Glaucoma filtering surgery is fraught with various complications for the simple reason that it is designed to interrupt the integrity of the globe. In all other intraocular procedures, ophthalmologists try to restore the ocular compartments to prevent hypotony or the extrusion of intraocular contents or fluids. The goal in glaucoma surgery, however, is just the opposite. The globe is left in a non-physiologic state, which can result in the many complications described in this chapter.
BUTTONHOLING THE CONJUNCTIVA
Tiny inadvertent perforations of the conjunctival flap are often overlooked until the procedure is completed. In guarded filters, such as trabeculectomy, small perforations (e.g., from a suture needle) usually heal spontaneously, even in the presence of antimetabolites, within 24–72 hours by simply withholding steroid drops; subconjunctival Healon-5 can be used to retard the flow of such leaks and facilitate healing. Focal perforations 1–2 mm in size should be closed with a 10-0 nylon suture on a microvascular tapered needle (e.g., Ehicon BV100), using a mattress or purse-string closure. For large perforations, it may be necessary either to prepare a relaxing incision near the fornix that allows anterior sliding of fresh conjunctiva toward the limbus or to procure a piece of Tenon’s capsule from a remote site and incorporate it into the closure ( Fig. 36-1 ).
If the buttonhole exists at the limbal junction during a fornix-based flap procedure, a peritomy can be performed and the conjunctiva advanced and sutured directly to the corneoscleral junction or into a corneal groove ( Fig. 36-2 ). If the buttonhole is noted in friable conjunctival tissue before the creation of the sclerostomy, a new site may be selected for the procedure.
Because of the possibility of inadvertent buttonholes, some physicians defer applying antimetabolites until the conclusion of surgery, before the conjunctival closure. They assess conjunctival integrity at the conclusion of the operation and then apply cellulose sponges saturated with either 5-fluorouracil (5-FU) or mitomycin-C on top of the trabeculectomy flap before the final conjunctival closure. If a Seidel-positive leak is seen from the buttonhole in the postoperative period, subconjunctival injections of 5-FU can be deferred until the leak closes.
Postoperatively, it is useful to distinguish between point leaks (seen in 2% of eyes at 3 months following either 5-FU or mitomycin-C filtration surgery) and transconjunctival aqueous oozing (seen in 12% of eyes, especially in large avascular areas, and following digital massage). Often such defects can be carefully monitored and/or treated prophylactically with antibiotic drops, with the vast majority spontaneously resolving (and often benignly recurring.) Recurrent leaks have a higher association with blebitis or endophthalmitis. Patients, of course, need to be alerted to the symptoms of early infection, so as to seek immediate medical attention.
THE SHALLOW AND FLAT ANTERIOR CHAMBER
The appearance of the eye in the first days after filtering surgery depends on many variables, not all of which can be controlled. Although it is customary to conclude a filtration procedure after ascertaining that the chamber is formed and a bleb is present, it is not uncommon to find that the appearance has changed 24 hours later. The depth of the chamber and the extent of the bleb will depend on several factors, including whether a full-thickness or guarded procedure (trabeculectomy) was performed, the tightness of the scleral flap, the firmness of the eyepatch, the use of antimetabolites at the time of the surgery, and the use of intracameral viscoelastics.
The clinical classification of shallow chambers popularized by Spaeth is particularly useful in the postoperative management. In grade 1 ( Fig. 36-3 ), the anterior chamber is peripherally flat, with the peripheral iris and cornea touching but with preservation of the anterior chamber in front of the pupillary space. In the grade 2 shallow chamber ( Fig. 36-4 ), there is greater apposition between the mid iris and the cornea, but some space between the anterior surface of the lens (or vitreous) and the cornea in the pupillary region is retained. For daily reference, it is useful to estimate the actual depth of the small, central chamber in terms of how many ‘corneal thicknesses’ there are between the cornea and the pupillary plane. The grade 3 anterior chamber ( Fig. 36-5 ) is truly flat, with complete contact of the iris and the pupillary space with the posterior surface of the cornea ( Fig. 36-6 ).
