Fig. 36-14  Dellaporta technique – B. After a water-tight closure of the conjunctival wound (e.g., using 9-0 Vicryl suture), a dependent bleb forms from the persistent egress of fluid through the 1-mm trephine hole. Uveal prolapse is rarely seen, and the drainage of fluid, activated by the extraocular movements, can sometimes persist for several days, thus reducing the tendency for recurrent accumulation of suprachoroidal effusion.

(From Lieberman MF: Complications of glaucoma surgery. In: Charlton J, Weinstein G, editors: Ophthalmic surgery complications, Philadelphia, Lippincott-Raven, 1995.)

visual acuity. However, over three-quarters of phakic eyes developed cataracts within the first year, a complication worth explaining during informed consent.35

Flat anterior chamber in normotensive and hypertensive eyes

Normal or elevated IOPs with a flat anterior chamber indicate that excessive filtration is not the cause of the flat chamber. The flat anterior chamber in such eyes is caused by increased volume or pressure behind the lens–iris diaphragm. Four mechanisms need to be methodically considered: (1) pupillary block with an incomplete iridectomy; (2) expansion of the choroid or enlargement of the suprachoroidal space by blood or effusion; (3) an increase in vitreous volume caused by blood or effusion, or (4) the misdirection of aqueous. If an iridectomy is not present or conclusively patent, one should be created immediately either by laser or, if necessary, incisional surgery.

If a patent iridectomy exists, there are two common causes of flat chamber with normal or high IOP after glaucoma surgery: ciliary block (e.g., aqueous misdirection syndrome, malignant glaucoma) and suprachoroidal hemorrhage (SCH).

Ciliary block (malignant glaucoma)

The term ciliary block or malignant glaucoma refers to a spectrum of atypical angle-closure glaucomas that share several essential features.36 Other terms have been proposed for this condition, many of which purportedly point to the underlying pathophysiology. These terms include aqueous misdirection, hyaloid block glaucoma and posterior

aqueous entrapment. Historically this condition was commonly appreciated as a complication of a filtering procedure in eyes with preexisting angle-closure glaucoma or shallow anterior chambers (See Ch. 16 - Secondary Angle-Closure Glaucoma.)

There is good agreement in the literature about several essential features of this condition, but other features are more controversial. Clinically, ciliary block glaucoma is suspected in the presence of a grade 2 or 3 shallow chamber, with the prominent shallowing of the peripheral and central anterior chambers simultaneously.The pressure is usually higher than expected: in the early postoperative period it may simply be between 15 and 20 mmHg despite the appearance of what would seem to be an otherwise adequate bleb; in other cases the pressure can be quite high indeed.

To diagnose ciliary block glaucoma, it is essential to eliminate the possibility of pupillary block; hence a patent iridotomy must be established before this diagnosis can be considered. Sometimes the diagnosis is made only in retrospect, after evaluating the eye’s response to several interventions. For example, cycloplegics can be curative of malignant glaucoma and miotics can be exacerbative. If surgical intervention is necessary, disrupting the hyaloid face or collapsing the vitreous is usually curative.

Other aspects that are sometimes seen with ciliary block glaucoma include the rarity of spontaneous resolution – and hence its ‘malignant’ designation. It is usually bilateral in predisposition, and it is often worsened by conventional glaucoma surgery such as iridectomy or filtration procedures.The clinical presentation of ciliary block glaucoma is similar to that of other conditions, notably angleclosure glaucoma with ciliary choroidal detachment.37 For exam-

ple, some authors have observed the accumulation of fluid in the suprachoroidal space in some cases of ciliary block glaucoma,36,38

and this has been confirmed by ultrasonic biomicroscopy.39 Other situations that may overlap with the appearance of ciliary block glaucoma include eyes that have undergone cataract extraction, with or without lens implantation, with sequestration of aqueous behind the iris plane. These conditions have been referred to as ‘iridovitreal block’40 and ‘retrocapsular aqueous misdirection.’41

