- •CONTENTS
- •FOREWORD 1
- •FOREWORD 2
- •CONTRIBUTORS
- •PREFACE
- •ACKNOWLEDGMENTS
- •GLAUCOMA GENETICS
- •GONIOSCOPY
- •PERIMETRY
- •PRIMARY OPEN-ANGLE GLAUCOMA
- •CHILDHOOD GLAUCOMA
- •NEOVASCULAR GLAUCOMA
- •ADRENERGIC AGONISTS
- •ADRENERGIC ANTAGONISTS
- •CHOLINERGIC AGENTS
- •PROSTAGLANDIN ANALOGS
- •HYPEROSMOTIC AGENTS
- •NEUROPROTECTION
- •BASICS OF LASERS
- •LASER TRABECULOPLASTY
- •LASER IRIDOTOMY
- •CYCLODESTRUCTION
- •FILTRATION SURGERY
- •AQUEOUS SHUNTS
- •OCULAR HYPOTONY
- •INDEX
Chapter 46
OCULAR HYPOTONY
Mary G. Lynch, M.D., and Reay H. Brown, M.D.
Ocular hypotony is a serious, sight-threatening condition. Although trauma and inflammation can also produce hypotony, filtration surgery is now its leading cause. This is due to recent trends toward more aggressive surgical management of glaucoma and the widespread use of antifibrosis agents, which increase the occurrence of excessive, leaking, and overfiltering blebs.
Hypotony shortly after filtration surgery is common and can generally be managed conservatively. However, prolonged hypotony and its sequelae, such as hypotony maculopathy and lens–cornea touch, require aggressive, often surgical, management. Numerous techniques are now available for treating both bleb leaks and overfiltration, and their use depends on the etiology and duration of these abnormalities. Although hypotony often resolves with time, the long-term outcome of its sequelae is guarded. The best treatment remains prevention, with judicious choice and use of surgical techniques. If hypotony maculopathy does occur, aggressive, early reversal of the hypotony offers the best hope of visual recovery, often requiring the surgeon to choose visual acuity over bleb function.
The definition of ocular hypotony has ranged from 2 to 10.5 mm Hg, although clinical studies now often use a pressure below 6 mm Hg.1,2 However, some eyes remain asymptomatic despite extremely low intraocular pressures (IOPs), whereas others experience sight-threatening complications at pressures that are well within the low–normal range. Rather than using an absolute numerical pressure, it is best to define “clinical hypotony” as a pressure low enough to cause functional and structural changes that reduce visual acuity. This actual pressure level will vary for each patient, depending upon other factors such as age, refractive status, and race.
CLASSIFICATION OF OCULAR HYPOTONY
Hypotony is generally classified as related or unrelated to the presence of a filtering bleb. Hypotony following filtering surgery can be further categorized by its timing in relation to the surgery and the extent of anterior chamber shallowing. All of these considerations help direct both the timing and the approach to therapy.
Bleb-related hypotony results from either excessive overfiltration or from a leak in the bleb. Since the introduction of adjunctive antifibrotic agents with filtering surgery, the incidence of hypotony has doubled, from 10 to 15% of eyes undergoing trabeculectomy to as high as 32%.1,3,4 Histopathology of these blebs shows diminished numbers of fibroblasts and disorganized, widely spaced collagen fibrils.5 Many lack blood vessels entirely, giving them their characteristic, bone-white appearance (Fig. 46–1). Independent of the bleb, other factors that can contribute
PEARL... Clinical hypotony is a pressure low enough to cause functional and/or structural changes that reduce visual acuity.
FIGURE 46–1 Filtering surgery with an adjunctive antifibrotic agent often results in blebs that are thin, avascular, and prone to leaking or overfiltration.
498
to hypotony include inflammation, a cyclodialysis cleft, and ciliary body “shutdown.”
Because many eyes exhibit transient and uneventful low pressure shortly after filtration surgery, hypotony in the early postoperative period requires more conservative management than that which develops later or persists for weeks or months. Similarly, shallowing of the anterior chamber generally recovers and can be approached more conservatively than if there is lens–cornea touch.
SEQUELAE OF DELAYED
OR PROLONGED OCULAR HYPOTONY
Filtering surgery commonly results in a transient low pressure. However, hypotony that persists for several weeks to months, or develops long after the filtering procedure, can lead to sight-threatening sequelae. The most serious of these is hypotony maculopathy (Fig. 46–2A,B).
