Chapter 10 Surgical procedures for the glaucomas
The glaucomas in animals consist of a group of diseases that share the common feature of elevated intraocular pressure (IOP) and subsequent retinal ganglion cell (RGC) loss and optic nerve atrophy. In humans, an additional form of glaucoma, normal tension glaucoma, consists of progressive optic disk cupping and vision loss in the presence of normal levels of IOP. Normal tension glaucoma has not been reported in animals, although canine patients with progressive optic disk atrophy and gradual loss of vision, in the face of an apparent normal range of IOP, have been identified clinically.
Traditionally, the veterinary glaucomas are divided into: 1) breed-related or primary (either ‘open’ or ‘closed’ angle); 2) secondary, in which an underlying cause for the elevated IOP can be determined; and 3) congenital, in which embryonic developmental iridocorneal angle anomalies result in dramatically elevated IOP in very young animals.
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.
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.
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.
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.
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.
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.
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.
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.
Several basic diagnostic procedures are essential to manage the glaucomas pre- and postoperatively in animals. They include: tonometry, ophthalmoscopy (direct/indirect), and gonioscopy (visualization of the iridocorneal angle). These procedures should be used each time the patient is examined. Newer techniques, such as pattern electroretinograms and visual evoked potentials, that estimate damage to the retinal ganglion cells and their axons, detect the changes that precede overt clinical signs of glaucoma by many months to a few years in small animals. Confocal scanningmicroscopy (Heidelberg retinal tomography (HRT), optical coherence tomography (OCT), and nerve fiber analyzers) which is more commonly used in the monitoring of human glaucoma and select research situations, has not found wide usage in veterinary medicine based on cost prohibition as well as logistical challenges associated with patient restraint and poor operator reproducibility.
Only applanation tonometers are used in all of the different animal species to estimate IOP, and fortunately are fairly accurate (in spite of varying corneal diameters) within the normal range of IOP, though they tend to underestimate when pressure exceeds about 40 mmHg (Fig. 10.7). Rebound tonometry is increasingly used to estimate IOP based on its ease and excellent patient compliance. Ophthalmoscopy, especially the direct method, permits detection of IOP-related damage to the retina and optic disk.
Fig. 10.7 Instrumental tonometry is an essential diagnostic and monitoring procedure for glaucomatous small animal patients.(a) The TonoPen™ XL applanation tonometer.(b) Applanation tonometry in a dog with the TonoPen™ tonometer.
Gonioscopy, or the direct observation of the iridocorneal angle through a special contact goniolens, is the basis for classification of all glaucomas, monitors iridocorneal angle and cleft changes as the glaucoma progresses, and assists selection of the different medical and surgical treatments (Figs 10.8 and 10.9). In most primary open-angle and narrow-angle glaucomas in animals, the iridocorneal angle, as viewed by gonioscopy, progressively narrows and eventually closes with the secondary formation of peripheral anterior synechiae.
Fig. 10.8 Evaluation of the iridocorneal angle is important for classification of the glaucoma and to assist in selection of treatment methods. Beagle with gonioscopic lens on the cornea and examination with the portable slit-lamp biomicroscope.
(Courtesy of Dr Don Samuelson.)
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.
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.
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.
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.
Procedures for the surgical management of glaucoma require accurate knowledge of the anterior orbit, globe, and intraocular tissues, including the iridocorneal angle, lens, iris, and ciliary body (Fig. 10.10). The anatomy of the last three structures (the iris and ciliary body, and the lens) is presented in Chapters 9 and 11, respectively. However, some additional comments regarding the anatomy of this area are important for the effective performance of the different glaucoma surgical procedures.
