fusions (ciliochoroidal detachment) may occur. The suprachoroidal fluid is proteinaceous and strawcolored in nature and seems to be a transudate from the choroidal vessels.36 Suprachoroidal effusions are usually visible on indirect ophthalmoscopy as smooth light brown elevations beneath the peripheral retina. The visibility of the effusions, in addition to the hypotony, differentiates this cause of a shallow or flat AC from the other possible causes. Most suprachoroidal effusions will resolve spontaneously once the hypotony is treated. Therefore, revising a trabeculectomy flap by placing additional sutures to raise the IOP is the preferable treatment. Drainage of the effusions through sclerotomies combined with reformation of the anterior chamber is to be discouraged because the effusions may recur due to continued hypotony from excess aqueous egress.

Management of this problem is discussed from the retinal viewpoint in Chapter 26.

HYPOTONOUS MACULOPATHY

Hypotonous maculopathy with concomitant decrease in visual acuity may also develop. The fundus examination in hypotonous maculopathy commonly exhibits chorioretinal folds and disk edema.36 The loss of retinal pigment epithelium and a disturbance of adjacent outer retina may occur over the crests of the chorioretinal folds. This is the probable explanation for the visual acuity loss.59 The exact amount of time and level of IOP necessary to produce hypotonous maculopathy is variable. It certainly may occur after 1 to 2 months of hypotony. Late postoperative hypotony with secondary decreased vision due to maculopathy is an indication for treatment to modify the bleb and raise IOP as outlined above. If unsuccessful, surgical bleb revision is required.

SHALLOW OR FLAT ANTERIOR

CHAMBER—OTHER CAUSES

The shallow anterior chamber is usually secondary to hypotony due to excessive aqueous egress either beneath a trabeculectomy flap or through a cyclodialysis cleft. It is not likely to occur in NPTSs because Descemet’s window is usually intact, providing resistance to aqueous outflow. Another cause of anterior chamber shallowing or flattening, although rare, is the aqueous misdirection syndrome (malignant glaucoma, ciliary block glaucoma, posterior aqueous diversion). This syndrome consists of a shallow or flat anterior chamber and elevation of IOP. It occurs typically after intraocular surgery in eyes with prior angle-closure glaucoma with a crowded anterior segment, short axial length, and nanophthalmos. It has

rarely been reported after cataract surgery and even various laser surgeries in eyes with open angles.60 The aqueous misdirection syndrome may occur in the presence of phakia, pseudophakia, or aphakia. This syndrome is unresponsive to conventional medical and surgical therapy for glaucoma, thus the name “malignant glaucoma.” The pathophysiology of this condition is unclear. The accepted theory is that aqueous is diverted and trapped in or behind the vitreous. This leads to increased pressure in the vitreous and the retrovitreal space. Forward movement of the vitreous ensues. The anterior hyaloid face comes in apposition to the lens and ciliary processes in phakia and pseudophakia, and to the iris and ciliary processes in aphakia.60 With the posterior pressure increase, the anterior chamber shallows.

The treatment for aqueous misdirection is initially medical, to which approximately 50% of patients respond within a 4- to 5-day period.60 Optimal medical therapy includes concurrent use of (1) mydriaticcycloplegic drops (2.5% phenylephine, 1 gtt (drop) q.i.d. and 1% atropine, 1 gtt q.i.d.); (2) a topical betablocker, 1 gtt b.i.d.; (3) 2-agonist (0.2% Alphagan or 0.5% Iopidine, 1 gtt t.i.d.); (4) carbonic anhydrase inhibitors (topical Trusopt or Azopt t.i.d. or Diamox 250 mg po q.i.d. or IV Diamox); and (5) a hyperosmotic agent (45% isosorbide solution, 1.5 g/kg body weight po b.i.d.; or maximum tolerated frequency, or 50% glycerin, 1 to 1.5 g/kg body weight po b.i.d.; or maximal tolerated frequency, or 20% mannitol solution IV, 2 g/kg body weight qd or b.i.d.).60

The remaining 50% of patients who do not respond to medical treatment require surgical treatment. This includes one or more of the following: (1) argon laser treatment of ciliary processes, if visible;

(2) YAG laser disruption of the anterior vitreous face in pseudophakes and aphakes; (3) Chandler’s vitreous operation (which involves disruption of the anterior hyaloid face with an 18-gauge needle and removing 1.0 to 1.5 mL of fluid from the vitreous cavity); or (4) Chandler’s vitreous operation using an automated vitrectomy unit.60

Other causes of anterior chamber shallowing or flattening must be ruled out prior to making a diagnosis of aqueous misdirection syndrome. The differential diagnosis will include excess aqueous egress due to overfiltration or a cyclodialysis cleft, pupillary block, suprachoroidal effusion, and suprachoroidal hemorrhage.