In hypotony maculopathy, low IOP leads to chorioretinal folds in the macula, optic disc swelling, and, occasionally, a peripheral choroidal detachment (Table 46–1).6–9 Animal studies have shown that hypotony can disrupt axonal cytoarchitecture and slow axonal transport.10 Symptoms include decreased central visual acuity and metamorphopsia, which some patients describe as “looking through Venetian blinds” or a cracked window.
Hypotony maculopathy generally does not occur if the pressure is greater than 6 mm Hg. However, patients can describe visual aberrations with pressures in the 8 to 12 mm Hg range. Because the fundus can appear relatively normal or be obscured by hazy media due to the hypotony, a fluorescein angiogram may help reveal a wrinkled posterior pole.
Although the incidence of hypotony, as defined by IOP, after filtering surgery can be as high as 32%, only about 14% of patients will develop clinical maculopa-
|
CHAPTER 46 OCULAR HYPOTONY • 499 |
TABLE 46–1 HYPOTONY MACULOPATHY |
|
|
|
|
|
Symptoms |
Decreased central acuity |
|
Metamorphopsia |
Signs |
Low intraocular pressure |
|
(generally less than 6 mm Hg) |
|
Chorioretinal folds in the macula |
|
(may require fluorescein angiography) |
|
Optic disc swelling |
|
Peripheral choroidal detachment |
|
|
thy.2,4,6,11 However, early recognition of this complication is important. In general, reversal of maculopathy is inversely related to the duration of the hypotony,3,12 and pressure should be restored to the normal range, or above, within several weeks of developing posterior pole changes.
Although hypotony maculopathy generally occurs shortly after filtering surgery with antimetabolites, it can also develop long after the procedure. Additional risk factors include young age,6,8,12,13 myopia,6,8,13 Caucasian race,6 and previous exposure to carbonic anhyrase inhibitors.12 The risk of developing hypotony maculopathy is lower in African Americans,11 probably due to their overall decreased incidence of hypotony after filtering surgery.14
Other sequelae of prolonged hypotony include cataract formation, corneal edema,15 fixed folds in the retina, visual field loss,9 bleb infections, and endophthalmitis.16,17
HYPOTONY INDEPENDENT
OF BLEB PATHOLOGY
INFLAMMATION
Inflammation following either filtration surgery or trauma can produce hypotony through iridocyclitis, ciliochoroidal detachment, and traction detachment of the ciliary body.
A B
FIGURE 46–2 (A) In hypotony maculopathy, the posterior pole often shows a diffuse pattern of chorioretinal folds as well as
(B) optic nerve swelling.
500 • SECTION VII SURGICAL THERAPY OF GLAUCOMA
Iridocyclitis may both diminish aqueous production and enhance uveoscleral outflow.18,19 Treatment usually includes topical steroids and cycloplegia, and systemic steroids in cases with severe inflammation or ciliary body detachment.
Ciliochoroidal detachments, which diminish aqueous humor production, can occur in up to 34% of eyes after filtering surgery15,20 and usually result from inflammation, an overfiltering bleb, or both. Although large detachments are easily seen by direct or indirect ophthalmoscopy, ultrasound biomicroscopy may be required to detect anterior or diffuse detachments.21 Usually, topical and systemic steroids, as well as cycloplegics, are necessary to resolve a choroidal detachment caused by inflammation. When an overfiltering bleb is the cause, treatment usually requires correcting the underlying problem.
Inflammation can also cause ciliary body traction and detachment by encouraging membrane formation in the anterior vitreous cavity. In the setting of proliferative vitreoretinopathy, such membranes must be removed by pars plana vitrectomy and membrane stripping.21–24
CYCLODIALYSIS CLEFT
A cyclodialysis cleft, or separation of the ciliary body from the scleral spur, creates hypotony by allowing the escape of aqueous through the cleft into the suprachoroidal space. This can produce diffuse choroidal thickening or a bullous choroidal detachment. These clefts usually result from blunt or penetrating trauma. However, they may also complicate cataract or filtration surgery, generally from inadvertent manipulation and/or traction of the iris or incisional entry posterior to the scleral spur. These clefts are usually located close to the surgical site.
