John F Salmon
MALIGNANT GLAUCOMA
INTRODUCTION
The term malignant glaucoma was first used by von Graefe to describe a rare and severe form of glaucoma that occurred after ocular surgery.[1] This complication was associated with elevated intraocular pressure (IOP) and shallowing or flattening of the anterior chamber. The word malignant was used to indicate the uniformly poor visual prognosis. Although the term is still commonly used, it should be emphasized to patients with malignant glaucoma that the term does not indicate a neoplastic process, that glaucomatous atrophy is not always a consequence of the condition and that the prognosis is good with modern laser and surgical approaches. Other terms have been suggested which emphasize the purported mechanisms responsible for this condition, such as ciliary block glaucoma, direct lens block glaucoma and aqueous misdirection syndrome.[2-4]
The diagnosis of malignant glaucoma is made when shallowing or flattening of the central (axial) anterior chamber occurs in association with increased IOP.(Fig. 212.1) Absence of pupillary block needs to be confirmed by the presence of a patent iridectomy or iridotomy and there should be no evidence of supra-choroidal effusion or hemorrhage. The raised IOP does not reduce in response to miotic treatment, but usually responds to mydriatic-cycloplegic therapy, aqueous suppressant and/or osmotic treatment. The condition is usually cured by disruption of the anterior hyaloid face by laser or vitreous surgery.
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FIGURE 212.1 Axial flattening of the anterior chamber. |
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Key Features: Malignant Glaucoma |
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CLINICAL FEATURES
Classic Malignant Glaucoma
Classic malignant glaucoma is the most common form of the disease and typically follows incisional surgical intervention for primary angle-closure glaucoma. It is reported to complicate 0.6-4% of these cases.[5,6] Neither the type of surgery nor the level of IOP immediately before surgical intervention appears to be related to the postoperative development of malignant glaucoma.[6] However, partial or total closure of the anterior chamber angle at the time of surgery is associated with an increased incidence of this complication.[6] Acute angle closure is a predisposing factor and the condition may rarely follow prophylactic iridectomy, even when the angle is narrow but open.[7] Shallowing of the chamber and elevated IOP may occur during the surgery, immediately afterwards, after the cessation of cycloplegics, after the initiation of miotics, or a considerable time later.[8-12] The first symptom is often an improvement in near vision secondary to a myopic shift in refraction, as the lens moves forward. If one eye develops malignant glaucoma after surgery, there is a high risk of a similar problem affecting the contralateral eye.
Nonphakic Malignant Glaucoma
This term has been used to describe malignant glaucoma in patients with persistent preexisting malignant glaucoma after cataract extraction, and in patients with malignant glaucoma occurring after routine cataract extraction. It occurs after cataract surgery in eyes with or without preexisting glaucoma.[6,13] It has been described in eyes of patients who have undergone anterior chamber and posterior chamber intraocular lens implantation and after combined posterior chamber intraocular lens and filtration surgery.[13-20]
Other Malignant Glaucoma Syndromes
Numerous clinical entities share some or all of the findings of classic phakic and nonphakic malignant glaucoma. Clinical findings consistent with classic malignant glaucoma may occur, but do not necessarily arise after typical incisional surgery. An extensive review of case reports in the literature has been published (Table 212.1.[21]
TABLE 212.1 -- Other Malignant Glaucoma Syndromes
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After Laser Treatment in Glaucoma Patients |
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After Miotics[28,29] |
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After Trauma[30] |
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Associated with Retinal Disease |
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Associated with Inflammation[30] |
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Associated with Infection |
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Spontaneously[37] |
PATHOGENESIS
Malignant glaucoma is a multifactorial disorder, which occurs in anatomically predisposed eyes. While the exact mechanism remains unclear, three theories have been proposed: posterior pooling of aqueous secondary to ciliolenticular block or anterior hyaloid obstruction, laxity of lens zonules and choroidal expansion. (Fig. 212.2)
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FIGURE 212.2 Diagrammatic representation of malignant glaucoma showing forward movement of the lens-iris diaphragm secondary to ciliolenticular block in the presence of an intact anterior hyaloid face. |
Posterior Pooling of Aqueous
Shaffer[38] suggested that aqueous accumulates behind a posterior vitreous detachment, which causes a forward movement of the iris-lens or iris-vitreous diaphragm, so-called 'aqueous misdirection syndrome'. The mechanism responsible for the posterior aqueous misdirection is not clear. Using ultrasound biomicroscopy in malignant glaucoma it has been shown that anterior rotation of the tips of the ciliary processes may occur which press against the lens equator in the aphakic eye or against the anterior hyaloid in aphakia, thus preventing forward flow of aqueous (hence the term 'ciliary block' glaucoma).[39,40] An intact anterior hyaloid face appears to be important in preventing the forward movement of aqueous that has been trapped behind the vitreous (Epstein DL: Unifying concepts in malignant glaucoma. Glaucoma Under Pressure 1997 Symposium. American Academy of Ophthalmology Specialty Day, San Francisco, October 1997).[41] It has also been demonstrated experimentally that a decrease in the permeability of the anterior vitreous gel to the forward movement of fluid occurs when the IOP is increased.[42,43]
Laxity of Lens Zonules
Chandler and Grant[30] thought that abnormal slackness or weakness of the zonules of the lens, as well as pressure from the vitreous, might cause forward movement of the lens-iris diaphragm in malignant glaucoma. The concept that the lens subsequently pushes the peripheral iris into the anterior chamber angle led to the proposed term of 'direct lens block angle closure'.
Choroidal Expansion
Quigley[44] suggested that the precipitating event is an increase in choroidal volume which causes an increase in the pressure in the vitreous cavity resulting in a compensatory outflow of aqueous and therefore shallowing of the anterior chamber. Since there is a decrease in the permeability of the anterior hyaloid and vitreous in an eye with increased pressure, transvitreal flow is insufficient to equate the pressure differential, the vitreous becomes condensed, further decreasing its fluid conductivity and a vicious cycle is established. Fluid builds up behind the vitreous which moves forward, carrying the lens and iris with it.
DIFFERENTIAL DIAGNOSIS
Malignant glaucoma is most commonly confused with pupillary block, choroidal effusion, and suprachoroidal hemorrhage. Ultrasound biomicroscopy, where available, may be useful in the differential diagnosis of malignant glaucoma and malignant glaucoma-like syndromes.
Pupillary Block
In pupillary block, the pressure is usually elevated and the anterior chamber is shallow or flat, particularly peripherally. (Fig. 212.3) If a previous iridectomy has been undertaken, careful slit-lamp examination needs to be undertaken. The iridectomy should be full thickness and not occluded by ciliary processes, inflammatory debris, the anterior hyaloid face, vitreous, retained lens material or an intraocular lens. If the iridectomy is clearly patent, a pupillary block mechanism is unlikely. If patency cannot be confirmed, then the clinician should proceed to undertake a laser iridotomy, which will result in deepening of the anterior chamber in pupillary-block glaucoma.