When cyclodialysis, posterior sclerotomy, and anterior chamber shunts are performed in small animals, the surgeon should be familiar with the anterior orbit and, in particular, the extraocular muscular insertions to the globe (Table 10.1). The dog orbit has considerably more room for instrument manipulations and glaucoma surgeries than the cat. Entry through the sclera (posterior sclerotomy for cyclodialysis) is usually performed at the 12 o’clock position because of improved surgical exposure. Like cataract patients, use of neuromuscular blocking drugs during surgery enhances maximal exposure of the globe, reduces intraorbital pressure on the globe, and facilitates anterior chamber surgeries. Placement of the episcleral portion of the anterior chamber shunts is usually performed between the dorsal rectus muscle and medial or lateral rectus muscle insertions. If the anterior chamber shunt is wider than the space between these muscles, portions of it may be manipulated under these muscles. If the implant is long, it may extend posteriorly beyond the equator of the globe and upon the insertions of the retractor oculi muscles. Subsequent implants (if deemed clinically necessary) may be placed in the dorsonasal, ventrolateral, and ventronasal quadrants in that order of preference. At the insertions of the major rectus muscles, both arterial and venous connections with the anterior globe occur. Incision of these rectus muscle insertions should be avoided since any hemorrhage in the wound field will further disseminate and stimulate those growth factors which mediate subsequent bleb fibrosis and failure. Meticulous wet-field cautery facilitates a blood-free surgical site. With most gonioimplants, placement at least 10–14 mm behind the limbus is recommended in dogs.
Most glaucoma surgeries are performed in the dorsal or dorsolateral one-half of the globe because of limited surgical exposure medially and ventrally in small animals. The 9 and 3 o’clock positions of the sclera are avoided because of the medial and lateral long posterior ciliary arteries. These two vessels provide the majority of the blood supply to the anterior uvea, and should not be disturbed surgically or during laser or cryothermy destruction of the ciliary body.
If a scleral incision is being performed (such as in the case of sclerotomy, cyclodialysis or iridencleisis), the proper distance of the scleral incision from the limbus is critical. This distance is also important in judging the site of probe application when applying transscleral laser photocoagulation. Ideally, the scleral incision is positioned directly over the pars plana ciliaris or posterior portion of the ciliary body. Anterior penetration increases the risk of intraocular hemorrhage because of damage to the ciliary body processes. Scleral incisions that are too far posterior, overlying the ora serrata or peripheral retina, have an increased risk of producing a retinal hole and secondary retinal detachment. With globe enlargement that is frequent with small animal glaucoma, selection of the site over the pars plana is more difficult. Dorsal sclerotomy is performed at the 12 o’clock position, and its anterior and posterior borders are about 4–5 and 7 mm, respectively, from the limbus. The length of the pars plana ciliaris varies in dogs by quadrant, with the medial aspect the shortest.
For laser and cryothermy destruction of the ciliary processes, measurements from the limbus to the ciliary body processes (pars plicata (corona) ciliaris) are critical for placement of the probe. These measurements change in the glaucomas when dog and cat globes are enlarged, and the sclera stretches. For measurement of the exact distance from the limbus, calipers are recommended. In the dog, laser cyclophotocoagulation is applied 5 mm behind the dorsal limbus. Application of laser transscleral cyclophotocoagulation or cyclocryothermy at the incorrect position attenuates the anticipated results.
The iris is a highly vascular and spongy tissue. Tearing of the iris of the dog usually results in variable hemorrhage which can be controlled only by electrocautery. The large major iridal arteriolar circle is located about 50% of the time in either the base of the iris or the anterior ciliary body of dogs. Hence, incision of the basal iris (as with a peripheral iridectomy) may cause excessive hemorrhage in about 50% of dogs. Iridectomies in dogs usually require wet-field cautery for hemostasis, applied simultaneously with the electrocautery for excision of the iris or following sharp incision by iris scissors.
An embryologic cleavage line is present between the sclera and the underlying iris and ciliary body. This area can be traversed, without significant hemorrhage, by a cyclodialysis spatula inserted through the sclera about 5–7 mm posterior to the limbus, and extending into the anterior chamber. If the spatula is malpositioned within the outer aspects of the iris and ciliary body, copious hemorrhage results.
While the macroscopic anatomy of the iridocorneal or anterior chamber angle of the dog and cat differs somewhat from the radial canal of Schlemm in humans and non-human primates, the ultrastructure of the trabecular meshwork and the aqueous humor dynamics are remarkably similar (Fig. 10.11). In dogs and humans the percentage of aqueous humor that exits the trabecular meshwork is about 85–90% (conventional outflow), and about 10–15% leaves by the uveoscleral route. The rates of aqueous humor turnover in dogs, cats, and humans appear quite similar (about 5.0–6.0 μL/min), although cats have been thought to have a much higher rate (about 15 μL/min). In horses, the best studies to date suggest that the majority of aqueous humor leaves through the uveoscleral outflow pathway. Hence, aqueous humor gradually flows posteriorly through the base of the iris and ciliary body to enter the subscleral space between the choroid and sclera.