Diagnosis of a cyclodialysis cleft is often complicated by coexistent corneal edema, hyphema, and shallowing of the anterior chamber, all of which impede its visualization by gonioscopy. These obscure clefts can be identified using ultrasound biomicroscopy25,26 or by deepening the anterior chamber with a viscoelastic prior to gonioscopy.27 A more invasive approach involves injecting balanced salt solution with added fluorescein into the anterior chamber and recovering fluorescein-stained fluid from the supraciliary space through a sclerotomy.28
PITFALL... Coexistent corneal edema, hyphema, and shallowing of the anterior chamber can all prevent gonioscopic detection of a cyclodialysis cleft.
The literature describes many procedures for treating cyclodialysis clefts, providing strong testament to the difficulty of treating this condition (Table 46–2). Clefts that occur shortly after surgery occasionally close following cycloplegia and termination of topical steroids. In cases with good visualization, several investigators
TABLE 46–2 MANAGEMENT OF CYCLODIALYSIS CLEFTS
Cycloplegia and discontinuation of steroids Direct photocoagulation using a gonioprism: argon laser
Cryotherapy
Indirect photocoagulation Diode laser
Trans-scleral yttrium-aluminum-garnet (YAG) laser Diathermy
Suturing Nonvisualized passage Direct cyclopexy
Pars plana vitrectomy, cryotherapy, gas tamponade
have reported success with direct argon laser photocoagulation through a gonioprism,27,29,30 often with a peribulbar anesthesia. Confluent applications of 100 m spots at 0.1 to 0.2 sec and 500 to 1000 mW are delivered to the base of the cleft, followed by postoperative cycloplegics. Some cases require repeat treatments to progressively close the cleft.
Poorly visualized clefts can be treated indirectly from the outside by cryotherapy, or photocoagulated with either a diode or trans-scleral yttrium-aluminum-garnet (YAG) laser.31–33 Diode laser treatment uses the contact hand piece (G-probe) to deliver two rows of 1500 mW contiguous applications for 1500 msec each over the cleft, beginning 1.5 mm posterior to the limbus. All of these indirect approaches require a local anesthetic block for comfort, and postoperative cycloplegics.
More aggressive surgical therapy involves external diathermy to the bed of a scleral flap that is created over the cleft.28,34 This can be combined with suturing the cleft closed with 9-0 or 10-0 nylon through the scleral bed,35 either with or without direct visualization.36,37 Particularly recalcitrant clefts may require pars plana vitrectomy, cryotherapy, and tamponade with sulfur hexafluoride gas.38,39
Once a cleft is closed, the eye can experience a period of extremely high pressure. Commonly, the patient undergoes treatment and is sent home with cycloplegia, only to call the surgeon several hours later in tremendous pain. The surgeon should always warn the patient of this possibility and consider prescribing prophylactic aqueous suppressants.
S P E C I A L C O N S I D E R A T I O N
Shortly after a cyclodialysis cleft is closed, the eye often goes through a period of extremely high pressure that is accompanied by tremendous pain.
CILIARY BODY SHUTDOWN
Ciliary body shutdown can occur after filtering surgery if the eye is treated with an aqueous suppressant. This has been reported with topical beta-blockers, and both topical and systemic carbonic anhydrase inhibitors.40–43 This phenomenon, usually associated with a choroidal detachment, probably results from drug supersensitivity because discontinuing the medication usually resolves the hypotony.
Ciliary body shutdown and aqueous suppression may also result from the toxic effects of antifibrotic agents on the ciliary body.44,45 These findings may help explain the higher incidence of hypotony following the use of antimetabolites.
HYPOTONY SECONDARY
TO BLEB PATHOLOGY
In the early postoperative period, up to one third of eyes experience overfiltration and a low IOP (i.e., less than 6 mm Hg).46 In the absence of lens–cornea touch and massive choroidal detachment, the hypotony will generally resolve and require only topical steroids and cycloplegics. Surgical intervention is needed if the cornea or retina is in jeopardy, or if the hypotony persists or develops later in the postoperative period.
PATHOGENESIS OF OVERFILTERING BLEBS
Aqueous Production
Proper development of filtering blebs depends, in part, on continued production of aqueous humor. Limiting aqueous production, especially in the early postoperative period, can reduce the height of a bleb, and ultimately its function.
