlargement of the globe, lens displacement, breaks in Descemet’s membrane of the cornea, and eventual buphthalmos (enlargement of the globe due to stretching) result (Fig. 10.2). Pain is usually manifested by behavioral changes and sometimes periorbital pain rather than blepharospasm, or not at all.

Fig. 10.1 Early glaucoma in the dog is often associated with moderate mydriasis, conjunctival congestion, and corneal edema. Repeated tonometry may be necessary to detect the brief bouts of elevated intraocular pressure.

Fig. 10.2 Glaucoma and subluxated lens in a dog.

Treatment of the secondary glaucomas, which are often unilateral, is determined based on the underlying disease. The most frequent cause of secondary glaucoma in the dog is lens displacement, manifested as subluxation, anterior luxation, or posterior luxation (Fig. 10.3). However, with megaloglobus and subtle but gradual increases in IOP, secondary lens subluxation is also common in the primary glaucomas as tension of the lens zonules eventually results in their tearing, usually just below their attachment to the lens equator. In addition, lens-induced uveitis (LIU) is common in the dog, secondary to leakage of lens proteins from cataracts. Occasionally the iridocorneal angles of globes affected by LIU become plugged with lens proteins and inflammatory cells; peripheral anterior synechiae then form, sufficient to elevate IOP. In both of these mechanisms of secondary glaucoma in dogs, lens or cataract removal may be important in the treatment of elevated IOP.

Fig. 10.3 Acute anterior lens luxation in a Smooth Fox Terrier. The periphery of the lens is easily visible because corneal edema has not developed.

Secondary changes, such as peripheral anterior synechiation due to iridocyclitis, preiridal membrane formation, and filtration angle and cleft closure may necessitate additional medical and/or surgical treatments. Primary and secondary intraocular neoplasms commonly produce secondary glaucoma in dogs and cats. Enucleation is usually the preferred treatment for glaucoma resulting from advanced primary intraocular neoplasms.

Secondary pigmentary glaucoma occurs in the Cairn Terrier, manifested by a progressive and relentless infiltration of the anterior uvea and drainage structures by large, round, pigment-laden cells. The optimal treatment for pigmentary glaucoma has not been established, and the visual prognosis for these animals remains poor.

A syndrome of iridociliary cystic and pigment-dispersive glaucoma is also recognized with increased frequency in the Golden Retriever. This disease is typically chronic in its development, manifested by the development of thin-walled iridociliary cysts, cataract formation, proteinaceous exudation, pigmentary dispersion, and ultimately glaucoma associated with trabecular meshwork remodeling and cleft collapse. These animals do not typically display iridocorneal abnormalities gonioscopically, and the disease (although often asymmetrical in presentation) is typically bilateral in nature.

With the increased frequency of extracapsular and phacoemulsification cataract surgery in dogs, aphakic glaucoma is not infrequent postoperatively. True postsurgical glaucoma should be differentiated from ‘postoperative hypertension’ (POH), which represents an increase in postoperative IOP following phacoemulsification and which occurs 6–12 h postoperatively and typically resolves (with or without adjunctive treatment). This secondary glaucoma results from closure of the iridocorneal angle and subsequent cleft collapse due to peripheral anterior synechiation, or occlusion of the pupil, secondary to annular posterior synechiation. Aphakic glaucoma, with pupillary blockage, requires surgery within 24–48 h after onset.

New glaucomas, observed in dogs, are those occurring secondary to silicone oil in the anterior chamber, and those secondary to rhegmatogenous retinal detachments. Silicone oil is used in the repair of retinal detachments in dogs (see Chapter 12). Leakage of this oil into the anterior chamber results in epithelial toxicity, impaired aqueous outflow, and increased IOP, and the oil must be removed from the anterior chamber. Subconjunctival silicone oil appears relatively inert.

Retinal detachments in dogs are usually associated with ocular hypotony (low IOP), presumably from increased uveoscleral aqueous humor outflow. However, rhegmatogenous detachments in dogs, especially in those patients with giant retinal tears (90° or more), may release outer rod and cone fragments into the subretinal fluids and vitreous that eventually enter the anterior chamber. This cellular debris in the aqueous humor outflow pathways elevates IOP.