The pathophysiologic sequence of ciliary block glaucoma is thought to be as follows.42,43 After some initiating event (e.g., shal-

lowing of the chamber during trabeculectomy) there is cause for misdirection of the aqueous to circulate into or behind the vitreous body.This apparently leads to an alteration of the vitreous volume and its compaction, with a cycle of increasing vitreous swelling and reduced conductivity of aqueous anteriorly. (A recent model proposes that choroidal expansion, suspected as an initiating event in acute angle-closure glaucoma, may also be a contributory event for anterior vitreal movement in malignant glaucoma, and hence the clinical association of the two disorders.44) The enlarging vitreous body is unable to exchange aqueous across the hyaloid face at the junction of the zonules, vitreous face, and ciliary processes.This progressive vitreal engorgement results in shallowing both axially and peripherally in the anterior chamber, with increasing apposition of the peripheral iris into the angle, setting up a further cycle of angle-closure glaucoma.

The management of ciliary block glaucoma is straightforward. It is important to eliminate the possibility of pupillary block glaucoma by verifying or creating a patent iridotomy. Miotic medications should be discontinued, and vigorous cycloplegia as well as the use of topical steroids should be instituted. Other agents to reduce aqueous production, such as topical -agonists or -blockers, carbonic anhydrase inhibitors, or osmotic agents, can be used to reduce the pressure. A waiting period of approximately 5 days has been advised

Fig. 36-15  Phakic malignant glaucoma. With the sequestration of aqueous within the vitreous body, there is compression of the anterior chamber both axially and peripherally (arrows), causing central shallowing of the chamber with forward movement of the lens and peripheral angle closure.

(From Lieberman MF: Complications of glaucoma surgery. In: Charlton J, Weinstein G, editors: Ophthalmic surgery complications, Philadelphia, Lippincott-Raven, 1995.)

Fig. 36-16  Capsular malignant glaucoma. In the presence of a posterior capsule with a posterior chamber intraocular lens there are multiple sites in which aqueous can be sequestered, and these sites must be sequentially eliminated: (A) aqueous pockets between the iris and anterior capsule;

(B) pockets within the capsular bag and lens implant; (C) pockets between the posterior capsule and hyaloid face, and (D) aqueous trapped within the vitreous cavity behind an intact hyaloid face.

(From Lieberman MF: Complications of glaucoma surgery. In: Charlton J, Weinstein G, editors: Ophthalmic surgery complications, Philadelphia, Lippincott-Raven, 1995).

with this intensive medical regimen to see if there is resolution, with as many as half of the cases resolving during this interval.45

In the event that surgical intervention is necessary, either a needle aspiration of vitreous through the pars plana46 or pars plana vitrectomy47 will usually be curative in phakic eyes (Fig. 36-15). Eyes that have cataract extraction – with or without a lens implant – and a retained posterior capsule offer a less complicated intervention: direct incision of the hyaloid face using the neodymium: yttrium-aluminum-garnet (Nd:YAG) laser.48,49 In this presentation with a retained posterior capsule (Fig. 36-16), it is necessary to sequentially eliminate pupillary block, retrocapsular block, and hyaloid block by respectively lasering through the iris, posterior capsule, and hyaloid face.36 In the acapsular eye (e.g., aphakia) (Fig. 36-17), hyaloidectomy centrally and peripherally can be undertaken with the Nd:YAG laser or with incisional surgery.

Vigorous surveillance is still necessary in these eyes because recurrent cases of ciliary block glaucoma have been reported, especially after vitreous aspiration or vitrectomy, which may not have been sufficiently anterior in the phakic eye to interrupt the obstruction of the hyaloid face. In rare cases, it is necessary to

Fig. 36-17  Acapsular malignant glaucoma. In the absence of a posterior capsule – such as aphakia or, as seen here, an anterior chamber intraocular lens – the abnormal vitreous forces compress the anterior chamber axially and peripherally (arrows), but the abnormal hyaloid surface is accessible to laser or incisional surgery.