(Courtesy of Dr Don Samuelson.)
Aqueous humor outflow pathways have the following boundaries: 1) the limbus and anterior chamber; 2) inwardly the pectinate ligaments, base of the iris, and inner aspects of the ciliary or sclerociliary cleft or sinus; 3) posteriorly the deeper aspects of the ciliary cleft or sinus; and 4) outwardly the sclera anteriorly and the outer aspects of the ciliary or sclerociliary cleft posteriorly (Fig. 10.12). Canine and feline aqueous outflow pathways differ slightly from those of humans by a cleavage of the anterior ciliary body which contains most of the trabeculae, and the iris base that directly communicates with the peripheral anterior chamber. Pectinate ligaments of various sizes and shapes connect the inner posterior limbus and termination of Descemet’s membrane to the anterior base of the iris. Although these pectinate ligaments appear to play no direct role in aqueous humor outflow unless significantly malformed/imperforate, they do provide stability for the iris. These iridocorneal angle anatomic differences between humans, non-human primates, and other animal species are thought to be associated with lens accommodation rather any differences in aqueous humor outflow physiology.
Fig. 10.12 The flow (arrows) of aqueous humor in the dog and cat. Formation by the ciliary body process, into the posterior chamber, through the pupil, into the anterior chamber, and exit through the corneoscleral trabeculae and uveoscleral pathways.
In horses, very stout pectinate ligaments span the opening of the sclerociliary cleft and are often visible without a gonioscopic lens at the nasal and temporal quadrants. The uveal trabecular meshwork (UTM; 74%), corneoscleral trabecular meshwork (CSTM; 22%), and angular aqueous plexus (AAP; 4%) have been quantified in horses; conventional trabecular aqueous humor outflow, as measured by pneumatonography, is 0.90 μL/min (about four times greater than in humans, dogs, and cats). The intertrabecular spaces of the uveal trabecular meshwork are very wide compared to the corneoscleral meshwork; this suggests that a significant resistance to aqueous humor outflow occurs in the latter trabeculae. Using microsphere perfusion studies it also appears that the majority of aqueous humor exiting the equine outflow pathways moves more posteriorly to enter mainly the vortex venous system.
The anatomic differences in the outflow pathways in many species of animals appear related primarily to the needs of accommodation rather than physiologic and morphologic differences in aqueous humor dynamics. The musculature of the ciliary body in dogs and cats is less developed than in humans, as accommodation, i.e. changes in the lens shape, is limited. The limited ciliary musculature and very large lenses in horses and cows suggest very limited accommodation. Aqueous humor leaves most of the non-human primate species through the corneal or corneoscleral trabecular meshwork (conventional or pressure-sensitive outflow) to enter eventually the episcleral plexus anteriorly, or uveal meshwork, and to pass through the ciliary body posteriorly (unconventional/uveoscleral or pressure-insensitive outflow).
In humans, microsurgical techniques have been developed that include suture cannulation of Schlemm’s canal and excision of segments of the corneoscleral trabecular meshwork (external trabeculectomy). Other procedures, such as goniosynechiolysis (restoring areas of the iridocorneal angle closed by peripheral anterior synechiae) and goniotomy (incision of congenital tissues obstructing aqueous humor flow into Schlemm’s canal), have not been reported in small animals. These microsurgical procedures represent the current refinement of human glaucoma surgical techniques, and suggest future possibilities for small animals. However, most primary glaucomas in the dog, when first presented to the veterinarian, already exhibit narrow-to-closed iridocorneal angles and clefts. The above techniques are more applicable to open iridocorneal angles. Nevertheless, experimental procedures such as goniotomy, trabecular meshwork transplantation, and gene transfer to the trabecular cells are future techniques worthy of investigation.