Another cause of shallowing of the AC is pupillary block. When pupillary block occurs aqueous cannot pass from the posterior chamber to the anterior chamber. This can occur due to apposition of the iris and lens (crystalline or pseudophakic), iris and vitreous (aphakes), or because of posterior synechiae. It is differentiated from aqueous misdi-

rection by visualizing bulging of the iris. Moreover the central AC depth may be shallower in aqueous misdirection compared with pupillary block. This is due to the posterior flow of aqueous into the vitreous, which will push the iris-lens diaphragm anteriorly. In pupillary block, only the iris is bowed forward (iris bombe) and the lens remains relatively stationary, creating a relatively deeper central AC. A laser peripheral iridectomy will cure pupillary block but not aqueous misdirection.

CYCLODIALYSIS

A cyclodialysis is a separation between the ciliary body and the scleral spur. It allows aqueous to flow from the anterior chamber into the supraciliary/ suprachoroidal space, greatly increasing the uveoscleral outflow.61 The size of the cyclodialysis does not necessarily correlate with the level of hypotony and even a tiny cleft can result in profound hypotony.

A cyclodialysis may occur inadvertently at the time of cataract or glaucoma surgery. It may also occur from ocular trauma. In the past cyclodialysis surgery was performed to treat glaucoma. This has been generally abandoned due to the inability to titrate the final IOP. Even though an inadvertent cyclodialysis rarely occurs, it is more likely to occur with trabeculectomy surgery than it is with NPTS. NPTS is less invasive and does not usually involve a primary entrance into the anterior chamber with manipulation of the uvea. It is, however, a diagnosis that must be considered when a patient has persistent hypotony after surgery.

The diagnosis of a cyclodialysis cleft may be difficult to make because the low eye pressure causes the cornea to deform when a gonioscopy lens is applied. This makes it difficult to visualize the cleft. Filling the anterior chamber with viscoelastic will firm the eye and may allow the cleft to be visualized. Another diagnostic modality that may be helpful in identifying a cleft is ultrasonic biomicroscopy.62 Finally, the injection of fluorescein into the anterior chamber may be seen escaping from a supraciliary sclerotomy placed over an existing cleft.63 In the posttrabeculectomy patient, a clue in distinguishing a cyclodialysis cleft from excessive filtration as the cause of hypotony is the lack of a bleb when a cleft is present. Assuming there is no conjunctival wound leak, excessive outflow of aqueous beneath the trabeculectomy flap will create an elevated bleb.

Spontaneous closure seldom occurs after 6 weeks.64 A cyclodialysis cleft that is causing hypotonous retinopathy should be treated. Closure of a cleft may be achieved with various techniques. Rarely a cleft may close spontaneously by using topical atropine. This is thought to relax the ciliary muscle,

bringing it in closer proximity to the sclera. Promoting inflammation through discontinuation of topical steroids may be helpful.59 Argon laser photocoagulation is probably the next least invasive modality. This has been used successfully by Ormerod and coworkers.59 It is necessary to use viscoelastic in the AC to firm the eye, and pilocarpine 2% to maximally open the cleft, before proceeding with the laser therapy of both the internal sclera and the ciliary body.59 If this is not successful in closing a cleft, other modalities include suturing of the detached ciliary body to sclera under direct visualization,65 or indirectly with McCannel retrievable sutures,66 transscleral cryotherapy,67 ciliochoroidal diathermy,68 and temporary anterior scleral buckling procedures.69

FAILURE OF TRABECULECTOMY

OR NPTS

TRABECULECTOMY

Failure of a trabeculectomy or NPTS may be categorized as early (within the first month) or late. Late failure implies that adequate IOP control existed for the first month. Early failure is usually manifested by a flattened, hyperemic bleb associated with a high IOP. It may be due to blockage of the sclerostomy, a tight scleral flap, or subconjunctival/episcleral fibrosis. Early recognition of a failing trabeculectomy may enable intervention and salvage of the procedure.

Topical corticosteroids have been shown to increase the success rate of glaucoma filtering surgery70 and are routinely used 6 weeks to 2 months after surgery. However, the optimal length of treatment with corticosteroids is not known.46 My approach is to continue corticosteroids on a tapering schedule, until the conjunctival and episcleral hyperemia has subsided. This is often 2, and sometimes 3, months.