Surgical Bleb Construction
and Postoperative Management
Several factors during and after surgery significantly influence the behavior of a filtering bleb: (1) assessment of conjunctival integrity, (2) flap construction, (3) sclerectomy size, (4) antimetabolite use, (5) preservation of Tenon’s capsule, (6) intraoperative assessment of the conjunctival wound for leaks, and (7) timing of suture-lysis.
By evaluating the thickness and integrity of the conjunctiva with a wet cellulose sponge, the surgeon can identify residual conjunctival scars and choose a different site for the incision, if possible. Eyes with thinner conjunctiva and Tenon’s capsule may require a lower concentration of antimetabolite or a shorter exposure time.
In general, a thin flap offers less resistance to aqueous outflow than a thicker flap. Large sclerectomy holes also
CHAPTER 46 OCULAR HYPOTONY • 501
enhance aqueous outflow, as do holes located close to the edge of the scleral flap. In a highly myopic eye, the surgeon should make the sclerectomy small relative to the flap size. Alternatively, a relatively thick scleral flap can allow for a more generous sclerectomy. A corneal safetyvalve incision, using a narrow scleral flap tunneled anteriorly into clear cornea, may result in less hypotony.47
Antifibrosis agents should be used with caution, particularly in young myopes and other individuals at high risk for complications from hypotony. This includes substituting 5-fluorouracil for mitomycin in primary filters.
If there are any concerns about possible overfiltration postoperatively, the surgeon should close the flap with several sutures. Extra sutures generally provide greater flexibility in suture lysis, which can be performed sequentially, allowing adequate time to assess its effect. Antimetabolites can allow the surgeon to delay suture lysis or removal by up to 2 months after surgery.48
Bleb Instability, Evolution,
and Repetitive Trauma
The structure and function of filtering blebs can also change years after the surgical procedure.49 A “stable,” well-functioning bleb can evolve into a large, avascular bleb that causes hypotony despite years of adequate pressure control. Most of these changes result from the continued internal pressure of aqueous outflow against the unstable, weak conjunctiva.
PEARL... Over time, a “stable,” well-functioning bleb can become a large, avascular bleb that causes hypotony despite years of adequate pressure control.
External, repetitive trauma, such as chronic eye rubbing by the patient or inadvertent pressure during sleep, also can cause a bleb to extend and become thinner and multilobulated. Any case of excessive filtration should suggest a history of trauma or ocular irritation producing continued rubbing or scratching.
PATHOGENESIS OF LEAKING BLEBS
“Traumatic” tears usually occur from a single event, such as an injury. These bleb tears usually appear as slits or flaps, and their edges are often relatively “raw.” They usually heal with aqueous suppression and patching.
Atrophic holes generally develop in thin, avascular conjunctiva. This type of leak looks more like a “hole” with a raised cuff around the opening. Because the edges of the opening may be lined with conjunctival epithelium, these threadbare holes generally require more aggressive surgical intervention than acute tears.
502 • SECTION VII SURGICAL THERAPY OF GLAUCOMA
MANAGEMENT
OF EARLY OVERFILTRATION
Transient overfiltration and hypotony commonly occur 2 to 3 days after filtering surgery.46 Most eyes without lens–cornea touch or marked choroidal detachment respond well to conservative management. However, a persistent, shallow anterior chamber may encourage peripheral anterior synechia formation, damage to the corneal endothelium, cataract formation, and filter failure. Decreased steroids and the addition of strong cycloplegics, such as atropine, usually help deepen the anterior chamber.
If these medical maneuvers are ineffective, a compression, or “torpedo,” patch placed over the scleral flap can help deepen the anterior chamber. This type of patch consists of the inner cotton from an eye pad, rolled into a tube shape and folded in half. This is then placed on the closed eyelid directly over the bleb, and held in place with two or three eye pads.
Oversized bandage contact lenses, available in diameters up to 24 mm, can also be used to tamponade the flap.50 The lens is placed on the eye and the patient checked every 2 days for removal and cleaning of the lens and IOP measurement. The average duration of a bandage lens for overfiltration is about 7 days.
The Simmons’ shell can also tamponade a brisk filter.51 This is a fenestrated methylmethacrylate lens with an internal ledge that depresses the bleb when placed over the cornea, followed by an eye patch. A large-diam- eter bandage contact lens flattened with peripheral radial incisions can minimize irritation from the shell itself. A large, brisk, or recalcitrant leak should be sutured with either 10-0 nylon or Bisorb, or 9-0 monofilament Vicryl, using a vascular, noncutting needle.