The pathophysiology of glaucoma surgery is influenced by the type and stage of glaucoma, the presence of secondary changes, and the type of glaucoma surgery performed, as well as changes resulting from either cryo- or cyclociliary destruction. For the majority of the primary glaucomas in dogs, the anatomic and biochemical status of the aqueous outflow pathways during the genesis of elevation of IOP have not been determined. Progressive narrowing and eventual closure of the iridocorneal angle occurs with all primary glaucomas in dogs, but these changes may be secondary to gradual enlargement of the lens and/or globe, iridal irritation, lenticular subluxation and instability, iridocorneal angle and trabecular meshwork remodeling in the face of chronic inflammation and/or cellular infiltration, and secondary instability of the ciliary cleft. These changes, whether primary or secondary, further complicate the medical and surgical treatment of primary canine glaucoma.
The initial presentation of canine glaucoma is typified by narrow-to-closed anterior chambers and iridocorneal angles. The distances between the basal iris and posterior limbus, as well as the anterior opening of the ciliary cleft, are reduced or closed as viewed by gonioscopy. Hence, surgical entry into the anterior chamber through a limbal incision in the glaucomatous eye must compensate for these changes.
The term ‘goniodysgenesis’ has unfortunately been applied inappropriately to many of the primary glaucomas in dogs. Goniodysgenesis refers to a diverse group of congenital iridocorneal anomalies in children that result in glaucoma in early life and infancy. Congenital glaucomas in puppies and kittens resulting from goniodysgenesis are rare.
The term goniodysgenesis was first applied to the presence of large areas of consolidated pectinate ligaments (mesodermal bands) in primary glaucoma in the Basset hound. Primary glaucoma in the Basset hound, like most breeds of dogs with breed-predisposed glaucoma, occurs in adulthood, and is not considered a congenital glaucoma. For these areas of consolidated pectinate ligaments to significantly impair the outflow of aqueous humor, essentially the entire iridocorneal angle would need to be affected. Often ‘flow holes’ are present in these consolidated pectinate ligaments (pectinate ligament dysplasia), permitting aqueous humor to traverse the entire filtration angle. The physiologic status of the trabecular meshwork environment, as well as stability of the ciliary cleft in the primary glaucomas with pectinate ligament dysplasia, remain a mystery, and may be the key to the treatment of these glaucomas.
The persistence of large, poorly differentiated sheets of pectinate ligaments in dogs should be classified as dysplasia of the pectinate ligaments. It appears that, in the dog, the formation of primary and secondary pectinate ligaments is often imperfect, and the range and relative size of the persistent areas of dysplastic ligaments in normal dogs and selected breeds need to be established, with a significant variation in the ‘normal’ population likely being present. The presence of dysplastic pectinate ligaments in dogs correlates to, but does not parallel, the genesis of the primary glaucomas. Significant diseases of the adjacent trabecular meshwork, not yet defined, may underlie the mechanisms of glaucoma. Surgery of the pectinate ligaments, as it relates to the outflow of aqueous humor, has not been reported in dogs, but these broad sheets of pectinate ligaments may be of increased relevance in those glaucoma surgeries that invade the iridocorneal angle.
Pre-iridal fibrovascular membranes (PIFMs) are common in advanced glaucomas in dogs. These membranes are potential sources of fibrin and other proteins, as well as erythrocytes and inflammatory cells that are released when the anterior chamber is opened and IOP lowered abruptly to 0 mmHg (Fig. 10.13). These same membranes may bridge the anterior iridocorneal angle, contributing to the formation of peripheral anterior synechiae (PAS), and even extend across the pupil and anterior lens capsule, and into the posterior chamber.
Fig. 10.13 Pre-iridal membrane (arrows) on the anterior surface of the iris in a Chow Chow with advanced glaucoma. These vascular membranes may impair aqueous humor outflow through the iridocorneal angle and interfere with glaucoma filtering surgical procedures in small animals. H & E, 100×.
Both PIFMs and PAS interfere with surgical entry into the anterior chamber by scalpel blade or hypodermic needle, and may contribute to early failures of many of the traditional filtering procedures in dogs. Experience suggests that glaucoma filtering procedures in the primary glaucomas in dogs are more successful when performed in the early phases of the disease. This opportunity usually occurs in the fellow asymptomatic eye as opposed to the opposite symptomatic eye which often exhibits end-stage glaucoma and blindness at the initial presentation.