(From Lieberman MF: Complications of glaucoma surgery. In: Charlton J, Weinstein G, editors: Ophthalmic surgery complications, Philadelphia, Lippincott-Raven, 1995.)

sacrifice the lens to access the hyaloid itself. Chronic atropine drops may be needed, and great attention should be paid to the fellow eye, which is at a high risk for recapitulating the events of the first eye’s ciliary block glaucoma attack.

Suprachoroidal hemorrhage (sch)

Fortunately, SCH after glaucoma surgery is rare.50 It occurs more commonly in traumatized eyes, in aphakia, in vitrectomized eyes, and in large eyes with pathologic myopia or congenital glau- coma.51–58 Patients taking systemic anticoagulants and eyes with significant post-operative hypotony are also at higher risk.59 In a large prospective study of antimetabolite usage,60 there was a remarkably strong association between the appearance of SCH and the preoperative IOP level. Among the patients with IOPs under 30 mmHg, there was no incidence of SCH; the incidence of SCH was 6% in eyes with IOPs between 30 and 39 mmHg and 11% in eyes with IOPs of 40–49 mmHg; and in three patients with IOPs over 50 mmHg the incidence of SCH was nearly 20%. A different analysis using a case-control methodology also identified the risk factor of elevated IOP and specifically called attention to the greater risk for SCH in the presence of an axial length greater than 25.8 mm.61 Suprachoroidal hemorrhage can appear after virtually any glaucoma operations, with or without antimetabolites; there may be a higher frequency following glaucoma shunt procedures.59

It is rare for a hemorrhage to occur during surgery in the phakic eye. More commonly, the patient experiences a sudden, severe pain accompanied by sudden loss of vision during the first 4 or 5 postoperative days. If the hemorrhage is severe, the pressure may be quite high and the patient may have nausea and vomiting.

If aqueous suppressants and hyperosmotic agents fail to lower the IOP, the hemorrhage may require drainage. Four to five days are usually necessary for a clot to lyse in the suprachoroidal space.Therefore, if drainage can be delayed for that period of time, drainage will be more easily accomplished through a posterior sclerostomy placed directly over the area of elevated choroid.

If pain and pressure cannot be controlled or the pressure elevation is very high, earlier drainage is required. In such cases, the clot will not have lysed, so a large scleral incision (possibly as large as 10–12 mm) may be required for the clot to slide out of the suprachoroidal space.62

The sclerotomy incision should be placed near the center of the choroidal elevation as determined visually or by ultrasound. If the clot has not lysed, it may have the appearance of choroid.The surgeon should not try to pull the clot from the wound with an instrument but rather express it with gentle pressure while gradually enlarging the sclerostomy site as needed.

If the clot has lysed, a 2-mm sclerostomy is usually adequate to allow the escape of the xanthochromic fluid followed by the black ‘sludge’ of the clot. Balanced salt solution (BSS), air, or viscoelastic can be injected gently to re-form the anterior chamber via a paracentesis opening63; or, as with re-formation of flat anterior chambers, an anterior chamber maintaining device is helpful to prevent intraoperative hypotony. Maintenance of high-normal IOP helps force more of this dissolved clot out through the sclerotomy opening. It is helpful to inject viscoelastic into the anterior chamber at the conclusion of the procedure to maximally maintain ocular integrity, and to allow the eye to run pressures in the 25–35- mmHg range a few days before intervening medically.

The goal of this surgical intervention is to allow the blood residue to escape from the suprachoroidal space while restoring the normal intraocular relationships. Every effort should be made to prevent choroidal injury, which might cause blood to get into the vitreous cavity where it promotes inflammation and scarring.