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FIGURE 212.3 Acute pupillary block, showing shallowing of the anterior chamber in the periphery. |
Choroidal Effusion
Choroidal effusion is associated with a shallow or flat anterior chamber after filtering surgery and the IOP is usually low. On ophthalmoscopy, light brown peripheral choroidal elevation containing a straw-colored fluid can be seen (Fig. 212.4). If visibility is poor and choroidal effusion cannot be discerned, B-scan ultrasonography may be needed. Most serous choroidal detachments will resolve spontaneously. However, those that are persistent or massive can be treated by undertaking a posterior sclerotomy, with drainage of the choroidal fluid and anterior chamber re-formation. A series of patients has been reported with occult annular ciliary body detachment giving rise to angle-closure glaucoma that is clinically indistinguishable from malignant glaucoma.[45,46] Ultrasound biomicroscopy is useful to confirm this diagnosis and may help to guide subsequent management.[46]
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FIGURE 212.4 Choroidal effusion associated with low IOP after filtering surgery. |
Suprachoroidal Hemorrhage
Patients with a suprachoroidal hemorrhage present with sudden onset of severe ocular pain and inflammation, associated with a shallow or flat chamber either at the time of surgery or during the first postoperative week. The IOP is normal or elevated. Findings on examination are similar to those seen in patients with choroidal effusion, except for a darker brown or dark red appearance of the choroidal elevation.(Fig. 212.5) In most patients the suprachoroidal hemorrhage will clear spontaneously in time, but if surgery is required the approach is the same as for serous choroidal detachment, with drainage of the blood from the suprachoroidal space through sclerotomies and re-formation of the anterior chamber.
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FIGURE 212.5 Suprachoroidal hemorrhage showing a dark-brown choroidal elevation. |
MANAGEMENT OF MALIGNANT GLAUCOMA
Careful clinical assessment, early detection and appropriate and timely intervention are critical to the successful management of malignant glaucoma. With modern therapeutic approaches the prognosis is good.
Medical Treatment
Medical therapy should be initiated immediately and has been reported to be curative in 50% of patients within 5 days.[5,6] Current treatment consists of atropine (1%) drops and phenylephrine (2.5-10%) drops, both instilled up to four times daily.[30] This combination tightens the zonules and helps to pull the anteriorly displaced lens backwards. Aqueous secretion should be decreased by using ?2-agonists, ?-blockers and carbonic anhydrase inhibitors. An oral osmotic agent (50% glycerol or isosorbide) or intravenous 20% mannitol in a dosage of 1-2 g/kg can be useful, as these preparations reduce vitreous volume, deepen the anterior chamber, and possibly increase vitreous permeability.[47] Topical steroids should be used to reduce inflammation. Oral steroids have been recommended for some cases of pseudomalignant glaucoma.[48] In most cases, further treatment using laser or surgery should be undertaken, but if this is not possible, administration of a topical cycloplegic will need to be used permanently to prevent relapse.
Laser Techniques
Argon laser treatment of the ciliary processes, with or without adjunctive medical therapy, has been advocated for phakic and aphakic malignant glaucoma.[49,50] Neodymium:yttrium-aluminum garnet (Nd:YAG) laser may be fired through a patent iridectomy in order to disrupt the anterior hyaloid face. In pseudophakia with malignant glaucoma posterior capsulotomy with disruption of the anterior hyaloid face is often effective.[51,52] Carasson et al[53] reported that a single session of contact transscleral cyclophotocoagulation using the diode laser (20 4-J spots over 360°, 1.5 mm posterior to the limbus) was successfully used in five patients with malignant glaucoma in whom anterior hyaloidotomy and vitreolysis had failed. The success of the procedure was attributed to the posterior rotation of ciliary processes secondary to coagulative shrinkage, which helped to eliminate the abnormal vitreociliary relationship. Although it is not currently recommended, cyclocryotherapy has been reported in the past as a treatment for malignant glaucoma.[54]
Surgical Therapy
When medical or laser therapy is not successful in relieving malignant glaucoma, then a surgical procedure on the vitreous should be undertaken. Chandler[55] described a technique of vitreous aspiration through an 18-gauge needle via an incision 4 mm behind the limbus in conjunction with anterior chamber re-formation with saline. This and similar techniques have remained in common use and with successful outcome in many eyes. However, because of improved microsurgical equipment and techniques, more recently pars plana vitrectomy with or without lensectomy has become the surgical method of choice in patients with malignant glaucoma.[56-63]
The primary aim of surgery is the removal of the anterior vitreous to increase aqueous flow into the anterior chamber. In patients with phakic eyes, the results of vitrectomy without lens extraction have been poor, primarily because of the difficulty of removing the anterior vitreous without damaging the crystalline lens.[56,57,61,62] It is likely that residual anterior vitreous is responsible for the failure of vitrectomy in many cases and consequently primary lens extraction with posterior capsulotomy has been advocated to facilitate removal of the anterior hyaloid.[56,62] (Fig. 212.6)
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FIGURE 212.6 Primary lens extraction with posterior capsulotomy and removal of anterior vitreous with a vitrector. |
The loss of accommodation associated with lens extraction is particularly undesirable in young prepresbyopic patients without preexisting cataract and a new technique of video-endoscope-guided fluorescein-assisted vitrectomy has been reported with a successful result.[63] Retrospective studies on patients with pseudophakic malignant glaucoma report good results with pars plana vitrectomy. However, Lois et al recently reported complete resolution of malignant glaucoma in five consecutive patients who underwent zonulectomy, hyaloidectomy and anterior vitrectomy through a peripheral iridectomy or iridotomy via the anterior chamber.[64] If extensive peripheral anterior synechiae are present, then vitrectomy can be combined with tube shunt implantation through the pars plana.[65]
Management of the Contralateral Eye
After an episode of malignant glaucoma in one eye, the risk of malignant glaucoma in the contralateral eye is significant if surgery is needed. Patients should be warned of the risk before any therapy is commenced. If acute angle-closure glaucoma is present, every effort should be made to break the attack before surgery is undertaken and, if the attack cannot be broken, mydriatic-cycloplegic therapy should be used vigorously after iridotomy and continued thereafter. Miotic agents should be discontinued before surgery, as these contribute to anterior rotation of the lens-iris diaphragm. A drop of atropine 1% should be used at the conclusion of glaucoma filtration surgery, particularly in phakic patients and continued for several months after surgery. Malignant glaucoma may occur when the atropine is eventually stopped.
GLAUCOMAS IN APHAKIA OR PSEUDOPHAKIA
INTRODUCTION
The glaucomas considered in this section are related by the fact that they develop after cataract extraction. In many instances, ocular hypertension occurs, but this can result in glaucomatous atrophy if untreated. Because these conditions differ in their pathogenesis, clinical features, and treatment, the terms pseudophakic glaucoma and aphakic glaucoma are inappropriate and should not be used. The glaucomas are broadly described as predominantly open-angle or angle-closure in mechanism, although both components may occur simultaneously. The postsurgical onset of the IOP elevation can provide important clues to the diagnosis (Table 212.2).[66]
TABLE 212.2 -- Classification of the Glaucomas in Pseudophakia
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Open-Angle Mechanism |
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Closed-Angle Mechanism |
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Adopted from Tomey KF, Traverso CE.: The glaucomas in aphakia and pseudophakia. Surv Ophthalmol 1991; 36:79, Review 1991.
The incidence of glaucoma after cataract extraction with intraocular lens implantation has dropped significantly in recent years as microsurgical techniques have improved. Uncomplicated phacoemulsification with implantation of a lens into the capsular bag does not predispose to chronic glaucoma, although a transient increase in the IOP may occur during the postoperative period.
In most cases, the raised IOP can be controlled by simply treating the underlying cause. However, treatment for glaucoma in an individual who is pseudophakic can be difficult. Life-long medical treatment is frequently justified as laser or surgical approaches are not always successful.