The most important determination after classifying the chamber depth is to determine whether the intraocular pressure (IOP) is either higher than expected or excessively low in conjunction with one of these three configurations of shallow chamber. By and large, grades 1 and 2 will almost always reverse spontaneously with time, responding to moderate intervention such as atropine cycloplegia. The grade 3 flat chamber is a ‘medical urgency,’ which requires frequent monitoring and possible surgical intervention (e.g., choroidal drainage) if not spontaneously resolved within a short period (3–7 days).
FLAT ANTERIOR CHAMBER WITH HYPOTONY
Hypotony with a flat anterior chamber after filtration surgery most commonly results from overfiltration or bleb leaks; it is very often seen in the first few days after full-thickness surgery. As many as one-third of trabeculectomies show an IOP (less than 8 mmHg) near the hypotonous range for as long as 2 weeks postoperatively. However, low IOP in the first postoperative weeks does not correlate with poor IOP control later.
Immediate postoperative hypotony is often accompanied by choroidal effusions or detachment. Such effusions can appear as either a low, annular detachment – sometimes appreciated only because of the ease with which the ora serrata is visualized – or as large choroidal effusions that may compromise the visual axis when two detachments ‘kiss’ in the midvitreal cavity. In a national survey of complications of glaucoma surgery among 1240 cases performed throughout the United Kingdom, early complications included hypotony (24%), wound leak (18%), and choroidal detachment (14%). These arose independent of whether the surgeon was a subspecialist or performed glaucoma surgery frequently; they bespeak of common intraoperative or postsurgical events in glaucoma surgery. A not dissimilar pattern of events was reported in the United States.
The choroidal detachment becomes of greatest clinical concern when the anterior chamber progressively shallows over time – even progressing to a grade 3 flat chamber. If effusions are seen in the absence of a conjunctival wound leak, however, most surgeons defer any surgical intervention. Indications for surgery are usually reserved for the persistence of ‘kissing choroidals,’ in which the retinal surfaces are in contact astride large bullous choroidal detachments ( Fig. 36-7 ), or a grade 3 flat chamber with actual or potential compromise of the corneal endothelium. Shy of these two events, however, the choroidal effusions will often resolve with time, and with the use of atropine cycloplegia and steroids to reduce inflammation. One exceptional circumstance that often fails to respond to medications and requires early surgical intervention is an eye with chronic angle-closure glaucoma and an extremely shallow chamber after trabeculectomy; such circumstances predispose to aqueous misdirection (malignant glaucoma) syndrome.
A large soft contact lens, a symblepharon ring ( Fig. 36-8 ), or the Simmons shell may impede aqueous flow through the sclerostomy, encourage any buttonhole to heal, and help form the chamber sooner. Such a sequence is more likely if no intraoperative antimetabolite was used. In the event of a small wound dehiscence, either topical cyanoacrylate or tissue glue covered with a bandage contact lens (see section on Thin-Walled Blebs, p. 522–4) or a compression suture can be attempted. The compression suture is rendered by 9-0 nylon that is attached at the corneal limbus, fashioned in an X-crossing at the leak site, and anchored in episcleral tissue posterior to the edge of the bleb. It can remain for several weeks before removal.
If the lens or IOL is pushed against the cornea, the endothelium may be rapidly damaged, causing corneal decompensation. There is an increased loss of endothelial cells when the eye passes from a grade 2 to grade 3 shallowing of the chamber. In cases of truly flat grade 3 anterior chambers, an attempt to re-form the chamber at the slit lamp should be made immediately through a paracentesis, either by air or viscoelastic injection or by intraocular gas. If a paracentesis opening does not exist or cannot be found, injection with a disposable 30-gauge needle passed into the anterior chamber through the cornea ( Fig. 36-9 ) can be used.
If the injected material passes out of the eye through the sclerostomy site, as is commonly seen with full-thickness or hyperfiltrating trabeculectomy procedures, it may be necessary to return to the operating room for drainage of the suprachoroidal fluid with or without surgical modification of the filteration site. For drainage, one or more sclerostomies inferiorly are made 4 mm behind the limbus and over the pars plana; the anterior chamber is re-formed with balanced salt solution (BSS) or viscoelastic, and attempts are made to drain the suprachoroidal effusion while maintaining the chamber at as normal a depth as possible ( Fig. 36-10 ). Intraoperative hypotony can be obviated by using an intracameral maintainer device (e.g., Lewicke anterior chamber; Figs 36-11 and 36-12 ). Another drainage approach involves 1-mm trephination through the sclera, anterior to the inferior rectus muscle, which remains open for several days to allow suprachoroidal fluid to drain subconjunctivally ( Figs 36-13 and 36-14 ).