The status of the ciliary body and its ability to form aqueous humor are important considerations when planning glaucoma surgery. Extensive damage to the ciliary body may occur in cases of advanced glaucoma, and is influenced, in part, by the severity and chronicity of IOP elevation, as well as the presence of inflammation. Marked elevations in IOP in the dog are often followed by brief (usually a few days) ocular hypotony; this is presumably the result of reduced rates of aqueous humor formation due to pressure-associated pathology at the ciliary body (sometimes termed ‘ciliary body shock’). If this damage is extensive and irreversible, phthisis bulbi results when normal aqueous humor outflow cannot be re-established. The rate of aqueous humor formation, as measured by fluorophotometry, has not been performed clinically in glaucomatous dogs, and therefore the status of the ciliary body and its ability to produce normal levels of aqueous humor are determined by clinical history and evaluation, tonography, and daily monitoring of IOP prior to surgical intervention.
The position of the lens can markedly influence the success or failure of glaucoma surgeries in all animal species. The lens may intermittently occlude the pupil, causing the basal iris to contact the inner posterior limbus and stimulate formation of peripheral anterior synechiae. These abrupt and temporary increases in IOP may hasten progressive damage to all ocular tissues, including the retina and optic disk. Lenticular instability (as well as increased lens/iris contact and microabrasion) may also stimulate chronic, low-intensity inflammation and pigment dispersion. Free melanin pigment dispersion has been demonstrated with the trabecular meshwork of advanced glaucomatous globes (including those affected by primary structural or dysplastic changes). Inflammatory cells may contribute to trabecular meshwork atrophy and subsequent ciliary cleft collapse which typifies end-stage glaucomatous globes. The exact relationship between these factors during the genesis of the canine glaucomas, however, remains poorly understood.
An anteriorly luxated lens, stuck in the anterior chamber, often has vitreous still affixed at its hyaloideocapsular (Wieger’s ligament) attachments that can completely occlude the pupil and cause marked elevations in IOP posterior to the pupil. Subluxation or luxation of the lens posteriorly into the vitreous can displace vitreous into the pupil and anterior chamber.
In most types of glaucoma the vitreous frequently undergoes partial liquefaction (syneresis). Hence, during many surgical procedures for glaucoma when the anterior hyaloid membrane has been already torn, presentation of the vitreous may occur within the anterior chamber. To minimize vitreous disturbances, osmotic agents are essential not only to reduce IOP, but also to dehydrate the vitreous, reducing its size. In advanced glaucoma eyes, syneresis of the vitreous is often complete. Preoperative administration of an osmotic agent provides the additional benefit of minimizing the dangers presented by rapid decompression of a hypertensive globe.
Potentially the most significant complication associated with the glaucoma surgeries is the pronounced inflammatory response which occurs at the surgical site in which aqueous humor is redirected into the episcleral space and surrounding tissues. This response results in considerable fibrosis about the area, and ultimately contributes to the failure of filtration blebs or drainage setons. Of interest, the normal passage of aqueous humor through the uveoscleral pathway all the way posterior to the optic nerve head does not incite this inflammatory response! Although not fully understood, the mechanism of this response appears to follow the general parameters of the wound-healing cascade, with growth factors mediating fibroblastic recruitment and transformation. Connective tissue growth factor (CTGF) and transforming growth factor beta 2 (TGF-β2) have been shown to mediate these initial events in multiple animal models (Tables 10.2a and 10.2b). Subsequent tissue fibrosis and cicatricial remodeling is at least partially matrix metalloproteinase mediated. Successfully controlling this postoperative fibrotic response is crucial to improving the long-term success rates of all glaucoma surgeries. Ultimately, this may require a ‘chemotherapeutic’ approach involving multiple targeted intraoperative and postoperative medications (applied topically as well as systemically). Achieving this goal represents the single greatest challenge in the successful long-term surgical treatment of this disease complex!