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Key Features: The Glaucomas in Pseudophakia |
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EFFECT OF CATARACT SURGERY ON IOP
Cataract extraction has a complex and dynamic effect on IOP. In the early postoperative period, the IOP is often elevated, particularly in glaucomatous eyes.[67,68] This is likely to be a consequence of decreased aqueous outflow facility, particularly in those eyes which demonstrate reduced outflow facility.[69] McGuigan et al[67] found a slight reduction in mean IOP in the early postoperative period after extracapsular cataract extraction in nonglaucomatous eyes compared with a mean increase of 10.2 mmHg in nonfiltered glaucomatous eyes. Kooner et al[70,71] reported a rise in IOP in 4% of eyes after standard extracapsular cataract extraction and in 11.3% of eyes undergoing secondary anterior chamber implantation. Most evidence indicates that cataract extraction alone produces a late, sustained reduction in IOP; however, the effect is generally small (1 mmHg to 4 mmHg).[71-74] Radius et al[74] reported no significant long-term change in mean postoperative IOP in a large group of normal and a smaller subgroup of glaucomatous eyes. In a single-surgeon ten-year follow-up study of IOP after phacoemulsification with intraocular lens implantation in patients without glaucoma, Suzuki et al[75] found no significant change between the mean preoperative and the mean postoperative IOP after ten years. However, in a prospective study examining the effects of phacoemulsification with intraocular lens implantation on IOP in glaucoma patients, Gimbel et al[76] found that two years postoperatively the mean IOP was 3.8 mmHg lower than the preoperative level. Shingleton et al[77] studied the effect of phacoemulsification with intraocular lens implantation on IOP in patients without glaucoma, glaucoma suspects and glaucoma patients and reported a significant reduction in IOP in the first two groups after 1 year, but not in the glaucoma patients and noted that the glaucoma patients needed less medication after surgery.
The type of incision used for phacoemulsification may influence the effect on IOP in nonglaucomatous eyes. Tennen and Masket[78] retrospectively studied the effect of incision location on IOP in 135 eyes of 89 randomly selected patients without glaucoma having phacoemulsification with intraocular lens implantation. One year after surgery, the mean IOP in the group having clear corneal phacoemulsification dropped from 15.57 mmHg preoperatively to 13.65 mmHg postoperatively, but in the group that had undergone phacoemulsification with intraocular lens implantation performed through a scleral tunnel there was no significant reduction in mean IOP.
Numerous studies have reported that Nd:YAG laser capsulotomy may be associated with a significant, but transient, rise in the IOP in some patients.[79,80] The presumed mechanism of IOP elevation after Nd:YAG laser capsulotomy is reduced aqueous flow through the trabecular meshwork secondary to inflammation associated with a breakdown in the blood-aqueous barrier.[81] The pressure rise may be detected within the first few hours and usually returns to baseline within 1 week, although in some cases the effect may last for several weeks. Several large studies have shown a persistent or late-onset IOP elevation in 0.8-6% undergoing this procedure.[82] In individuals with glaucoma, this can cause progressive visual deterioration. Risk factors for significant IOP elevation after Nd:YAG laser capsulotomy include preexisting glaucoma, a preoperative IOP above 20 mmHg, a large capsulotomy, the total laser energy used, a lens in the ciliary sulcus (rather than the capsular bag), the absence of a posterior chamber lens, myopia, vitreoretinal disease and vitreous prolapse into the anterior chamber.[83] The effect on the IOP can be minimized by using apraclonidine (0.5% or 1%) before and after treatment.[84]Pretreatment with timolol or acetazolamide has also been shown to be effective.[85]
CLINICAL FEATURES
Open-Angle Mechanism
Early onset (within the first postoperative week): usually self-limiting
Viscoelastic agents
Viscoelastic agents are universally used to maintain the anterior chamber, protect the corneal endothelium, and improve access to the capsular bag. The viscoelastic substances that are useful in ophthalmic surgery share certain rheologic properties including viscosity, molecular volume, chain length, molecular rigidity and shear, which may also be responsible for their tendency to induce or exaggerate IOP elevation after cataract extraction.[86] Sodium hyaluronate (Healon) is a large polysaccharide molecule that is a physiologic component of human vitreous as well as other connective tissues. Some studies have shown no significant postoperative IOP rise after the use of sodium hyaluronate, whereas others have reported high IOP in the first few days after surgery.[86-88] The mechanism by which sodium hyaluronate increases postoperative IOP is thought to be related to a reduction in outflow facility secondary to mechanical obstruction of the trabecular meshwork.
Other viscoelastic agents have been investigated and are also associated with IOP elevation.[89-99] Alpar et al[89] compared a formulation of chondroitin sulfate and sodium hyaluronate (Viscoat) with sodium hyaluronate alone and found that Viscoat caused a significant IOP rise in the immediate postoperative period in many patients. Barron et al[90] confirmed this finding. A modified sodium hyaluronate viscoelastic (Healon GV), which has higher molecular weight, viscosity and sodium hyaluronate concentration than Healon, was found by Caparossi et al[91] to be associated with a comparable postoperative IOP course to Healon. Healon 5 was found to have a lower IOP in the postoperative period compared with patients receiving Viscoat, although other studies found no difference in postoperative IOP spike when comparing Healon 5 to other viscoelastics.[92,93] Methylcellulose has not been found to cause a significant postoperative pressure rise in animal or human eyes, although one study reported a similar effect on IOP as sodium hyaluronate 1%.[94]
A number of investigators have noted dampening of the IOP effect with all viscoelastics when an anterior chamber washout is undertaken. The effect is unpredictable, however, and great care should therefore be exercised in patients with compromised optic nerve function. Complete removal of viscoelastic, at the end of surgery, is the key to the prevention of this condition. Intracameral acetylcholine and carbachol have been reported to be effective prophylaxis against postoperative IOP rise.[100-103] Pilocarpine gel, ?-blockers, apraclonidine, and carbonic anhydrase inhibitors are also helpful.[104-106]Examination at 6-8 h postoperatively increases the likelihood of observing the elevated IOP.
Hyphema
Most hyphemas occur in the first few days after cataract surgery (Fig. 212.7). The elevation of IOP in this setting tends to be transient. Patients may notice blurred vision, but unless there is a significant rise in IOP, they are otherwise asymptomatic and pain free. The source of bleeding in the immediate postoperative period is usually from the iris, iris root, or the corneoscleral incision. Bleeding tends to be more common with posteriorly located corneoscleral incisions. As in posttraumatic hyphema, the mechanism of IOP elevation is physical obstruction of the trabecular meshwork with red blood cells, fibrin, and other blood proteins. Patients with underlying trabecular dysfunction (i.e., primary open-angle glaucoma) typically experience higher and more prolonged IOP elevation postoperatively if there are red blood cells in the anterior chamber. It is generally possible to control the secondary glaucoma medically, but anterior chamber irrigation is occasionally necessary.
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FIGURE 212.7 A small hyphema after cataract surgery. |
Late-onset hyphema most commonly occurs as a result of hemorrhage from fine arborizing neovascularization of the inner aspect of the cataract incision.[107] These blood vessels are fragile and can bleed spontaneously or as a result of minor trauma such as eye rubbing. In one study, the average time between surgery and presentation was 4 years.[108] Patients most often complain of painless blurring of vision, especially on awakening which usually resolves over several hours. When the bleeding stops and the blood clears, the offending blood vessels can be gonioscopically visualized and ablated using argon laser goniophotocoagulation or limbal cryopexy.[109] In addition to this mechanism, posterior chamber intraocular lens haptics may erode into the ciliary sulcus, causing late-onset hyphema.[110] More commonly, an anterior chamber intraocular lens may produce a hyphema in association with uveitis and IOP elevation (uveitis-glaucoma-hyphema syndrome).[111]
Inflammation
Transient postoperative inflammation occurs to some degree in every patient immediately after cataract extraction. In most cases the inflammation can be controlled with topical steroids. However, the inflammatory response and associated ocular hypertension may be particular prominent when lens fragments are lost into the vitreous after complicated extracapsular cataract extraction or phacoemulsification.[112] (Fig. 212.8) The risk of postoperative uveitis is increased when an anterior chamber lens has been inserted or when a posterior chamber lens is placed into the ciliary sulcus.[113] In these circumstances, the cause of the inflammation is thought to be the contact between the iris and a rough implant surface or the haptics.[114] Late inflammation after uncomplicated phacoemulsification and implantation is rare. Fluorophotometric studies have shown that pseudophakic eyes with a posterior chamber lens and an intact posterior lens capsule have minimal alteration in the blood-aqueous barrier.[115] Ultrasonography can be helpful in detecting malpositioned haptics (especially with posterior chamber lenses) and planning subsequent surgical intervention.[116]
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FIGURE 212.8 Anterior uveitis and keratic precipitates after loss of nuclear fragments during complicated phacoemulsification. |
?-Chymotrypsin
?-Chymotrypsin was commonly used to facilitate enzymatic zonulysis during intracapsular cataract extraction and commonly resulted in raised IOP;[117] however, it is no longer used.