The benefits of choroidal drainage may take several months to fully manifest: in one retrospective series of 94 procedures, 60% of effusions resolved by 1 month, increasing to 90% by 4 months, accompanied by slight loss of IOP control but statistically improved visual acuity. However, over three-quarters of phakic eyes developed cataracts within the first year, a complication worth explaining during informed consent.
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, oneshould 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. 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 pre-existing 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 theperipheral 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 angle-closure glaucoma with ciliary choroidal detachment. For example, some authors have observed the accumulation of fluid in the suprachoroidal space in some cases of ciliary block glaucoma, and this has been confirmed by ultrasonic biomicroscopy. 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’ and ‘retrocapsular aqueous misdirection.’
The pathophysiologic sequence of ciliary block glaucoma is thought to be as follows. After some initiating event (e.g., shallowing 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. ) 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 α-agonists or β-blockers, carbonic anhydrase inhibitors, or osmotic agents, can be used to reduce the pressure. A waiting period of approximately 5 days has been advised with this intensive medical regimen to see if there is resolution, with as many as half of the cases resolving during this interval.
In the event that surgical intervention is necessary, either a needle aspiration of vitreous through the pars plana or pars plana vitrectomy 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. 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. 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 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. It occurs more commonly in traumatized eyes, in aphakia, in vitrectomized eyes, and in large eyes with pathologic myopia or congenital glaucoma. Patients taking systemic anticoagulants and eyes with significant post-operative hypotony are also at higher risk. In a large prospective study of antimetabolite usage, 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. Suprachoroidal hemorrhage can appear after virtually any glaucoma operations, with or without antimetabolites; there may be a higher frequency following glaucoma shunt procedures.
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.
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 opening ; 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 posterior sclerostomy has allowed evacuation of the suprachoroidal blood.
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. Prognosis is particularly poor if there is concomitant retinal detachment or a 360° SCH.
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 ).
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. This has been noted in approximately 20% of suchcases and appears to be more common in the more severely involved side of bilateral cases. A posterior sclerotomy may allow suprachoroidal effusion to escape and may resolve the problem (as in nanophthalmos).
|Young eyes usually with relatively high IOP
|Secure the wound as best possible; administer atropine
|Hemangioma (e.g., Sturge-Weber syndrome); effusion (nanophthalmos)
|Recognize choroidal elevation; secure the wound; perform posterior sclerotomy that does not perforate choroid (for drainage of subchoroidal fluid); administer atropine
|Rare in phakic eyes unless it is buphthalmic
|Recognize vitreous loss; secure the wound; perform posterior sclerotomy over choroidal elevation area to drain blood; administer atropine
|Ciliary block (malignant glaucoma)
|Absence of choroidal elevation; anterior chamber flattens and eye firms as balanced salt solution is injected into the anterior chamber
|Secure the wound; confirm the absence of choroidal expansion or suprachoroidal hemorrhage; perform vitrectomy or aspiration 3 mm posterior to the limbus; inject air into the anterior chamber; administer atropine
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 used frequently in the early postoperative period. The eye should be observed carefully for recurrence of the ciliary block if the atropine is discontinued.
Hemorrhage may accompany any intraocular procedure, particularly in the first 3–5 postoperative days. Where compatible with general health, anticoagulants which are risk factors for intraocular bleeding during surgery should be discontinued. Consultation with the patient’s provider of primary care, cardiologist, or other appropriate specialist is appropriate before discontinuing these agents. While some feel that the risks are low, studies have shown anticoagulant therapy to be a significant risk factor for intra- and post-operative bleeding ; similarly, low-dose aspirin or ginkgo biloba preparations may need to be preoperatively discontinued, although the evidence for serious bleeding difficulties while using these agents is not convincing. Bleeding is usually from the iris, anterior ciliary body, or corneoscleral wound, producing a hyphema that commonly subsides without intervention. Activities must be restricted, and a protective eye shield should be worn during the critical follow-up period. Evacuation of the hyphema is rarely necessary, unless the IOP is persistently elevated or the corneal health threatened. If the hyphema remains for several days or increases, laser photocoagulation of localized hemorrhaging in the angle or stoma site may be possible through a clear portion of the anterior chamber. Rarely, the incision area must be re-entered to apply wetfield cautery to the bleeding site. Clot lysis, with prompt resolution of the hyphema, can be effected with intracameral or subconjunctival administration of tissue plasminogen activator or urokinase.