The feline glaucomas

Glaucomas in cats occur predominately secondary to anterior uveitis and neoplasia; however, primary open-angle glaucoma also occurs at a very low frequency. In one report, based on 131 enucleated eyes, feline glaucomas were associated with chronic lymphocytic–plasmacytic anterior uveitis (53 eyes), diffuse iridal melanoma/melanocytoma (38 eyes), other neoplasms (14 eyes), lens rupture (4 eyes), anterior lens luxation (4 eyes), primary glaucoma (3 eyes), and other causes (15 eyes). In clinical reports, the most frequent form of glaucoma in cats occurs secondary to anterior uveitis, and neoplasia (Fig. 10.4). In cats with inflammatory-related secondary glaucomas, topical and systemic corticosteroids frequently reduce the anterior uveitis sufficiently to lower IOP. Cats, usually older than 10 years, may also develop lens luxation in the absence of iridocyclitis (Fig. 10.5). Some feline eyes have normal levels of IOP; in others the IOP is elevated. The globe is usually slightly enlarged, but the eye often remains visual. Gonioscopy of affected cats (which, unlike dogs, may be performed without the aid of a refracting goniolens) usually reveals open iridocorneal angles; in fact, some iridocorneal angles appear recessed posteriorly in enlarged globes and are wider than normal. Lens removal in normotensive eyes may resolve the problem. If glaucoma is already present, lens removal alone may not sufficiently address the elevated IOP because of permanent outflow abnormalities.

Fig. 10.4 Glaucoma secondary to iridocyclitis in the cat. Note the numerous posterior synechiae.

Fig. 10.5 Anterior lens luxation, cataract formation, and secondary glaucoma in an aged cat.

An apparently unique feline manifestation of glaucoma is represented by the syndrome of aqueous misdirection. In this poorly understood condition, expansion of the vitreous body (potentially resulting from an inappropriate ‘misdirected’ shunting of aqueous into this space) results in marked anterior chamber shallowing, and iridocorneal angle and ciliary cleft compromise. Glaucoma which results from aqueous misdirection is typically chronic in development, and many cats appear to tolerate elevated IOPs surprisingly well. Medical management of this situation is, however, generally less successful with progression. Lenticular phacoemulsification and limited vitrectomy likely represent the most effective surgical course of action when faced with progressively escalating IOP.

The equine glaucomas

Glaucomas in horses have been classified into congenital, primary, and secondary to anterior uveitis, lens luxation, and intraocular neoplasia. Aging, persistent anterior uveitis, and breed (Appaloosa is most often affected) are predisposing factors. The signs of elevated IOP in the horse are more subtle, and include enlargement of the globe, variable corneal edema, and corneal striae or deep linear band opacities. Intraocular pressure tends to fluctuate more than in small animals, and higher levels (30–40 mmHg) tend to occur more frequently. Topical medications should be attempted before diode laser cyclophotocoagulation to reduce any existing anterior uveitis and lower IOP. Topical medications which may be used for treatment of glaucoma in the horse include beta adrenergic agents (i.e. 0.5% timolol) and carbonic anhydrase inhibitors (2% dorzolamide). Topical prostaglandins, i.e. latanoprost, may lower IOP only slightly, and their use is tempered by side effects including miosis and ocular irritation.

Congenital glaucoma in rabbits

Glaucoma in this species may be encountered by the small animal veterinarian, as pet rabbits become more popular, as well as by the laboratory animal veterinarian. Congenital glaucoma in rabbits, occurring most frequently in New Zealand whites, is inherited as an autosomal recessive trait. Affected rabbits may grow less than normal littermates, and a 25% mortality of affected rabbits occurs. This same form of glaucoma occurs in all breeds of pet and pigmented rabbits. Congenital glaucoma results from iridocorneal angle anomalies, including disorganization and lack of development of the trabecular meshwork, and posterior displacement of the aqueous plexus within the sclera.