Idiopathic
IOP may rise after cataract extraction without any detectable cause. The IOP rise usually starts within hours of the surgery and may last for weeks thereafter. The exact mechanism by which IOP rises temporarily in an otherwise perfectly normal eye following cataract extraction is not yet fully understood, but several theories have been proposed: inflammation, trabecular meshwork edema, and angle de-formation by sutures.[66]
Intermediate-onset (after the first postoperative week)
Corticosteroid-induced glaucoma
Steroids are typically prescribed after cataract extraction and may be responsible for a rise in IOP. When steroid-induced IOP elevation does develop, the duration of drug use can be as short as 3 days but more commonly is 2-3 weeks in cases of topical administration.[118] In general, the propensity for IOP elevation is correlated with antiinflammatory potency, frequency of application and drug concentration.[118]Patients with open-angle glaucoma are especially prone to develop ocular hypertension when treated for an extended period with topical steroids. Most patients who develop IOP elevation return to baseline IOP over days to weeks with the cessation of the steroid medication. In some patients, the effect persists and requires standard medical therapy for open angle glaucoma. In the past 3 years, the use of intravitreal triamcinolone to treat a range of conditions including postoperative cystoid macular edema, has become popular.[121] This may cause a significant rise in IOP and may necessitate an urgent trabeculectomy.
Lens particle or retained cortex after cataract extraction
Retained cortical material which can be sequestered out of sight in the capsular bag or small nuclear remnants which have dropped into the vitreous after complicated phacoemulsification, may induce an inflammatory reaction and ocular hypertension.[114,120,121] (Fig. 212.9) Liberated cortical material has been shown to block trabecular outflow pathways in enucleated human eyes.[120] The role of high molecular weight soluble lens proteins, macrophages, and other cellular responses to the lens material is not clear.[121] However, the infrequency of lens particle glaucoma implies an inherent capacity of the normal trabecular meshwork to handle this material. Clinically, cortical material may be visible in the anterior chamber and typically appears as fluffy white material, often associated with a significant inflammatory response. (Fig. 212.10) The onset of IOP elevation typically occurs days to weeks after surgery. The level and severity of glaucoma appears to be correlated with the load of cortical material. Medications that suppress aqueous production are most useful in managing this disorder.[120] Miotics should be avoided. Corticosteroids should be used to suppress the inflammatory response and prevent synechia formation. If medical therapy does not control the inflammation, surgical aspiration of lens material is required.[112,120]
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FIGURE 212.9 Dislocation of a fragment of lens material and intraocular lens into the vitreous cavity. |
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FIGURE 212.10 Residual lens particles in the anterior chamber following incomplete irrigation. |
Ghost cell glaucoma
Campbell et al[122] described a late-onset secondary glaucoma which developed as a consequence of retained intraocular blood. In this condition obstruction of the trabecular meshwork by degenerative spherical erythrocytes (erythroclasts) occurs secondary to the loss of normal erythrocyte pliability. Generally, the degeneration of red blood cells occurs in the vitreous cavity and therefore requires disruption of the anterior hyaloid face. While in the vitreous, red blood cells lose hemoglobin and convert to spherical transparent cell remnants whose plasma membranes are stippled with denatured hemoglobin clumps, which can be observed using phase-contrast microscopy of anterior chamber aspirates.[123] The transformation tends to occur over weeks to months. In the setting of cataract extraction, any event that places blood in the vitreous cavity can be responsible for the subsequent emergence of ghost-cell glaucoma; for example: postoperative hyphema associated with cataract extraction which has been complicated by vitreous loss.[124] The immediate postoperative period can be complicated by fresh red blood cells causing IOP elevation, but this is not necessary. Typically, 1-3 weeks later, IOP elevation may occur secondary to ghost cell-induced obstruction of the trabecular meshwork. The anterior chamber contains floating tan cells, which can easily be mistaken for white blood cells. If a pseudohypopyon is present, ghost-cell glaucoma may be confused with an inflammatory process. Diagnostic clues include the absence of keratoprecipitates and a limited response to steroids. Medical treatment may provide sufficient therapy for self-limited disease, but surgical intervention is most often necessary. Anterior chamber washout alone can temporize, but IOP again increases after 1-3 days unless vitrectomy is included to eradicate the reservoir of ghost cells in the vitreous cavity.[125]
Pigmentary glaucoma
Pseudophakic pigmentary glaucoma is most often associated with posterior chamber lenses, although this may occur after the implantation of phakic refractive intraocular lenses.[126-127] The mechanism appears to be rubbing of the iris pigment epithelium against the haptics of the intraocular lens, leading to the dispersion of pigment granules that obstruct the trabecular meshwork, similar to the situation found in patients with phakic pigmentary glaucoma. If the degree of pigment dispersion is excessive it can lead to transient IOP elevation in aphakic or pseudophakic eyes with the latter occasionally leading to chronic glaucoma (Fig. 212.11). The most characteristic finding is iris transillumination defects at the sites of contact with the implant[128] (Fig. 212.12). Gonioscopy reveals heavy pigmentation of the trabecular meshwork. The onset may be immediate and associated with marked increased IOP or can be delayed by several months.[129] Should the problem occur, then the best treatment is to exchange the implant. The complication can be avoided by placing the intraocular lens implant into the capsular bag.
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FIGURE 212.11 Capsular fibrosis and pigment deposition on the intraocular lens. |
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FIGURE 212.12 View of the same eye on retroillumination. |
Vitreous in the anterior chamber
Grant described a mechanism of acute open-angle glaucoma in which vitreous humor fills the anterior chamber after cataract surgery[130] (Fig. 212.13). This mechanism is extremely rare in the age of phacoemulsification with intraocular lens implantation.
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FIGURE 212.13 Vitreous in the anterior chamber after intracapsular cataract extraction. |
Angle-closure mechanism
With pupillary block
Relative pupillary block occurring in phakic patients is due to the anatomic relationship of the iris with the crystalline lens which offers increased resistance to the passage of aqueous from the posterior to anterior chamber. In aphakic and pseudophakic patients, a functional anatomic pupillary block can exist, but one frequently encounters synechiae formation between the iris and the ocular structures; typically the hyaloid, lens remnants, posterior capsule and intraocular lens.[131]
Aphakic pupillary block, typically presents as iris bombé with angle closure. The condition often follows a transient flat anterior chamber secondary to a wound leak and is seen these days after surgery for congenital cataract. The time course of presentation is variable. Pupillary block may present in the immediate postoperative period but has been described weeks to years after surgery (Fig. 212.14). Unfortunately, many cases are asymptomatic and are recognized at the time of routine examination. The anterior chamber is shallowed peripherally to a greater extent than centrally. Irregular shallowing of the anterior chamber may be seen in eyes in which broad iridovitreal adhesions result in loculation of aqueous pools posterior to the iris, resulting in segmental pupillary block. The least reliable clinical feature of aphakic pupillary block is the level of IOP.[132] Normal IOP most commonly results from wound leak, a choroidal detachment associated with increased uveoscleral outflow, and inhibition of aqueous production. Inflammation also predisposes to aqueous hyposecretion, pupillary membranes, and iridovitreal adhesions. Aphakia is often marked by broad adhesions of the vitreous to the iris, thus the popularity of the term iridovitreal block. In round-pupil intracapsular cataract extraction, the development of functional and synechial pupillary block is increased.[133] Prolapse of an intact hyaloid face through the round pupil results in pupillary block, and the vitreous itself can block a patent iridectomy. For a vitreous-related episode of pupillary block to occur, an intact hyaloid face is usually found because aqueous is capable of percolating through a broken hyaloid face. Undertaking a peripheral iridectomy usually prevents this complication.