Very rarely, the surgeon will encounter a large, clotted hyphema postoperatively. This is usually associated with some other precipitating factor such as the use of salicylates or other clotting inhibitors, trauma, inflammation, or rubeosis iridis. Its management must be tailored to the particular situation. High pressure can be relieved by periodically depressing the posterior lip of the sclerostomy or of the paracentesis incision if one exists.
Clot removal from the anterior chamber can be accomplished with a vitrectomy, but which significantly risks causing a cataract. Careful aspiration with an irrigation/aspiration unit can, in conjunction with intracameral viscoelastic for visualization, be successful. In the absence of such phacoemulsification machinery, repeated drainage and irrigation of the anterior chamber via a 2-mm paracentesis incision can also be successful. Here too the use of intracameral fibrinolytic agents (e.g., tissue plasminogen activator or urokinase) may be useful.
Late hyphema is rare; it is usually the result of a small capillary or vein in the filtration site that ruptures during a Valsalva maneuver. If the site of bleeding can be visualized gonioscopically, it can be cauterized with argon laser. Failing that, a single application of cryotherapy over the area of the bleeding site may stimulate scarring and closure of the vessel, though occasionally at the cost of scarring the filtration site.
Fortunately, infection is a rare complication after glaucoma surgery. As with any intraocular procedure, infections can occur in the early postoperative period but may also be seen months to years later when a filtering bleb is present. After filtering surgery, all patients should be thoroughly informed about the symptoms and signs of infection, including pain, reduced vision, and purulent discharge; patients should be instructed to contact an ophthalmologist immediately if these symptoms occur. Intensive self-medication with sterile antibiotic eyedrops may be begun while awaiting ophthalmologic evaluation. If infection is even suspected, smears and cultures should be obtained from the lids, conjunctiva, and filtering bleb.
The presence of a thin-walled bleb in general and of antimetabolite use in particular are major risk factors for intraocular infection. Other risk factors include myopia, thin-walled blebs with leaks, the presence of releasable sutures, concurrent upper respiratory infection, and blebs located at the inferior limbus. Onset of infection can be anywhere from the first few days to up to 20 years later. Other risk factors include unguarded filtration surgery, intermittent postoperative use of antibiotics, and diabetes mellitus.
Both of the most commonly used antimetabolites, mitomycin-C and 5-FU, have seemingly increased the frequency of postoperativeendophthalmitis – to estimates as high as a 2.0% incidence. In one study, following a primary trabeculectomy with 5-FU or mitomycin-C, the 5-year probabilities for postoperative complications of bleb leak, blebitis, and endophthalmitis were 18%, 6%, and 7.5% respectively. The morbidity of such infection can be appallingly high: nearly one-third of eyes following filtering surgery and treated for bacterial endophthalmitis with intensive medical treatment were at no light perception (NLP) at 1 year following infection. Positive bacterial cultures carried a worse visual prognosis.
An important distinction has been made between bacterial infection confined to the bleb with limited anterior chamber reaction (‘blebitis’) and infection that penetrates into the vitreous cavity (classic endophthalmitis). Blebitis is more likely to respond promptly to intensive antibiotic treatment; it can be treated in an outpatient setting ; and it has a more favorable visual outcome than does diffuse intraocular infection. Nevertheless, bouts of blebitis may be prodromal to frank endophthalmitis. Staphylococcus and Streptococcus species account for approximately half of the culture-positive organisms.
When hypopyon is present, fluid for culture should be obtained from the anterior chamber and vitreous. Antibiotics should be initiated while the specific causative organism is determined at the laboratory. Frank endophthalmitis usually requires aggressive vitrectomy with intracameral antibiotics (± steroids).