In affected rabbits, impaired aqueous humor outflow occurs by 3 months, and IOP elevates by 6 months. Corneal and globe enlargement are detectable in animals as young as 4–6 months old. Pet rabbits are typically presented with, at least, one buphthalmic eye (Fig. 10.6). Corneal edema, pupillary dilatation, and elevated IOP are present. Medical treatment of pet rabbits is generally limited to topical agents; however, miotics and beta adrenergics are less effective and of shorter duration than in dogs and cats. Glaucoma surgical procedures, including iridencleisis, can provide normal IOP for several months. Anterior chamber shunts in congenital glaucomatous rabbits have been successful for periods greater than 3 years; however, rabbits generally exhibit an even more aggressive healing and subsequent scarring response at the site of surgical intervention than dogs and cats.

Fig. 10.6 Inherited and congenital glaucoma in rabbits.(a) This disease is a bilateral inherited disease. Note the enlarged globes.(b) It manifests as mydriasis, corneal edema, and enlargement of the globe in animals 3–6 months old.

The bovine glaucomas

Glaucomas occur rarely in cattle. Primary glaucoma occurs in the Holstein breed and is concurrent with cataract formation, lens luxation, and globe enlargement. Secondary glaucoma from anterior uveitis and perforated corneal ulcers with iris prolapse occurs more frequently, but is not usually treated. In some of these inflammatory glaucomas, once the anterior uveitis decreases, IOP may return to normal.

Glaucoma classification as a guide to therapy

Classification of the etiology of glaucoma, based on ophthalmic, gonioscopic, and ultrasonographic examinations, assists in the optimal planning of clinical management and the preservation of vision (Box 10.2). With progressive iridocorneal angle closure that occurs in most canine glaucomas, the choice of medical, surgical or, most frequently a combination of both modalities, must be tailored. In the case of acute goniodysgenic/angle-closure glaucoma in dogs, surgical treatment is the first choice, with medical treatment usually providing only a few weeks to months of effective IOP control. Unfortunately, surgical treatments for the primary canine glaucomas and the maintenance of effective long-term IOP control have been notoriously challenging. However, diode laser cyclophotocoagulation and anterior chamber shunts appear to offer longer periods of successful control of IOP at this time. In horses, laser cyclophotocoagulation appears more successful than in dogs, although use of anterior chamber shunts is still under study.

Box 10.2 Recommended medical and surgical treatment modalities for the different glaucomas in animals

Primary open angle glaucoma

Short and long term

• Prostaglandins (not useful in horses and cats)

– Bimatoprost (0.03%) q12–24h

– Latanoprost (0.005%) q12–24h

– Travoprost (0.004%) q12–24h

– Unoprostone isopropyl (12% and 0.15%) q12–24h

• Miotics (limited use in horses)

– Pilocarpine (1–2%) q6–12h

– Carbachol (0.75–3%) q8–12h

– Demecarium (0.125–0.25%) q12–24h

– Echothiophate (0.125–0.25%) q12–24h

• Carbonic anhydrase inhibitors (CAI) (all species)

– Systemic CAI

Acetazolamide, 10–25 mg/kg PO q12h

Dichlorphenamide, 10–15 mg/kg PO, q8–12h

Ethoxyzolamide, 2–8 mg/kg PO q12h

Methazolamide, 2.5–10 mg/kg PO q12h

– Topical CAI

Dorzolamide (2%) q8–12h

Brinzolamide (1%) q8–12h

• Adrenergics (all species)

– Adrenaline (epinephrine) (1–2%) q8–12h

– Dipivefrin (0.1%) q8–12h

• Osmotics (all species)

– Mannitol, 1–2 g/kg IV

– Glycerol, 1–2 mL/kg PO

• Beta-blocking adrenergics (all species; caution in very small patients)

– Betaxolol (0.25%) q12–24h

– Levobunolol (0.25% and 0.5%) q12–24h

– Timolol (0.25% and 0.5%) q12–24h

• Corticosteroids and non-steroidal anti-inflammatory agents (all species)