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FIGURE 212.14 Angle closure due to aphakic pupillary block, demonstrating iris bombé. |
Pseudophakic pupillary block was once seen most often with anterior chamber and iris-supported lenses, but there are now numerous reports of this complication after posterior chamber lens implantation.[134-137] (Fig. 212.15) It usually appears in the early period after surgery, but may occur months or years later. With phacoemulsification and posterior chamber intraocular lens implantation, peripheral iridectomy is not commonly undertaken. However, pupillary block in this setting is still possible, particularly in patients with uveitic cataract where inflammatory membranes and hyphema may be responsible for pupillary seclusion. Diabetes mellitus is a risk factor for this complication.[136] Zonular dehiscence with an intact posterior capsule may be associated with vitreous prolapse and pupillary block. Vitreous can prolapse through an Nd:YAG laser capsulotomy or inadvertent posterior capsular rent.[137] Ultrasound biomicroscopy can be useful in the management of pseudophakic pupillary block glaucoma.[138]
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FIGURE 212.15 Iris bombé due to pupillary block may occur with an anterior chamber lens in the absence of an adequate peripheral iridectomy. |
Without pupillary block
Peripheral anterior synechiae and/or trabecular damage. In most cases of chronic glaucoma in aphakia or pseudophakia, peripheral anterior synechiae are present, presumably due to a flat anterior chamber or the presence of inflammation or debris in the postoperative period. A flat anterior chamber after cataract surgery may be caused by wound leak with subsequent hypotony and choroidal detachment. Late-onset progressive peripheral anterior synechiae have been reported with posterior chamber intraocular lenses.[139] (Fig. 212.16) The mechanism is related to posterior 'pushing', with closure of the overlying angle by the haptics of a posterior chamber intraocular lens. The incidence of peripheral anterior synechiae is higher (65-80%) with 10-degree anterior vaulted haptics and when these lenses are sulcus supported. In most cases, peripheral anterior synechiae are noted early and are nonprogressive. Anterior chamber intraocular lenses are also responsible for loss of functional trabecular meshwork through fibrosis and cocooning of the lens haptics.[140] Chronic uveitis may be associated with peripheral anterior synechiae or pupillary seclusion and pupillary block.
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FIGURE 212.16 Gonioscopic appearance showing progressive synechiael closure. |
Malignant glaucoma. This has been discussed in the previous section.
Epithelial downgrowth. This is considered in the following section.
MANAGEMENT
Prevention of IOP Rise after Cataract Surgery
The risk of postoperative IOP elevation can be significantly reduced by meticulous attention to detail during the cataract surgery. The tissues need to be gently handled with minimal intraocular manipulation in order to reduce the risk of excessive inflammation, pigment dispersion and hemorrhage. Judicious use of viscoelastic substances and thorough removal of the material at the end of the surgery may also help to minimise the risk of postoperative IOP elevation. This is particularly important in individuals with preexisting glaucoma and those with pseudoexfoliation syndrome. It has been shown that a surgeon's experience is more important than prophylactic medication in preventing IOP elevation after phacoemulsification.[141]
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Key Features: In the Management of Ocular Hypertension or Glaucoma in Pseudophakia |
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Injecting acetylcholine into the anterior chamber to constrict the pupil has been shown to be associated with lower IOP at 3 h and 6 h postoperatively, although the difference is not significantly different at 24 h.[101] The combination of preoperative acetazolamide and intraoperative acetylcholine appears to be more effective than either drug alone in controlling postoperative IOP elevation.[68] There is evidence to suggest that intracameral carbachol is more effective than acetylcholine at 24 h, two days and 3 days postoperatively.[103]
A number of drugs have been evaluated for efficacy in controlling the early IOP rise in eyes with an open anterior chamber angle. Oral acetazolamide and topical ?-blockers have been shown to be useful in these cases.[104-106] Apraclonidine is useful in controlling postoperative IOP elevation, particularly when given 1 h preoperatively rather than immediately after surgery.[142] In a double-blind randomized study comparing IOP lowering efficacy of the various drops, Schwenn et al[143] reported that, a combination of timolol 0.5% and dorzolamide 2% produced the greatest IOP reduction during the first 24 h after phacoemulsification with intraocular lens implantation. Topical steroids are not effective in reducing IOP, but can be helpful if the mechanism of IOP elevation is severe inflammation. Topical prostaglandins should be avoided because of their tendency to increase inflammation and cystoid macular edema, particularly in cataract surgery that has been complicated by posterior capsular rupture.[144-146]
Treatment of the cause of IOP elevation
As a general principle in these cases, IOP elevation can often be controlled by dealing with the underlying cause. For example, when uveitis and glaucoma are associated with retained lens fragments in the vitreous, pars plana vitrectomy with removal of the fragments will solve the problem.[112] In individuals with recurrent UGH (uveitis, glaucoma, hyphema) syndrome, lens exchange should be considered.[147] If pupillary block occurs in aphakia or pseudophakia, the block can often be broken by using mydriatics, followed by a laser iridotomy.[124] If this is unsuccessful, then alternative surgical approaches can be considered, especially pars plana vitrectomy with separation of the iris from the vitreous adhesion.[148]
Surgical Intervention
It is common practice to use long-term medical treatment for the glaucomas in the presence of aphakia and pseudophakia because the surgical options in these eyes are usually less successful and can carry greater morbidity than in phakic eyes.[149-151] This is usually undertaken with drugs which reduce aqueous production, such as carbonic anhydrase inhibitors, ?-blockers, ?2-agonists and miotics. Because of the risk of cystoid macular edema, topical prostaglandins should be avoided during the first postoperative month, and not be used at all in individuals who have undergone cataract surgery with vitreous loss.[144-146] Argon laser trabeculoplasty (ALT) may have a role in the treatment of patients once the eye is stable and quiet.[152-153] The results in general, are not as effective as those found in phakic eyes. Pseudophakic eyes respond relatively better to ALT than aphakic eyes.[154]
Surgical intervention is rarely required in the immediate postoperative period and in general, is limited to the use of paracentesis to lower the IOP. The decision to proceed to surgery in a pseudophakic patient should follow the guidelines adopted in phakic patients.[1] When choosing a glaucoma procedure in these circumstances, it is important to consider the surgeon's experience, the potential intraoperative and postoperative risks and finally the operative success rate.[151,154] In glaucoma associated with pseudophakia, there may be mild, moderate or severe conjunctival scarring. Particularly when large incisional surgery has been previously undertaken, conjunctival adhesions, limbal ectasia and altered limbal anatomy may be present which may make the dissection of a trabeculectomy scleral flap difficult.[155] Elderly patients may have friable scleral tissue that easily tears during dissection. Corneal edema may reduce visualisation of anterior chamber contents. There may be vitreous in the anterior chamber, intraocular lens implant malposition, and posterior or peripheral anterior synechiae.