Prevention of such a devastating complication is problematic. Even the role of postoperative antibiotics in preventing endophthalmitis following routine cataract surgery has not yet been definitively established; nevertheless such usage remains common standard practice for nearly all intraocular surgeries. The importance of patient awareness cannot be stressed enough: to detect new and unusual symptoms, to promptly seek medical attention, and to initiate antibiotic drops if a delay is encountered being seen by an ophthalmologist.
Sympathetic ophthalmia may arise 2 weeks to many years after any form of intraocular surgery, but it is more common after procedures that involve intentional or unintentional incarceration of the iris or ciliary body (e.g., following vitrectomy or cataract surgery or after ciliary body destruction with either cryotherapy or transcleral laser. An incidence of 0.08% has been estimated after glaucoma operations.
Although rare, sympathetic ophthalmia is severe enough that ophthalmologists should be alerted to its symptoms and signs to make the diagnosis. Symptoms and signs include photophobia, blurred vision, and redness first in the traumatized eye and then in the fellow eye. Keratitic precipitates, iris nodules, and anterior chamber flare and cell are part of the granulomatous uveitis. Dalen-Fuchs nodules form in the peripheral fundus and appear ophthalmoscopically as yellow-white spots. Fundus fluorescein angiography has characteristic patterns that establish the correct diagnosis. A thorough evaluation is advised to establish the correct diagnosis, which then requires aggressive immunosuppressive therapy, atropine, and possibly enucleation of the exciting eye.
Failure of filtration surgery can occur any time during the first weeks after surgery or may be delayed for months or years. Early failure may result from surgical complications or technical error or simply from a vigorous healing process in the eye. The use of antimetabolites during and after filtration surgery has reduced the frequency of bleb failure from scarring, but at the cost of thinner blebs that are more prone to leak and be infected. Management of filtration failure depends on the cause and the interval since surgery.
Digital pressure also known as ocular massage, is a useful technique that is used to try to salvage and retain failing filtering blebs. It is based on the observation that forcing aqueous through a closing sclerostomy may (1) prevent closure of the sclerostomy; (2) elevate the conjunctiva and episcleral tissues away from the external opening of the sclerostomy and retard or prevent scarring, and (3) allow aqueous to flow into the filtering cicatrix to weaken its collagen structure, resulting in a more permeable bleb.
In the early postoperative period, the goal is to separate the edges of the healing scleral incision. When applied after 3 months following surgery, no effect was seen in a controlled study. Pressure at one side of that incision will indent it and break adhesions forming within it. This massage should be performed by the surgeon at the slit lamp. A simpler and equally effective technique is for the surgeon, at the slit lamp, to apply firm, momentary pressure through the upper lid adjacent to the bleb ( Fig. 36-19 ). Putting pressure along the limbal or lateral edges of a trabeculectomy flap depresses the plane of the sclera while increasing the pressure in the eye. The combination of forces causes the scleral flap of the trabeculectomy to lift off of its bed so that aqueous escapes from the eye. In a thermal sclerostomy incision, point pressure with any small blunt instrument can be placed at the posterior wound edge, which will tend to rupture and reopen the slit-like sclerostomy. Based on experimental investigations, the IOP after mechanical wound distortion should be checked 40 minutes after manipulation to most accurately assess efficacy.
If the sclerostomy incision is open but the bleb appears to be sealing down over it, digital pressure can be applied on a regular basis by the patient, through the closed eyelid, at any point on the globe away from the filtration site. One useful method is to instruct the patient to press through the upper lid on the lateral aspect of the globe until the eye just begins to ache and to hold the pressure for 10 seconds. After a 30-second pause, this can be repeated three or four times sequentially, four to six times daily. The surgeon should have the patient perform the technique in the office to measure its effect and instruct the patient appropriately. If the eye softens easily and rapidly, the patient should not be permitted to apply excessive digital pressure for fear of collapsing the globe. In diffuse blebs, the pressure reduction may last for several hours.