In aphakia, the choroid and often the retina are pushed so far forward that they present in the pupillary space. Immediate attention is warranted for such eyes. Air, fluid, and intraocular gas have been used to push the choroid and retina back after a pos-

terior sclerostomy has allowed evacuation of the suprachoroidal

blood.56,57,63–65

If there is no extrusion of intraocular contents other than aqueous and liquified vitreous, if blood does not break through into the vitreous cavity, and if high IOP is not sustained, the prognosis for these eyes is reasonably good, with visual recovery in the majority of cases. Outcome is usually favorable in eyes with focal SCHs or if surgical drainage is undertaken within 14 days.54 Prognosis is par-

ticularly poor if there is concomitant retinal detachment or a 360° SCH.66

Postoperative SCH seems to occur most often in aphakic eyes with other pathology. The vitreous is often synergetic. In a hypotonous eye with little resistance to outflow through a glaucoma filtration site, liquified vitreous offers an insufficient tamponading effect to prevent expansion of the hemorrhage. Thus in such eyes, more secure closure of the guarding scleral flap may increase this resistance and reduce the likelihood of hypotony. After a few days, when inflammation from the surgery has subsided and the conjunctiva has healed enough to offer some resistance to the aqueous outflow, the scleral flap sutures can be lasered transconjunctivally to increase the scleral opening. Re-formation of the chamber with a viscoelastic substance also increases the resistance to expulsion of the intraocular contents and should be considered in high-risk eyes.

Intra-operative expulsive SCH is rarely seen in eyes undergoing glaucoma surgery. If it does occur, the limbal incision must be closed instantly and a posterior sclerotomy performed immediately over the presumed site of bleeding to allow the blood to escape from the suprachoroidal space without causing extrusion of intraocular contents or bleeding into the vitreous cavity. An anterior chamber maintainer can be inserted to maintain control of IOP. If the hemorrhage is small, it may not be located easily and therefore will be impossible to drain. In the phakic eye, it will absorb enough to allow the chamber to form, usually in 1–2 days (Fig. 36-18).

Fig. 36-18  Self-limited intraoperative subchoroidal hemorrhage below the inferior temporal arcade during trabeculectomy. This absorbed spontaneously.

(Photo courtesy of Douglas Day, MD, Atlanta.)

Intraoperative flat anterior chamber

Anterior chamber flattening during glaucoma surgery may occur from causes other than suprachoroidal hemorrhage (Table 36-1). In Sturge-Weber syndrome or other glaucomas with elevated venous pressure, lowering the IOP at surgery may cause immediate expansion of a choroidal hemangioma with both suprachoroidal and subretinal effusion.67 This has been noted in approximately 20% of such cases and appears to be more common in the more severely involved side of bilateral cases.68,69 A posterior sclerotomy may allow suprachoroidal effusion to escape and may resolve the problem (as in nanophthalmos).68

Sometimes, however, intrachoroidal expansion of the hemangioma occurs, and a posterior sclerotomy will reveal only the choroid, even when it is placed over the apparent mass. It is imperative that this choroid not be penetrated because it will result in massive hemorrhage and probable loss of the globe. Instead, the surgeon should close the trabeculectomy site and wait.

After a few days, as the IOP returns to preoperative levels, the anterior chamber will re-form and the choroidal mass will subside. This phenomenon probably results from arteriolar communications to the choroidal hemangioma. When IOP falls below the arteriolar pressure level of approximately 30 mmHg, there is not enough resistance to keep the hemangioma from expanding, creating a serious dilemma for both the surgeon and the patient (see the section on Sturge-Weber syndrome in Chapter 19.) In all such high-risk surgeries, the anterior chamber maintainer is invaluable.

Ciliary block glaucoma may occur during surgery when saline injected into the anterior chamber is inadvertently diverted into the vitreous cavity and the chamber becomes shallow while the eye becomes firm. One may close the trabeculectomy flap securely and try to re-form the chamber through a paracentesis opening. If this fails, 0.5–1.0 ml of liquified vitreous should be removed through a sclerostomy positioned 3 mm posterior to the limbus. If the chamber then cannot be re-formed with saline, viscoelastic substance or a large air bubble should be placed into the anterior chamber to maintain it. Atropine and topical steroids should be