Trabeculectomy without the use of antiscarring agents has a higher failure rate in eyes that have undergone previous cataract surgery than in eyes without previous ocular surgery.[156] The failure rate of glaucoma filtration surgery can be reduced by the use of postoperative subconjunctival 5-fluorouracil injections.[157] This approach has been superseded by the use of intraoperative 5-fluorouracil or mitomycin C.[158-160] The adjunctive use of mitomycin C reduces the failure rate, produces good long-term IOP control and eliminates or reduces the need for postoperative glaucoma medication. (Fig. 212.17) Typically mitomycin C is used in a concentration ranging from 0.2 mg to 0.5 mg/mL and is applied for a period of 1-5 min. However, the use of mitomycin C may result in significant postoperation complications including chronic ocular hypotony, bleb leak and late bleb-related endophthalmitis. Intraoperative 5-fluorouracil is less effective than mitomycin C, but there is less risk of late complications as a consequence of its use.
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FIGURE 212.17 Thin-walled avascular filtration bleb after the use of mitomycin C in the pseudophakic eye. |
Should trabeculectomy with mitomycin C fail, or should there be extensive superior conjunctival scarring, then the insertion of a drainage implant is a good surgical option.[161] The results with this surgery are similar to those obtained with trabeculectomy and intraoperative mitomycin C.[162-163] Transscleral Nd:YAG laser used in the continuous-wave mode or cyclodiode therapy can be effective in treating chronic glaucoma in aphakia or pseudophakia, but is usually reserved for patients with poor visual potential or in those patients in whom incisional surgery is not possible or is thought to have a limited change of success.[164-165]
GLAUCOMA ASSOCIATED WITH EPITHELIAL AND FIBROUS DOWNGROWTH
INTRODUCTION
Intraocular proliferation of epithelium from the ocular surface is a rare but devastating complication of anterior segment surgery. Although it is most commonly found after cataract extraction, it may also occur after keratoplasty and penetrating ocular injuries. Ingrowth of fibroblasts from episceral connective tissue or cornea may mimic epithelialization and often the two conditions coexist. The epithelium usually penetrates the anterior chamber through a fistula which may be associated with iris, lens material or vitreous incarceration in the wound, or by epithelial implantation from surgical instruments or sutures (Fig. 212.18). The incidence of this condition has fortunately decreased in recent years with modern microsurgical techniques and meticulous wound closure. A variety of treatments have been proposed for eradicating the epithelial cells from the anterior chamber. However, even with aggressive surgical treatment of the epithelial downgrowth, many affected eyes develop intractable glaucoma. Fibrous ingrowth is generally less destructive to the eye than epithelial proliferation, but is nevertheless associated with substantial morbidity including glaucoma and vitreous traction.
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FIGURE 212.18 Molteno implant in a patient with an anterior chamber IOL. |
CLINICAL FEATURES
Epithelial Downgrowth
The original description of epithelialization of the anterior segment is often accredited to Collins and Cross in 1892.[166] Epithelialization was grouped by Perera[167] in 1937 into three categories: pearl tumors, posttraumatic cysts of the iris, and epithelial downgrowth.
Pearl tumors occur most often after penetrating trauma in which epithelial elements associated with a cilium are implanted into the eye. The epithelial wall of the pearl cyst may be keratinized, contributing to its pearly lustre and opacity. Pearl tumors may remain dormant for extended periods of time, but may expand to fill the anterior chamber and cause secondary angle-closure glaucoma.
Posttraumatic cysts of the iris or epithelial inclusion cysts are thought to occur when surface epithelium is implanted into the eye as a result of surgical or accidental trauma (Fig. 212.19). They may develop months or even years after the original injury. It is believed that the iris provides nutritional support for the epithelial cells. The cyst wall may have various degrees of pigmentation. These cysts are often translucent, and large epithelial cells and cellular debris may be visible in the cavity of the cyst. They may demonstrate progressive growth, filling the pupil and anterior chamber.
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FIGURE 212.19 Anterior chamber cyst after corneal graft. |
Epithelial downgrowth may occur when surface epithelium is given the opportunity to grow into the anterior chamber (Fig. 212.20). It occurs most commonly after cataract extraction. In a 30-year clinicopathological review published in 1989, an incidence of 0.08-0.12% was reported after cataract surgery.[168] Epithelial downgrowth has been described as early as 4 days after cataract extraction and as long as 10 years after surgery.[169] Most cases, however, are noted within the first 12 months of intraocular surgery. In the past, the diagnosis of epithelialization after cataract surgery was usually not made until the eye was enucleated and examined pathologically. Earlier diagnosis is now possible because clinicians are able to recognize the early signs of epithelialization, perhaps resulting in fewer eyes requiring enucleation. Although epithelial downgrowth is decreasing in incidence with modern microsurgical techniques, it still represents an important cause of eyes being lost after cataract surgery.
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FIGURE 212.20 A translucent posterior corneal membrane with a scalloped border and pupillary distortion. |
In its earliest stage, epithelial downgrowth can be difficult to diagnose unless specifically considered. It is often associated with persistent inflammation that does not respond to steroid therapy. As the process continues, a characteristically scalloped migration line of epithelium appears on the endothelial surface of the cornea. The anterior chamber angle is initially anatomically open, but physiologically obstructed. Over time, peripheral anterior synechiae begin to form. Many eyes with this complication have a fistula, and careful examination of the surgical or traumatic wound with 2% fluorescein to find a leak of aqueous is important. The pupil may be updrawn, and vitreous may be incarcerated in the wound. The normal iris architecture may be altered by the epithelial sheet.
A major aid in the diagnosis and treatment of epithelialization involves applying photocoagulation burns to the iris in suspected cases.[170] Areas of epithelial membrane turn white (Fig. 212.21). Commonly used settings on the argon laser are 0.2 s, 200-500 mm spot size, and 200-500 mW power, but higher energy levels may be needed to penetrate a hazy cornea. This technique is also used to outline the extent of the epithelial membrane on the iris surface for preoperative planning. Specular microscopic findings of the leading edge of the epithelial sheet was described by Smith and Parrett and provides an additional clinical means of confirming the diagnosis.[171] When specular microscopy is performed at the scalloped margin of the advancing epithelial membrane, an interface between intact endothelium and affected areas may be appreciated. Focusing slightly deeper in the areas of suspected epithelial membrane may reveal the outline of epithelial cells.
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FIGURE 212.21 Left: Typical advancing front (arrows) of epithelial downgrowth on the corneal endothelium. Right: Edge of epithelial downgrowth (arrows) over iris as outlined by argon laser photocoagulation, causing blanching of the treated epithelium. |
Virtually all eyes with epithelial downgrowth develop secondary glaucoma and several mechanisms may play a role.[172] Dysfunction of anterior chamber angle structures may be masked by an open fistula or inadvertent filtration, resulting in low pressures. Fistulous tracts eventually tend to close, which results in high IOP. Many of these eyes have preexisting peripheral synechiae from a shallow anterior chamber. As the epithelial membrane advances over angle structures, secondary open-angle glaucoma results. The epithelial membrane results in secondary disorganization of the trabecular meshwork. Progressive anterior synechiae may develop secondary to contraction of the epithelial membrane and chronic inflammation, causing secondary angle-closure glaucoma. (Fig. 212.22) Pupillary block may occur as the epithelial membrane advances across the iris to the anterior vitreous face.
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FIGURE 212.22 Histopathology of epithelial downgrowth demonstrating the epithelial membrane of the iris and posterior surface of the cornea with broad peripheral anterior synechiae. |
Fibrous Ingrowth
The term fibrous ingrowth is synonymous with stromal ingrowth or stromal overgrowth.[173] The term retrocorneal membrane is used by some authors for fibrous ingrowth, especially after penetrating keratoplasty. Fibrous ingrowth and epithelial downgrowth occur under similar circumstances and is usually seen after anterior segment trauma or surgery, when wound healing has been poor. Fibrous ingrowth may occur in a limited fashion or may be massive, with resulting loss of the eye. Because of the relatively indolent nature of fibrous ingrowth compared with epithelial downgrowth, a smaller percentage of eyes with fibrous ingrowth eventually require enucleation.