Shallow anterior chambers that do not resolve spontaneously generally require surgical reformation using a viscoelastic agent, occasionally combined with surgical revision of the flap. Eyes with lens–cornea touch can quickly develop corneal endothelial cell damage and require this aggressive approach relatively early.
PEARL... The best treatment for overfiltration is to avoid it.
The best approach to early overfiltration is to avoid it. This requires meticulous surgical technique including careful closure of the flap, sparing use of antifibrotic agents, and evaluation of the surgical wound for leaks.52 Suture lysis also should be delayed, preferably for several days after surgery.52,53
MANAGEMENT
OF PROLONGED HYPOTONY
In general, a conservative, nonsurgical approach is appropriate (1) for acute bleb tears, (2) for a monocular patient with adequate vision, (3) when central acuity is preserved,
(4) for a reliable patient who will notify the physician of any change in symptoms, and (5) for an eye without severe macular changes.
More aggressive, generally surgical, therapy is needed for (1) an eye with a chronic “threadbare” hole,
(2) a history of bleb-related infection, (3) an expanding, unstable, overfiltering bleb, (4) a monocular patient with inadequate vision, (5) an unreliable patient for whom repeated trauma is a possibility, and (6) an eye with poor central acuity or marked anisometropia.
MANAGEMENT OF CONJUNCTIVAL LEAKS
The surgeon should always try to repair a conjunctival leak because a leaking bleb is at increased risk of infection and hypotony and will not develop the height necessary to achieve long-lasting filtration (Table 46–3).54
Small, early leaks resulting from inadequate conjunctival closure or inadvertent, acute bleb tears often close with aqueous suppression and patching55 using either a torpedo cotton pad, an oversized bandage contact lens,3,56 or the Simmons’ shell.
Chronic, atrophic holes are more difficult to close and often resist both patching and suturing. Although cyanoacrylate adhesive can seal holes in filtering blebs, a collagen shield or a soft contact lens is often necessary for comfort and to keep the hard glue pellet from tearing the fragile conjunctiva and enlarging the hole.57,58
Atrophic holes often require treatment of the entire bleb to thicken the tissue and induce inflammation. However, the most definitive treatment for a chronically leaking
TABLE 46–3 MANAGEMENT OF CONJUNCTIVAL LEAKS
Patching
Large-diameter bandage contact lens
Simmons’ shell
Aqueous suppression
Topical antibiotics
Cyanoacrylate glue
Suture closure
Fibrin adhesive
Thicken bleb (induce inflammation)
Excise conjunctiva
bleb is conjunctival advancement or transplantation, usually following removal of the thin, avascular portion of the
bleb.57,59–61
MANAGEMENT OF PROLONGED
OVERFILTERING BLEBS
The choice of technique usually begins with the least aggressive course. However, the stepwise approach discussed here is not an absolute sequence because therapy also depends upon the location and cause of the problem.
Reduce the Extent or Elevation of the Bleb
Continued aqueous production can exert ongoing “barotrauma” to a thin, overfiltering bleb. Decreasing this production with topical and, occasionally, oral aqueous suppressants can “turn down the faucet” and allow some blebs to remodel lower and thicker, particularly in the early postoperative period.
Bleb Compression
Bleb compression with a torpedo patch, an oversized bandage contact lens,3,56 or a Simmons’ shell can also change the appearance and function of an overfiltering bleb. Such compression can also enhance the effectiveness of more aggressive therapies, discussed in the following text.
Suturing methods can also depress the bleb and tighten the scleral flap. One technique involves placing a 9-0 nylon mattress suture over the bleb, anchored anteriorly in the peripheral cornea and posteriorly in Tenon’s and conjunctiva.62 The suture is left in place for 1 to 4 weeks and the patient is followed weekly.
Thicken the Bleb
Medical approaches: Reducing or stopping steroids in the early postoperative period can allow the normal inflammation that follows surgery to thicken the bleb. Some topical antibiotics can irritate the conjunctival surface and promote inflammation, but can theoretically select resistant organisms. Trichloroacetic acid, applied to the bleb surface with the end of a small stick, can also shrink and thicken the conjunctival epithelium.63 Unfortunately, these medical approaches are relatively ineffective in treating overfiltering blebs.