Narrow/closed angle

Initial control

• Osmotics

• Prostaglandins or miotics

• Carbonic anhydrase inhibitors

• Adrenergics

• Beta-blocking adrenergics

• Corticosteroids and non-steroidal anti-inflammatory agents

Short and long term

• Surgery: filtering procedures, anterior chamber shunts

• Cyclocryotherapy

• Laser transscleral or endoscopic cyclophotocoagulation

Secondary glaucomas

• Address primary underlying condition

• Antihypertensive medications as necessary

End-stage glaucoma with buphthalmia and blindness (all species)

• Surgery: intrascleral prosthesis, enucleation

• Cyclocryothermy

• Intravitreal gentamicin (10–25 mg)

Surgical procedures for the treatment of the canine glaucomas have traditionally provided only short-term resolution because the filtering fistulae eventually close and fail in the face of inflammation and subsequent tissue remodeling and scarring. Newer anterior chamber shunts, with and without valves, offer improved results. Antifibrotic drugs, such as mitomycin C and 5-fluorouracil (5-FU), may delay or prevent scarring of the alternative aqueous outflow channels and prolong their function. Although intraoperative mitomycin C application has yielded less promising results in animals than those displayed by human patients, the postoperative use of 5-FU has significantly improved the survivability of filtration blebs. Indeed, systemic anti-inflammatory therapy, as well as careful postoperative ‘bleb’ management, appears key to maintaining the functionality of filtering surgeries for as long as possible. Hopefully, during the next decade, advances in surgical treatments of the primary glaucomas in the dog will be similar to those that occurred during the past two decades in cataract surgery in small animals. Recurrent studies in the canine primary glaucomas suggest that the aqueous humor contains high levels of myocilin, CD44, matrix metalloproteinases (MMPs), and other large proteins; these substances probably adversely affect aqueous outflow after the traditional glaucoma surgeries as well as laser cyclophotocoagulation. High concentrations of these substances are found not only within the trabecular meshwork, but also within the non-pigmented ciliary body epithelium. The inflammatory cascade induced by aqueous humor at the site of filtering surgeries has been characterized in several animal models, and an increased understanding of the major mediators of this process will underlie more effective postoperative treatment strategies.

The relatively recent introduction of endoscopic diode cyclophotocoagulation has permitted the direct observation of ciliary body processes as they are sequentially treated, significantly improving the efficacy of this treatment modality.

Medical and/or surgical treatment

The decision to employ medical and/or surgical therapy for the veterinary glaucomas is determined by the stage of the disease and the appearance of the iridocorneal angle as judged by gonioscopy, as well as the perceived viability of the visual structures and optic nerve. The dilemma that confronts the veterinarian is that both medical and those traditional filtering surgical procedures adopted from human ophthalmology do not usually provide long-term relief. As these patients are usually only of middle age, more successful surgical treatments need to be developed. Anterior chamber shunts and newer laser cyclophotocoagulation techniques offer this potential.

In general, horses, because of their size, are more difficult to manage medically long term, as the owners must medicate these patients themselves.

Medical treatments for the glaucomas either decrease the rate of aqueous humor formation or increase its outflow. A few drugs, such as 1% and 2% adrenaline (epinephrine), affect both aqueous humor outflow and formation. Medical therapy is most effective with open iridocorneal angles. Unfortunately, most forms of primary glaucomas in dogs exhibit narrow iridocorneal angles and outflow tracts, and result in eventual angle and cleft closure; thus medical therapy will be successful only short term or when combined with surgery. In some breeds, angle closure seems secondary and directly associated with enlargement of the globe (megaloglobus or buphthalmia). With narrow angles and closure, medical therapy that primarily affects aqueous humor outflow is ineffective for significant periods of time. Drugs that decrease aqueous humor formation rates are most useful whether the iridocorneal angle is open, narrow or closed. Intravenous osmotic agents are employed to rapidly lower IOP when the possibility for the return of vision is ascertained to be good and/or immediately before surgery. These drugs are typically effective at rapidly lowering IOP in the presence of an intact blood–aqueous barrier; however, their effect is short lived. The use of miotics after glaucoma surgery is recommended infrequently because these drugs may cause mild iridocyclitis and aqueous flare, which may contribute to the failure of filtering surgical procedures. Topical prostaglandins, introduced in the 1990s, can lower significantly IOP in dogs, but are not useful in cats or horses.