Patients presenting with fibrous ingrowth typically demonstrate a translucent membrane on the posterior surface of the cornea adjacent to the limbal or corneal wound. Swan[173] described this greyish fibrous membrane as having the appearance of woven cloth. The edges of the membrane tend to have tongue-like projections rather than the scalloped edge of epithelial membranes. Glaucoma occurs in fibrous ingrowth when peripheral anterior synechiae develops secondary to contraction of fibrous membranes.[173] Glaucoma can also occur from associated inflammation or hemorrhage. Posterior segment sequelae resulting from tractional forces produced by fibrous membranes include retinal tears or detachments and cystoid macular edema.
PATHOGENESIS
Epithelial Downgrowth
A major risk factor for the development of epithelial downgrowth is delayed closure or dehiscence of an incision after cataract extraction, creating a tract for entry of surface epithelium.[174] (Fig. 212.23) Recognized associated risk factors include a shallow anterior chamber, which places the invading epithelium in close proximity to the iris. Incarcerated iris, vitreous, retained lens material, or tags of surface epithelium may prevent wound healing and thus promote downgrowth. Healthy corneal endothelium probably has a protective role against epithelial downgrowth by contact inhibition and damage to the underlying endothelium has been reported to be a predisposing factor in this condition.[168,175] Hypotony and the associated plasmoid aqueous may provide more support to the ingrowth of epithelium than normal aqueous.
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FIGURE 212.23 Iris prolapse after large incisional surgery is a major risk factor for the development of epithelial downgrowth. |
Fibrous Ingrowth
The hallmark of this form of fibrous proliferation is a break in the corneal endothelium and Descemet membrane, which allows fibroblasts to enter the anterior chamber. The source of fibroblasts in fibrous ingrowth is believed to be either subepithelial connective tissue or corneal stromal fibroblasts. Metaplastic corneal endothelium and blood mononuclear cells are other suggested sources. Studies of the healing of limbal and corneal incisions confirm the role of subepithelial connective tissue and stromal keratocytes in normal healing. Overgrowth of these cells under proper conditions provides an obvious mechanism for fibrous ingrowth.
Prolonged inflammation is recognized as an important risk factor for fibrous ingrowth.[173] Poor wound apposition resulting from tissue incarceration or improperly placed sutures is also a recognized risk factor.[173] Henderson[176] observed that normal healing of limbal wounds involves downgrowth of subepithelial or corneal stromal connective tissue to the inner margin of the wound. Further ingrowth of connective tissue appears to be inhibited when the inner wound margins are bridged by endothelium by the second postoperative week. Therefore, damaged corneal endothelium is also a risk factor for stromal ingrowth even with a well-apposed wound. It has been suggested that posterior limbal incisions are more likely to be associated with fibrous ingrowth, whereas more anterior limbal incisions with poor healing are prone to develop epithelial downgrowth.[176] Swan[173] suggested that more posteriorly placed incisions are more often associated with hemorrhage and that hemorrhage is the important risk factor for fibrous ingrowth.
MANAGEMENT
The key to the management of epithelial downgrowth is to make an early diagnosis and then proceed to radical surgical intervention. Many techniques have been devised for the treatment of this condition. Whichever technique is used, the purpose of treatment must first be the complete eradication of invading epithelium to avoid recurrence and second, the control of IOP. Even if useful vision is not achieved with surgical intervention, the need for enucleation is reduced.[168]
Background to Surgical Approach
Maumenee et al[170] reported a series of 40 consecutive eyes with epithelial downgrowth undergoing surgical treatment. All eyes in the series were diagnosed when less than 25% of the cornea was involved. Eleven eyes (27%) achieved 20/50 vision or better with successfully controlled glaucoma. This remarkable result is probably due to an aggressive surgical approach which eliminated the invading epithelium, coupled with an early diagnosis. However, even with early diagnosis and treatment, morbidity remains high. Five eyes in this series required enucleation and five had persistent hypotony or atrophy.
The above surgical technique was modified by Stark et al,[177] who treated 10 patients with epithelial ingrowth using a pars plana vitrectomy approach.[177] After removal of the involved iris, intraocular air was inserted and cryotherapy was applied in a transcorneal and transscleral fashion to devitalize the epithelium remaining on the posterior surface of the cornea, in the anterior chamber angle and on the ciliary body. Corneal decompensation occurred in four eyes and penetrating keratoplasty was required. Postoperative visual acuity improved in eight patients, four achieving 20/40 vision or better. The postoperative IOP remained less than 21 mmHg in all cases, although two eyes required topical antiglaucoma medication. Peyman et al[178] also used a pars plana approach. The iris and epithelial tissue over the ciliary body were removed with intraocular scissors and a vitrector combined with unipolar diathermy and endophotocoagulation.
Friedman[179] proposed en bloc excision of the cornea, sclera, iris, ciliary body and vitreous, similar to the technique used for an intraocular tumor. Brown[180] used a similar surgical strategy, with complete resection of the affected tissues and extensive cryotherapy to eradicate epithelial downgrowth in fourteen patients with epithelial ingrowth involving 50% of the anterior iris and/or cornea. Naumann and Rummelt[181] reported a technique of simultaneous removal of adjacent iris, pars plicata of the ciliary body, and all layers of sclera and cornea in contact with the lesion acting as a shell. The resulting defect was covered by a tectonic corneoscleral graft. In 32 consecutive patients long-term visual acuity was better than 20/60 in 37.5% of patients. No recurrence of the downgrowth was noted and enucleation was not necessary.
If surgical treatment of epithelial downgrowth fails to control the disease, then intraocular 5-fluorouracil may be helpful. Shaikh et al[182] reported a case where an anterior chamber injection of 1.2 mg of 5-fluorouracil mixed with a viscoelastic, combined with viscodissection of the membrane itself, was successful in halting the disease process and prevented recurrence 14 months after treatment.
Surgical Approach
The initial step in the management is to determine the extent of epithelial invasion with argon laser application to the iris (Fig. 212.22). Photocoagulation is performed within 24 h of the planned surgical procedure because the treatment can cause moderate anterior chamber inflammation. Intraoperatively, a scratch incision into Bowman's membrane may be helpful to outline the extent of corneal involvement. Sharp dissection of a fornix-based conjunctival flap is then performed. A limbal incision is made posterior to the original section. Fluorescein solution is used to test for a fistula. If a fistula is present, the incision may be placed to bisect the fistula. The fistula is closed, if necessary using a hinged scleral flap. The involved posterior corneal surface is treated with cryotherapy using a double freeze-thaw technique. Other methods involve swabbing the posterior corneal surface with absolute alcohol or scraping the membrane off the posterior corneal surface. Involved areas of iris, ciliary body and vitreous are resected.[169] Alternatively, the iris and epithelial tissue over the ciliary body can be removed with intraocular scissors and a vitrector, combined with unipolar diathermy and endophotocoagulation; intraocular air is inserted and cryotherapy is applied in a transcorneal and transscleral fashion.[177] Postoperatively, the eye is treated with corticosteroids. Cycloplegics and aqueous suppressants are used as needed for inflammation and control of IOP.