Surgical approaches: Argon and YAG laser treatments can effectively stimulate inflammation within filtering blebs. In one approach, the conjunctival epithelium of large, cystic blebs with translucent walls is gently abraded with a cotton-tipped applicator soaked with anesthetic or 95% alcohol, followed by painting with methylene blue to absorb the laser energy.64,65 Argon laser applications, 500
CHAPTER 46 OCULAR HYPOTONY • 503
to 800 m in size with a duration of 0.17 to 0.50 sec, are then delivered, titrating the power from 300 to 500 mW to shrink the surface tissue without producing a crater. This technique also works with rose bengal, but has a higher risk of perforating the bleb surface.
A second procedure uses the Lasag Microrupter II neodymium:YAG (Nd:YAG) laser in the continuous wave mode to apply thermal energy to both the surface and base of the bleb.66 However, this laser is now generally unavailable.
Cautery67 and cryotherapy68–70 to the bleb surface have also been advocated for overfiltering blebs. Unfortunately, these methods used alone are frequently ineffective in reversing the hypotony.
Numerous investigators have reported on the efficacy and complications of injecting autologous blood into overfiltering blebs, which encourages fibroblast proliferation and collagen deposition.71–77 In this procedure, conducted at the slit-lamp with topical anesthesia, the surgeon draws venous blood from the patient and then puts a new, sterile 30-gauge needle on the syringe. This needle is advanced to the center of the bleb, and blood is injected, often into each of several lobes, if present (Fig. 46–3).
Such injections alone appear to succeed only half the time,3,52 although surface cryotherapy, aqueous suppression, and torpedo patching may improve this success rate. Complications include tracking of blood into the eye, which can be averted by first injecting a viscoelastic into the anterior chamber. Increased IOP, corneal blood staining, filter failure, and corneal graft rejection may also occur.
FIGURE 46–3 Appearance of a large, overfiltering bleb after injection of autologous blood into the bleb and a compression patch. Note subconjuctival inflammation and residual blood. The bleb eventually became lower and thicker, with increased intraocular pressure.
504 • SECTION VII SURGICAL THERAPY OF GLAUCOMA
A B
FIGURE 46–4 (A) Overfiltering and leaking bleb after a trabeculectomy with mitomycin-C. (B) The bleb was later excised and posterior conjunctiva advanced to cover the defect.
Reopen the Conjunctiva and Reinforce the Flap
When more conservative measures fail to raise IOP, the bleb must be surgically revised.78 This involves identifying and reopening the original conjunctival incision or creating a more posterior incision. After reinforcing the scleral flap with additional 10-0 nylon sutures, Tenon’s capsule and conjunctiva are closed separately with a running 9-0 monofilament Vicryl suture. Including a Tenon’s capsule autograft in the wound can further reinforce a thin, attenuated bleb.
A thin scleral flap or a full-thickness opening generally must be reinforced with a slightly oversized patch graft sutured over the flap with 10-0 nylon. This graft can be glycerin-preserved sclera,79–81 preserved pericardium, or a corneal allograft.82 Unlike a resutured scleral flap, tension on these patch grafts cannot be adjusted with suture lysis and may result in loss of the filtering bleb.
Conjunctival Advancement, Excision,
and Transplant
If the bleb is extremely thin or leaking, the surgeon may have to combine reinforcement of the scleral flap with conjunctival advancement59,63 or transplantation.83 Advancing a conjunctival flap may involve making a relaxing incision in the conjunctiva and Tenon’s capsule near the fornix to allow dissection and mobilization of these tissues from the episclera. The flap is then pulled forward and its anterior edge sutured to the peripheral cornea with 10-0 nylon. The posterior edge is sutured to the sclera or conjunctiva with 9-0 or 8-0 Vicryl (Fig. 46–4A,B).
If conjunctival scarring prevents the creation of a sufficiently mobile flap, then a conjunctival autograft may be necessary (Fig. 46–5). This involves excising the ischemic bleb and measuring the diameter of the defect with calipers. Using a corneal traction suture to rotate the eye upward, an area of inferior bulbar conjunctiva 50% larger than the defect is marked out, excised, and then sutured
to the defect with interrupted 9-0 Vicryl sutures posteriorly and 10-0 nylon at the conjunctiva–cornea interface. The donor site is allowed to heal through granulation tissue.