|MMP common name||Designation||Substrates and actions|
|Fibroblast collagenase||(MMP-1)||Cleaves single bond in native types I, II and III collagens|
|72 kDa Gelatinase||(MMP-2)||Degrades types IV, V, and VII collagens, gelatin, fibronectin; synthesized by fibroblasts and macrophages|
|92 kDa Gelatinase||(MMP-9)||Degrades types IV and V collagen, gelatin; synthesized by epithelial cells, macrophages, polymorphonuclear leukocytes|
|Stromelysin||(MMP-3)||Degrades proteoglycans, fibronectin, laminin, gelatin and types III, IV, and V collagen|
|Neutrophil collagenase||(MMP-8)||Similar to MMP-1, degrades type I, II, and III collagen|
|Epidermal growth factor||EGF||Synthesized by corneal epithelial cells, lacrimal gland; mitogen and chemotactic factor for all three types of corneal cell|
|Transforming growth factor alpha||TGF-α||Structurally and functionally similar to EGF; synthesized by corneal epithelial cells, lacrimal gland|
|Transforming growth factor beta||TGF-β||Three isoforms: TGF-β1, TGF-β2, TGF-β3; promotes formation of extracellular matrix; TGF-β2 present in aqueous humor; synthesized by multiple types of cell|
|Basic fibroblast growth factor||bFGF||Detected in basement membranes; synthesized by endothelial cells; mitogen for fibroblasts and endothelial cells; angiogenic|
|Acidic fibroblast growth factor||aFGF||Detected in basal layer of corneal epithelial cells and basement membranes; synthesized by endothelial cells; mitogen for fibroblasts and endothelial cells; angiogenic|
|Keratinocyte growth factor||KGF||Synthesized by keratocytes; stimulates corneal epidermal cell proliferation and migration|
|Hepatocyte growth factor||HGF||Synthesized by corneal epithelial cells; stimulates corneal epidermal cell proliferation and migration|
|Platelet-derived growth factor||PDGF||Synthesized by corneal epithelial cells; stimulates proliferation of stromal fibroblasts|
|Insulin-like growth factor I||IGF-I||Part of the IGF axis (comprising surface receptors, ligands, binding proteins and proteases). Involved in early healing and promotes cellular proliferation.|
|Connective tissue growth factor||CTGF||Stimulates fibrosis and mediates the actions of TGF-β on matrix formation|
|Tumor necrosis factor alpha||TNF-α||Proinflammatory cytokine with multiple effects including chemotaxis of leukocytes, increased production of MMPs, and induction of apoptosis; soluble TNF-α is released by TACE cleavage of transmembrane pro-TNF-α|
|Interleukin-1 beta||IL-1β||Proinflammatory cytokine synthesized by corneal epithelial cells; stimulates MMP production by keratocytes|
TACE, tumor necrosis factor-α converting enzyme.
Preoperative considerations in the treatment of glaucoma include: 1) preoperative control of IOP to levels consistent with normal RGC physiologic function (<25–33 mmHg); 2) suppression of concurrent anterior segment inflammation; and 3) vitreous body dehydration and shrinkage with osmotic agents. IOP must be reduced to the low normal range in patients prior to glaucoma surgery if at all possible. Fortunately, combinations of miotics, osmotic agents, adrenergic agents, and carbonic anhydrase inhibitors can usually lower IOP to 10–15 mmHg, albeit temporarily.
Surgical entry into the anterior chamber when IOP is 25 mmHg or higher can be hazardous to the eye and surgical outcome. If necessary, additional vigorous massage and hypotensive medical treatment should be initiated (such as an additional intravenous dose of osmotic agents) before the eye is entered. Glaucoma procedures in a globe with elevated IOP exhibit higher risk and lower surgical success rates. A glaucomatous eye without satisfactory ocular hypotension upon entry may exhibit choroidal hemorrhage, choroidal edema, vitreous protrusion through the pupil, and forward displacement of the iris. Intraocular hemorrhage is also more apt to occur in these globes. Cautious anterior chamber paracentesis may be performed in a glaucomatous eye that has not responded to vigorous medical treatment. Keratocentesis is usually performed under general anesthesia or deep sedation, and aqueous humor is removed slowly from the anterior chamber after first decompressing the syringe plunger (see Chapter 9).