The goal of digital pressure is to force primary aqueous into the bleb without causing hypotony. If the IOP is reduced much below 7–10 mmHg with digital pressure, secondary aqueous may be produced with its increased protein content, which could increase ocular inflammation and encourage bleb scarring. Fluctuating vision from optical distortion of the cornea with transient hypotony may also limit its effectiveness.
Gonioscopy should first be performed before pressure is used to force aqueous out of the eye, to ensure that the internal sclerostomy is not plugged by material such as iris, lens, or vitreous, which should not be forced out of the eye. Digital pressure should be used with caution in patients who have had penetrating keratoplasty or recent intraocular lens implantation. One case of corneal wound dehiscence occurred from digital pressure 10 years after penetrating keratoplasty.
FAILURE DURING THE FIRST POSTOPERATIVE WEEK
Pressure elevation within the first postoperative week usually indicates a surgical complication or technical problem such as those listed in Box 36-1 . If the chamber is flat with elevated IOP, the possibility of pupillary or ciliary block or a posterior segment-expanding mass must be investigated.
Iris, vitreous, clot, ciliary process, or lens-plugging sclerostomy
Retained viscoelastic substance
Imperforate Descemet’s membrane
Scleral flap too tightly sutured
Ciliary or pupillary block
PLUGGED SCLEROSTOMY SITE
If the chamber is formed, gonioscopy is imperative to rule out obstruction of the internal filtering site by iris, clot, vitreous, or lens. Iris usually plugs the sclerostomy site after a flat chamber or if the peripheral iridectomy is too small. Iris should be removed as soon as it is recognized as an obstruction to filtration because iris tissue can seal the internal opening of either a trabeculectomy or a full-thickness sclerostomy. Pilocarpine 2% or 4% may pull the iris out of the wound. If this fails, argon laser applications through a contact lens across the anterior chamber have been successful. Typical settings are 50-μm spot size and 1500 mW for 0.05-second exposure to chip the iris out of the sclerostomy. The beam is aimed at the point of adhesion between the iris and the wound, and the laser energy is used to cut the iris away from the wound. This may create a new iridotomy.
Nd:YAG laser can also be used to cut the iris away from the wound. Occasionally this can cause more bleeding, which may be prevented by first cauterizing the portion of the iris to be treated with argon laser energy. A 100-μm spot size at 400–600 mW for 0.1-second exposure is used, applying enough energy and applications to see contraction of iris tissue in the area receiving Nd:YAG bursts. The Nd:YAG settings depend on the energy concentration of the particular machine but should be similar to those used for iridectomy and should be initiated with a single-shot burst.
If a small blood clot is obstructing the sclerostomy internally, pressure on the posterior lip of the sclerostomy incision may be used, either with a blunt spatula or muscle hook, or with digital pressure exerted through the lid margin while it is positioned just posterior to the scleral incision (see Fig. 36-19 ). This should reopen the sclerostomy and establish filtration. If the clot is quite small and the pressure not very high, waiting 2–3 days to see if the clot will lyse is an option. Argon or Nd:YAG laser can be used, as described above, to break up the clot if it is large. Argon laser is less likely to cause bleeding.
Vitreous in the sclerostomy is a more difficult problem, usually occurring after filtering surgery in an eye with prior cataract surgery (especially aphakia). Vitreous itself is not impermeable to aqueous but entrapped vitreous strands provide a scaffold for cicatrization of the filtering site. The Nd:YAG laser can be used to lyse small vitreal bands, but it is often tedious and of uncertain benefit. The best management is prevention by using great care not to rupture the hyaloid face during surgery or by performing a good anterior vitrectomy from the sclerostomy, but this is often unsuccessful. It is often best to wait until the eye quiets to re-evaluate the need for repeat surgery.