Traditional surgical treatments of the canine primary glaucomas have enjoyed only limited success rates. These surgeries, including iridencleisis, cyclodialysis, and a combination of both procedures, are not difficult to perform, but these new surgical fistulae for the escape of aqueous humor usually seal and fibrose closed within 6–12 months. With the relatively recent introduction of antifibrotic agents, these techniques may be more successful. Although both contact and non-contact laser-induced partial destruction of the ciliary body (transscleral and endoscopic cyclophotocoagulation) have shown promise, at least 40% of the treated eyes develop cataracts within 6 months of the transscleral technique.

Recently, anterior chamber shunts consisting of silicone tubing introduced into the anterior chamber, a pressure-sensitive valve, and a biocompatible extrascleral base have shown promise in dogs. These drainage devices are not trouble free, as fibrosis around the episcleral bases can develop rapidly. Patients with successful postoperative control of IOP in excess of 3 years are, however, now common, especially when operated on early in the course of the disease.

Blind end-stage glaucomatous globes do represent suitable candidates for these complex surgeries, and are more ideally managed via ‘procedures of comfort’, including enucleation, gentamicin-induced ciliary body destruction, cyclocryoablation or intrascleral prosthesis placement in all animal species.

Iridencleisis

In the iridencleisis procedure, a radial section of iris is permanently positioned through a limbal incision into the subconjunctival spaces beneath the bulbar conjunctiva (Fig. 10.14). Reduction in IOP following iridencleisis is primarily related to the escape of aqueous humor through this area. Aqueous may also filter through the space between the two pillars of the iris, as well as through the iridal stroma itself. Iridencleisis may be used successfully in the management of narrow- and closed-angle glaucoma, acute iris bombé associated with annular posterior synechiae, and glaucoma associated with peripheral anterior synechiae. When the iris is thin, atrophied, or adhered to the lens with focal posterior synechiae, iridencleisis is not recommended.

Fig. 10.14 Iridencleisis 1 year postoperatively in a dog. A large posterior synechia is present as well as some pigment migration on the anterior lens capsule. Early cortical cataract formation is also present.

After the onset of general anesthesia, clipping of the eyelid hair, and cleansing of corneal and conjunctival surfaces with 0.5% povidone–iodine solution with swabs, the eyelids are retracted by speculum. The iridencleisis procedure is performed at the dorsal one-half of the limbus, usually at the 12 o’clock position. An alternative surgical site may be selected if other surgical procedures have been previously performed in the preferred site.

With curved blunt-tipped tenotomy scissors, a limbal-based 10 mm bulbar conjunctival flap is constructed. The flap is usually 12–18 mm long. Tenon’s capsule is identified and, if extensive, excised from the overlying bulbar conjunctiva and sclera in the area of the limbal incision (Fig. 10.15a). The anterior chamber is entered through the limbus with the Beaver No. 6500 microsurgical (Fig. 10.15b). The limbal incision is usually 8–10 mm long. A 1–2 mm section of sclera in the caudal aspect of the limbal incision is carefully excised (anterior sclerectomy). Hemostasis and limited tissue destruction are achieved by cautious electrocautery (Fig. 10.15c). The wet-field coagulator is superior in this region because of the frequent presence of aqueous humor. Limited application of electrocautery on the scleral aspect of the incision seems to facilitate maintenance of an open fistula and reduces the possibility of closure by fibrosis.