Many types of canine glaucoma exhibit concurrent aqueous humor flare, altered blood–aqueous barrier, and mild to chronic iridocyclitis. The iridocyclitis may also be a primary or secondary factor in the genesis of the glaucoma. Topical and systemic corticosteroids and non-steroidal anti-inflammatory drugs (NSAIDs) are indicated to suppress inflammation and reduce inflammatory cells and proteins in the aqueous humor. The iridocyclitis and aqueous exudates can compromise short- and long-term existing aqueous humor outflow pathways as well as the new surgical site. Aggressive systemic anti-inflammatory therapy may additionally contribute to arresting the destructive and self-perpetuating milieu of RGC death.
Control of the pupil immediately before surgery often contributes to the overall success rate of intraocular procedures. For most types of glaucoma surgery, the desired pupil size at the time of surgery is either normal or miotic. The pupil is usually constricted for surgical procedures, including iridencleisis, cyclodialysis, iridencleisis–cyclodialysis, corneoscleral trephination, and cyclocryothermy.
Pupil size when luxated lenses are removed depends on the position of the lens. For anterior luxated lenses, the pupil is constricted immediately before surgery to maintain the lens within the anterior chamber. Prior to surgery, 10% phenylephrine may assist in re-establishing pupillary flow and lower IOP in the posterior segment; sometimes a combination of 2% pilocarpine and 10% phenylephrine is alternated to provide a constantly moving and moderate-sized pupil. A miotic pupil may aggravate the glaucomatous process by creating an acute pupillary blockage related to the lens or adherent vitreous, or both. Before removal of subluxated and posterior luxated lenses, the pupil is dilated with several instillations of 1% tropicamide, 1% atropine or 10% phenylephrine, or some combination of these agents. At the time of mydriasis, IOP should be within normal limits. Following the intact removal of a luxated or subluxated lens, degenerate vitreous within the pupillary opening or anterior chamber should be carefully removed by the judicious use of automated vitrectomy where possible.
Surgical procedures for the treatment of the glaucomas may be divided into two types: 1) those that increase outflow of aqueous humor via alternative pathways of drainage; and 2) those that decrease the rate of formation of aqueous humor by destroying part of the pars plicata or corona ciliaris (Table 10.3). Procedures to increase the outflow of aqueous humor include iridencleisis, corneoscleral trephination, cyclodialysis, combined iridencleisis and cyclodialysis, posterior sclerectomy, and anterior chamber shunts (gonioimplants). Additional procedures to increase the outflow of aqueous humor include goniopuncture, iridosclerectomy, goniotomy, trabeculectomy, and sinusotomy, but these surgical procedures have not been described in dogs. Techniques used to reduce the rate of aqueous humor formation by partial destruction of the ciliary body include cyclocryothermy, cyclodiathermy, and diode laser transscleral or endoscopic cyclophotocoagulation. The popularity, staging, and combining of these different glaucoma surgical techniques are constantly evolving. However, as new antifibrosis drugs are developed, some of these older traditional selected filtration procedures may again be more useful.
|Mechanism||Type of surgery|
|Iridocorneal angle bypass||Corneoscleral trephination|
|Iridocorneal angle bypass||Anterior chamber shunts/gonioimplants|
|Decrease aqueous formation||Cyclocryotherapy|
|Decrease aqueous formation||Transscleral or endoscopic cyclophotocoagulation (diode laser)|
|Destroy ciliary body epithelia||Intravitreal gentamicin|
Additionally, minimizing the egress of blood into the surgical wound field during all forms of glaucoma surgery will help minimize the subsequent healing and scarring response which is mediated by red blood cell-delivered growth factors. Removal of the lens, although not commonly considered a surgical procedure for treatment of lens-induced glaucoma, may be necessary in the management of many canine glaucomas. Lens removal may be indicated for secondary glaucomas associated with lens-induced uveitis and cataract resorption, intumescent cataracts, anterior and posterior lens luxations, and subluxations. When the lens is displaced from its patellar fossa in a primary glaucomatous eye, maintenance of IOP within normal limits by surgical or medical treatment, or a combination of both modalities, may be impossible without first removing the luxated lens.
The canine lens may additionally need to be removed in the face of aggressive endoscopic cyclophotocoagulation in order to facilitate adequate exposure and reduce the necessity for subsequent cataract removal. Furthermore, the absence of the lens in the face of developing/outright glaucoma may contribute via decreasing lens/iridal contact and pigment shedding, anterior chamber crowding, and iridocorneal angle and/or ciliary cleft collapse.
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).
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.