RETAINED VISCOELASTIC MATERIAL
Some surgeons routinely use viscoelastic material to re-form the anterior chamber at the end of a filtering procedure to retain the anterior chamber and reduce bleeding. The viscosity of the material impedes aqueous egress from the anterior chamber. If aqueous production is high and the sclerostomy small, postoperative pressure elevation can be severe. Digital or direct pressure on the posterior lip of the scleral incision may widen the sclerostomy enough to allow aqueous and/or viscoelastic material to escape from the chamber. The viscous material may leave the chamber in a sudden bolus; thus the surgeon should be prepared to release the pressure quickly to prevent flattening the chamber. Most studies consistently find no essential differences among visco-dispersive agents – hydroxypropylmethylcellulose 2% (Methocel TM ), sodium hyaluronate 3% with chondroitin sulfate 4% (Viscoat TM ), or sodium hyaluronate 1% (Healon TM ) or 1.4% (Healon – GV) in relation to endothelial cell protection, postoperative endothelial cell density, intraocular inflammation, or IOP elevation when used incataract surgery. However, the visco-cohesive agent Healon-5 TM can take several days before dissolving within the eye, causing prolonged IOP elevation.
TIGHT SCLERAL FLAP: RELEASABLE SUTURES AND LASER SUTURE LYSIS
Perhaps the most common cause of increased IOP during the first week after surgery is a scleral flap that is too tightly sutured. Digital pressure can reduce elevated IOP initially when secondary aqueous, wound edema, and surgical debris all contribute to reduce aqueous outflow. If digital pressure is still required after 4–7 days, or if it is unsuccessful initially, one or more of the scleral flap sutures should be loosened. This window of intervention may last many weeks if antimetabolites were used; one study suggests waiting 4 months postoperatively in mitomycin-treated eyes, thereby reducing the risk of hypotony. In our experience, however, the window is usually under 3–4 weeks.
If access to a laser is limited and releasable sutures were placed at the time of filtration surgery, their sequential release has proven useful in forestalling shallow chambers in the immediate postoperative period by allowing relatively tight flap closure for the first several days as well as later permitting IOP reduction simply by slit-lamp manipulation of the sutures. Experimental studies suggest the alternative method of suture adjustment to be more effective than either suture lysis or posterior lip manipulation of the filtering wound. A variety of suturing techniques have been described, including double-armed sutures and tamponade configurations. Adjustable sutures, tied with four-throw slip knots and manipulated postoperatively at the slit lamp, have also been described for incremental reduction of IOP.
If an argon or diode laser is available, the nylon sutures routinely placed in the scleral flap are amenable to laser suture lysis. This depends both on the visibility of the sutures through the bleb and on the extent of flap adherence to the scleral bed – a situation that can be modified by the use of intraoperative mitomycin-C or 5-FU under the flap. Multiple instruments have been described for this procedure: the standard Zeiss four-mirror gonioscopy lens, the specially designed Hoskins stalk lens, specially designed suture lysis contact lenses by Ritch, Mandelkorn, or Blumenthal, and even test tubes and micropipettes. The common feature among these devices is their ability to compress the conjunctiva and underlying hydrated Tenon’s tissue to bring the nylon suture as close to the lens surface as possible for maximal laser effect. Argon laser settings typically are for 0.1-second duration at 400–600 mW with a 50- or 100-μm spot size. Conjunctival perforation and its possible complications of leakage and hypotony may be minimized by using the larger spot size and incrementally increasing power. The diode laser has also been used, but it typically requires a high power density contact lens such as the Mandelkorn or Blumenthal lens.
Although the short-term effects of laser suture lysis are dramatic and obvious at lowering the IOP and improving bleb function in the short term, the long-term effects are less certain. When compared with eyes that did not undergo suture lysis and bleb manipulation, the IOP results at 2 years were the same.
INADEQUATE OPENING OF DESCEMET’S MEMBRANE
In full-thickness surgery, and less often in guarded filtering procedures, there may be an inadequate opening of Descemet’s membrane. This is suspected early in the postoperative period when the internal sclerostomy site is clear, yet the pressure is high and digital pressure is ineffective. In such cases, the Nd:YAG laser can be carefully focused at and slightly deep to the internal sclerostomy site and several bursts of moderately high energy delivered. If it is successful, digital pressure will open the wound and elevate the bleb.
An encapsulated or encysted filtering bleb ( Fig. 36-20 ) is also referred to as exteriorization of the anterior chamber, walled-off bleb, Tenon’s cyst, high-domed bleb, and localized cystic bleb. This usually occurs during the second to fourth postoperative week, presenting as a dome-like elevation of the bleb that is walled off from the surrounding conjunctival tissue. The incidence may be as high as 9–15% after trabeculectomies.