Fig. 10.15 In the iridencleisis procedure, two pillars of iris are externalized into the subconjunctival tissues through a limbal incision. Filtration of aqueous humor occurs through the space between the iris pillars as well as within the pillars themselves.(a) A 10 mm wide limbal-based conjunctival flap is constructed with Steven’s tenotomy scissors.(b) The anterior chamber is entered at the limbus with a stab incision with the Beaver No. 6500 microsurgical blade. The limbal incision is lengthened with the scalpel blade or corneoscleral scissors to about 8–10 mm.(c) In the central of the limbal incision, a 1–2 mm section of sclera (anterior sclerectomy) is excised by scissors. Some cautery may be necessary for scleral hemostasis.(d) A blunt iris hook is carefully inserted into the anterior chamber to the pupillary margin to retract the iris into the limbal incision.(e) The iris is protracted further by thumb forceps.(f) The iris is then grasped with an additional thumb forceps and gradually torn to its base.(g) Each pillar of iris is anchored to the sclera with a 6-0 simple interrupted absorbable suture.(h) Any hemorrhage and/or fibrin is irrigated from the anterior chamber with lactated Ringer’s solution.(i) The conjunctival flap is apposed with a 6-0 to 7-0 simple continuous absorbable suture.

During the limbal incision and subsequent anterior sclerectomy, the iris may protrude into the incision. A blunt iris hook or serrated iris forceps is carefully manipulated into the anterior chamber to grasp the dorsal pupillary margin and protract the iris into the limbal incision (Fig. 10.15d). Using the iris hook and serrated forceps, the iris is carefully pulled from the anterior chamber into the limbal incision (Fig. 10.15e). With both iris forceps pulling in opposite directions, the iris is slowly torn radially to its base. Each pillar of the iris, with its pigmented epithelium exposed, is manipulated into the respective end of the limbal incision (Fig. 10.15f). To minimize the possibility of the iris pillar retracting back into the anterior chamber, each tag of the iris is attached to the sclera with a 6-0 simple interrupted absorbable suture (Fig. 10.15g). The anterior chamber is carefully irrigated with balanced salt solution to remove all fibrin and blood. With successful manipulation of the iris and judicious use of electrocautery, hemorrhage and fibrin in the anterior chamber at the conclusion of surgery are generally avoided. In the event that fibrin remains, or continues to be formed in the anterior chamber, tissue plasminogen activator (tPA; 25–50 μg) is injected between the two iris pillars into the anterior chamber (Fig. 10.15h).

The limbal wound is not apposed with sutures. The bulbar conjunctival flap is apposed with a 6-0 to 7-0 simple continuous absorbable suture (Fig. 10.15i).

Postoperative treatment after iridencleisis consists of: 1) maintenance of a pupil of normal size (neither dilated nor constricted); 2) maintenance of a normal range of IOP; and 3) suppression of postoperative iridocyclitis with topical and systemic corticosteroids, NSAIDs, or a combination of these agents. Topical and systemic antibiotics are administered to prevent postoperative infections. Phenylephrine (10%) and pilocarpine (2%) are alternately instilled to facilitate movement of the pupil and minimize the possibility of focal posterior synechiae. The ratio of these two drugs is varied depending on pupil size. In the event that a relatively normal-sized pupil cannot be obtained because of postoperative inflammation, 1% tropicamide is administered until a moderately dilated pupil is achieved. Topical and systemic carbonic anhydrase inhibitors are administered postoperatively if IOP exceeds 25 mmHg. They are not necessary if the IOP is normal and can be monitored daily.

Potential complications that may occur following iridencleisis include excessive/uncontrolled iridocyclitis, hyphema, posterior synechiation, iridal pigment shedding onto the anterior lens capsule, and cataract formation. Blebs usually occur following iridencleisis in the area of the limbal incision. These blebs may eventually flatten, but may still function. The bulbar conjunctiva in the area of the limbal incision usually demonstrates increased vascularity.

Failure of the iridencleisis procedure to satisfactorily control IOP is usually related to the short-term closure of the limbal incision with inflammatory products, secondary to postoperative iridocyclitis, or long-term loss of filtration secondary to fibrosis several months later. Gentle massage of the eye postoperatively for several months is recommended. Long-term administration of topical 1% prednisolone for 6 months or indefinitely may increase the success rate of the iridencleisis procedure.