If early failure of a trabeculectomy is due to blockage of the sclerostomy by iris, viewed gonioscopically, Nd:YAG laser pulses delivered to the anterior edge of the fresh synechiae may relieve the blockage. This same procedure is sometimes necessary after NPTS especially if there is a rent in Descemet’s window at the time of surgery. If this is unsuccessful in relieving the synechiae, then internal revision may be undertaken. This is done by filling the AC with viscoelastic and placing a cyclodialysis spatula through a paracentesis incision to manually relieve the iris adhesion. Treatment with pilocarpine 2% q.i.d. followed in 10 minutes each time with neosynephrine 10% may keep the iris maximally taut and prevent recurrence of synechiae.

If early failure of a trabeculectomy is due to a tight scleral flap, release of an externalized releasable suture or laser suture lysis is indicated. Only one suture should be removed or lysed at a time. This is essential if antimetabolites have been used because excess aqueous egress with ensuing hypotony may result. If mitomycin-C was used, suture removal or lysis may produce a pressure-lowering effect months after the surgery. If, however, suture release or removal does not lower IOP, fibrosis of the flap-bed interface is probably present. Early closure of a sclerostomy opening due to fibrosis may sometimes be reversed with Nd:YAG laser pulses applied through a gonioscopy lens.

If postoperative IOP in not adequately lowered, but it appears that some degree of episcleral/conjunctival fibrosis is present, subconjunctival injections of 5 mg aliquots of 5-fluorouracil (5-FU) up to a total of 105 mg 71 may be beneficial. This may create a more succulent bleb having a larger surface area. Although these injections were originally described as being given 180 degrees from the operative site,71 the author has found no adverse outcome from giving the injections adjacent to the bleb. Additionally, during the injection there is the benefit of being able to perforate newly forming fibrous tissue in the bleb wall with a 30-gauge needle. 5-FU may be used postoperatively even if mitomycin-C is used at the time of the trabeculectomy. The number of 5-FU injections that can be given is usually limited by the onset of corneal toxicity. The success of deep sclerectomy surgery is dependent on bleb formation, and therefore postoperative 5-FU injections may be beneficial in the early postoperative period.

Late failure of a trabeculectomy may be due to either subconjunctival/episcleral fibrosis or closure of the sclerostomy or a combination of both. The subconjunctival/episcleral fibrosis may be treated with needling using a 27or 30-gauge needle with or without 5-FU72,73 (Fig. 27–7) or mitomycin-C.74 The needle may also be cautiously slid under the scleral flap to lyse fibrous tissue in the sclerostomy. The technique for needling failing filtering blebs is described in Table 27–2.46 Nd:YAG75 and argon76 lasers may also be used transconjunctivally to treat some cases of bleb failure due to subconjunctival/episcleral fibrosis.

In late failing blebs, where obstruction to the sclerostomy is thought to be the etiology for failure, internal revision of the sclerostomy may be performed with argon77 or Nd:YAG78 laser application or with an older technique utilizing a goniotomy needleknife blade via a transanterior chamber approach.79 External revision of an obstructed sclerostomy, using a holmium laser via a subconjunctival approach, is another treatment option.80 If a sclerostomy cannot be salvaged, another glaucoma surgery, at a different site, may have to be considered.

FIGURE 27–7 Photograph of the needling of an encysted bleb with a 27-gauge needle. It is important to puncture the fibrous wall of the bleb multiple times with a forward and backward motion of the needle rather than a side-to-side motion.

NPTS

Early and sometimes late failure of a NPTS may be due to lack of drainage through Descemet’s window. This may be remedied by performing a YAG laser goniopuncture through Descemet’s window.19,21 This procedure is similar to performing a YAG posterior capsulotomy. Alternatively, if this were thought to be the cause of early failure of a viscocanalostomy operation, surgical revision could be performed by raising the superficial flap and making microperforations in Descemet’s window. This may be less inflammatory than YAG goniopuncture and may cause less of a chance for bleeding from the angle.26 Early failure of a viscocanalostomy may also be due to blockage in Schlemm’s canal or ostia. To differentiate blockage in Schlemm’s canal from poor percolation of aqueous through Descemet’s window, while observing the angle gonioscopically, a Valsalva maneuver is executed.26 If Schlemm’s canal is patent, reflux of blood will be seen in the canal and in the

TABLE 27–2 THE TECHNIQUE FOR NEEDLING A

FAILING FILTERING BLEB

The procedure can be done at the slit lamp or in the operating room

Topical anesthesia (e.g., proparacaine 0.5%) is used; a cotton pledget soaked in anesthetic can be applied to the area of injection; topical phenylephrine 2.5% or apraclonidine 0.5% can be used to vasoconstrict the conjunctival vessels (optional)