Both conjunctival advancement and transplantation result in normal conjunctiva over the trabeculectomy site. Additional sutures in the scleral flap are not always necessary and a bleb often re-forms over the original filter.
Lens Extraction
Removal of the crystalline lens can also reverse hypotony, and may be considered if any lens opacity is present, followed by a reassessment of bleb function and pressure control.84,85 This approach is supported by the difficulty of differentiating between decreased vision from hypotony maculopathy versus cataract, the fact that 52% of eyes will develop a cataract after trabeculectomy,46 and that many of the methods used to treat hypotony can actually accelerate cataract formation.40
FIGURE 46–5 An eye after excision of a leaking bleb, with the defect covered by a conjunctival autograft from the inferior fornix.
C O N T R O V E R S Y
Cataract removal may reverse ocular hypotony following filtration surgery. However, this does not always succeed, and lens extraction in a hypotonous eye presents many challenges.
However, lens extraction in a hypotonous eye presents several challenges. Reduced axial length from hypotony can complicate intraocular lens selection. A diminished view through the soft cornea, and rapid outflow of infused saline through the trabeculectomy site can also complicate phacoemulsification in this situation. Postoperatively, limiting steroid use to enhance inflammation and using aqueous suppressants to decrease the bleb height during the healing and remodeling phase may also help reverse hypotony.
PROGNOSIS
Spontaneous resolution of prolonged hypotony after filtering surgery is uncommon.8,13,86 Unfortunately, an increase in the IOP to a normal level does not always resolve the macular changes and return the visual acuity to baseline.6,13,66,86,87 Although elevating the pressure to a higher than normal range may successfully flatten the posterior pole,47,78,87 photoreceptor loss, choroidal thickening, pigmentary changes, and epiretinal membrane formation can still permanently affect vision.8
Some studies demonstrate an association between prolonged hypotony and ultimate failure of the filter and poor visual recovery.3,12 For this reason, early intervention (i.e., within 6 months) is often advocated.3 However, reversal of even prolonged hypotony can still occasionally produce a good visual outcome.9,73
Prevention remains the best treatment for hypotony. This includes limiting the use of antifibrotic agents to patients with a low risk for developing hypotony maculopathy, using lower concentrations of these agents for shorter time periods, and conservative suture-lysis. If symptomatic hypotony does occur, the surgeon should consider early intervention and be prepared to use multiple approaches.3
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3.Nuyts RMMA, Greve EL, Geijssen HC, Langerhorst CT. Treatment of hypotonous maculopathy after trabeculectomy with mitomycin C. Am J Ophthalmol 1994;118:322–331.
CHAPTER 46 OCULAR HYPOTONY • 505
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10.Radius R, Anderson DR. Morphology of axonal transport abnormalities in primate eyes. Br J Ophthalmol 1981;65:767–780.
11.Shields M, Scroggs MW, Sloop CM, Simmons RB. Clinical and histopathologic observations concerning hypotony after trabeculectomy with adjunctive mitomycin C. Am J Ophthalmol 1993;116:673–683.
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13.Stamper RL, McMenemy MG, Lieberman MF. Hypotonous maculopathy after trabeculectomy with subconjunctival 5-FU. Am J Ophthalmol 1992; 114:544–553.
14.Singh K, Byrd S, Egbert PR, Budenz D. Risk of hypotony after primary trabeculectomy with antifibrotic agents in a black West African population. J Glaucoma 1998;7:82–85.
15.D’Erno F, Bonomi L, Doro D. A critical analysis of the long-term results of trabeculectomy. Am J Ophthalmol 1979;88:829–835.
16.Hattenhauer JM, Lipsich MP. Late endophthalmitis after filtering surgery. Am J Ophthalmol 1971;72:1097.
17.Waheed S, Liebmann JM, Greenfield DS, et al. Recurrent bleb infections. Br J Ophthalmol 1998;82: 926–929.
18.Toris C, Pederson J. Aqueous humor dynamics in experimental iridocyclitis. Invest Ophthalmol Vis Sci 1987;28:477–481.
19.Bito LZ, Camras CB, Gum GG, Resul B. The ocular hypotensive effects and side effects of prostaglandins on the eyes of experimental animals. In: Bito LZ, Stjernschntz J, eds. The Ocular Effects of Prostaglandins and Other Eicosanoids. New York: Alan R. Liss; 1989: 349–368.
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