A topical antibiotic is used; alternatively, povidone-iodine 50% solution can be applied to the conjunctiva, eyelid margins, eyelashes, and eyelids

A lid speculum is used

On a tuberculin syringe, a 30or 27-gauge needle penetrates the conjunctiva 5 to l0 mm from the sceral fistula (through conjunctiva not treated with an antifibrosis regimen)

Balanced saline solution (or lidocaine) can be injected to raise the conjunctiva (optional)

The needle is then advanced into the bleb cavity and beneath the scleral flap; a sweeping motion or to-and- fro movements are made with the edge or the tip of the needle, respectively

Aggressive alternative: the needle can be advanced through the internal ostium until the needle is visualized in the anterior chamber (This procedure should be done with extreme caution in phakic eyes)

The end point is elevation of the bleb and intraocular pressure reduction

subscleral reservoir. Conversely, if no blood is seen, blockage in Schlemm’s canal or ostia is implied. This can sometimes be remedied by lifting the superficial flap and removing fibrous tissue from the base of the subscleral reservoir and ostia to Schlemm’s canal.26 Patency of Schlemm’s canal is then demonstrated by injecting saline and seeing blanching of the episcleral vessels. Stegman is experimenting with placing polyamide implants into the ostia to function as stents and to maintain patency.26

SYMPTOMATIC FILTERING BLEBS

Filtering blebs are usually fairly well tolerated. However, many patients have some degree of discomfort or foreign body sensation. These symptoms are usually associated with large blebs that are elevated or overhang the cornea. Symptomatic patients usually show signs of superficial punctate keratopathy or dellen formation. In addition, patients with large overhanging blebs may have visual complaints including blurriness of vision, loss of vision or visual field, or monocular diplopia.46

Treatment for discomfort includes artificial tears and ointments. If lubricants are not sufficient, symptoms due to large, elevated blebs can be diminished

or eliminated by shrinking the bleb size with various modalities. These include chemical irritant therapy with silver nitrate or trichloroacetic acid,46,49 argon laser,81 thermal Nd:YAG laser,51 cryotherapy,52 diathermy, and cauterization.46,82 Remodeling of a bleb may cause an increase in IOP. If these more conservative therapies are not successful, surgical excision or revision of a bleb may be tried. This may also compromise the IOP. Large blebs that overhang the cornea lie on the corneal surface rather than dissecting into the corneal tissue planes.46 Therefore, overhanging blebs can be bluntly dissected off the corneal surface and the excess excised with a cut parallel to the limbus.46,83 Usually, there is little or no leak after this overhanging bleb excision.46 Symptoms due to a large nasal bleb may sometimes be alleviated with a medial tarsorrhapy.46 This may cause remodeling of the bleb such that it will shift superiorly over a 1- to 2-month period. Then the tarsorrhapy may be reversed.46

BLEBITIS AND ENDOPHTHALMITIS

Bleb-associated endophthalmitis can be a devastating complication of filtration surgery. Factors that are thought to be associated with an increased risk of infection after filtering surgery are the use of 5-FU84 and mitomycin-C,85 inferior location of the filtering bleb,84 thin-walled blebs,86 bleb leaks,84 bleb manipulation and trauma,87 use of contact lenses,87 external disease including conjunctivitis,88 blepharitis87 and nasolacrimal duct obstruction,88 releasable sutures,89 upper respiratory infection,90 and systemic diseases that predispose to infection such as diabetes mellitus and AIDS.

Symptoms of blebitis and bleb-associated endophthalmitis may include foreign-body sensation, ocular pain, photophobia, tearing, and blurred or decreased vision. Signs of blebitis include a milkywhite appearance to the bleb with conjunctival and episcleral injection prominent in the region of the edge of the bleb. A pseudohypopyon may be present within the bleb as well as a purulent conjunctival discharge. Chemosis, corneal edema, anterior chamber cell and flare, keratitic precipitates, and hypopyon may be present. The anterior chamber may be deep with normal or elevated IOP, or shallow/flat with hypotony due to a bleb leak. As the infection progresses posteriorly, the vitreous will eventually become cloudy with inflammatory debris.

The most common organisms to cause blebitis and bleb-associated endophthalmitis are Streptococcus species, Haemophilus influenzae, and Staphylococcus species.46,84,85 Bacteria that cause blebitis and bleb-associated endophthalmitis probably arise from the ocular surface, but cultures of the ocular surface