Treatment of the Associated Glaucoma
The management of the associated glaucoma is extremely difficult. Generally, trabeculectomy fails secondary to closure of the sclerostomy by epithelial sheets. Loane and Weinreb[183] reported their results with trabeculectomy and 5-fluorouracil in one patient, noting that the retrocorneal membrane rapidly grew to block the sclerostomy after the 5-fluorouracil injections were stopped. Whether the use of intraoperative mitomycin C would be more advantageous than 5-fluorouracil is yet to be reported. The use of a drainage implant may be the therapy of choice in eyes with glaucoma secondary to epithelial downgrowth. Fish et al[184] reported their results of nine patients with advanced epithelial ingrowth who underwent Molteno implantation for medically uncontrolled secondary glaucoma. Substantial reductions in IOP was observed and in seven (78%) a final postoperative IOP of less than 22 mmHg was achieved.
In individuals with extensive disease who are poor candidates for surgical removal of the intraocular epithelium simply inserting an implant will frequently maintain some vision, control the IOP and avoid the rapid progression to absolute glaucoma with pain.[184] Costa et al[185] found the combination of penetrating keratoplasty and double-plate Molteno tube implantation effective in controlling pressure and maintaining visual acuity in two eyes with epithelial ingrowth.
Treatment of Cysts and Fibrous Downgrowth
Pearl tumors are rarely treated because they remain unchanged for extended periods. En bloc surgical excision of an anterior chamber cyst and involved iris is indicated if enlargement threatens other intraocular structures. Posttraumatic epithelial cysts usually require surgical intervention for progressive enlargement.
There is no specific treatment for fibrous downgrowth. Attention is directed at the complicating sequelae without necessarily eradicating the fibrous membrane as is necessary in epithelial downgrowth. Secondary glaucoma is managed medically or surgically as necessary. Penetrating keratoplasty may be required for visual rehabilitation. Release of vitreous traction by vitrectomy or Nd:YAG laser lysis may be indicated.
ACKNOWLEDGEMENT
Colour photographs for this chapter are courtesy of Jack J Kanski.
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Key Features: Epithelial Downgrowth |
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REFERENCES
1. von Graefe A: Beitrage zur Pathologie und Therapie des Glaukoms. Arch Ophthalmol 1869; 15:108.
2. Weiss DI, Shaffer RN: Ciliary block (malignant) glaucoma. Trans Am Acad Ophthalmol Otol 1972; 76:450.
3. Shaffer RN, Hoskins Jr HD: Ciliary block (malignant) glaucoma. Ophthalmology 1978; 85:215.
4. Levene R: A new concept of malignant glaucoma. Arch Ophthalmol 1972; 87:497.
5. Chandler PA, Simmons RJ, Grant WM: Malignant glaucoma: Medical and surgical treatment. Am J Ophthalmol 1968; 66:495.
6. Simmons RJ: Malignant glaucoma. Br J Ophthalmol 1972; 56:263.
7. Lowe RF: Malignant glaucoma related to primary angle closure glaucoma. Aust N Z J Ophthalmol 1979; 7:11.
8. Merritt JC: Malignant glaucoma induced by miotics postoperatively in open-angle glaucoma. Arch Ophthalmol 1977; 95:1988.
9. Gorin G: Angle-closure glaucoma induced by miotics. Am J Ophthalmol 1966; 62:1063.
10. Hoshiwara I: Case report of simultaneous malignant glaucoma occurring 3 years after glaucoma surgery. Arch Ophthalmol 1964; 72:601.
11. Jafar MS, Tomey KF: Malignant glaucoma manifesting bilaterally 15 months after peripheral iridectomy. Glaucoma 1982; 4:177.
12. Ellis PP: Malignant glaucoma occurring 16 years after successful filtering surgery. Ann Ophthalmol 1984; 16:177.
13. Wollensak J, Pham DT, Anders N: Ciliolenticular block as a late complication in pseudophakia. Ophthalmologe 1995; 92:280.
14. Hanish SJ, Lamberg RL, Gordon JM: Malignant glaucoma following cataract extraction and intraocular lens implant. Ophthalmic Surg 1982; 13:713.
15. Tomey KF, Senft SH, Antonios SR, et al: Aqueous misdirection and flat chamber after posterior chamber implants with and without trabeculectomy. Arch Ophthalmol 1987; 105:770.
16. Duy TP, Wollensak J: Ciliary block (malignant) glaucoma following posterior chamber lens implantation. Ophthalmic Surg 1987; 18:741.
17. Dickens CJ, Shaffer RN: The medical treatment of ciliary block glaucoma after extracapsular cataract extraction. Am J Ophthalmol 1987; 103:237.
18. Risco JM, Tomey KF, Perkins TW: Laser capsulotomy through intraocular lens positioning holes in anterior aqueous misdirection. Arch Ophthalmol 1989; 107:1569.
19. Reed JE, Thomas JV, Lytle RA, Simmons RJ: Malignant glaucoma induced by an intraocular lens. Ophthalmic Surg 1990; 21:177.
20. Boreham C: Combined extracapsular cataract extraction and posterior chamber intraocular lens implantation and trabeculectomy. Aust N Z J Ophthalmol 1987; 15:201.
21. Luntz MH, Rosenblatt M: Malignant glaucoma. Surv Ophthalmol 1987; 32:73.
22. Brooks AM, Harper CA, Gillies WE: Occurrence of malignant glaucoma after laser iridotomy. Br J Ophthalmol 1989; 73:617.
23. Robinson A, Prialnic M, Deutsch D, Savir H: The onset of malignant glaucoma after prophylactic laser iridotomy. Am J Ophthalmol 1990; 110:95.
24. Aminlari A, Sassani JW: Simultaneous bilateral malignant glaucoma following laser iridotomy. Graefes Arch Clin Exp Ophthalmol 1993; 231:12.
25. DiSclafani M, Liebmann JM, Ritch R: Malignant glaucoma following argon laser release of scleral flap sutures aftertrabeculectomy. Am J Ophthalmol 1989; 108:597.
26. Macken P, Buys Y, Trope GE: Glaucoma laser suture lysis. Br J Ophthalmol 1996; 80:398.
27. Hardten DR, Brown JD: Malignant glaucoma after Nd:YAG cyclophotocoagulation. Am J Ophthalmol 1991; 111:245.
28. Pecora JL: Malignant glaucoma worsened by miotics in a postoperative angle-closure glaucoma patient. Ann Ophthalmol 1979; 11:1412.
29. Rieser JC, Schwartz B: Miotic-induced malignant glaucoma. Arch Ophthalmol 1972; 87:706.
30. Chandler PA, Grant WM: Mydriatic-cycloplegic treatment in malignant glaucoma. Arch Ophthalmol 1962; 68:353.
31. Pollard AF: Secondary angle closure glaucoma in cicatricial retrolental fibroplasia. Am J Ophthalmol 1980; 89:651.
32. Kushner BJ: Ciliary block in retinopathy of prematurity. Arch Ophthalmol 1982; 100:1078.
33. Weiss IS, Deiter PD: Malignant glaucoma syndrome following retinal detachment surgery. Ann Ophthalmol 1974; 6:1099.
34. Weber PA, Cohen JS, Baker D: Central retinal vein occlusion and malignant glaucoma. Arch Ophthalmol 1987; 105:635.
35. Jones BR: Principles in the management of oculomycosis. Trans Am Acad Ophthalmol Otol 1975; 79:15.
36. Lass JH, Thoft RA, Bellows AR, Slansky HH: Exogenous Nocardia asteroides endophthalmitis associated with malignant glaucoma. Ann Ophthalmol 1981; 13:317.
37. Schwartz AL, Anderson DR: 'Malignant glaucoma' in an eye with no antecedent operation or miotics. Arch Ophthalmol 1975; 93:379.
38. Shaffer RN: The role of vitreous detachment in aphakic and malignant glaucoma. Trans Am Acad Ophthalmol Otol 1954; 58:217.
39. Trope GE, Pavlin CJ, Bau A, et al: Malignant glaucoma: Clinical and ultrasound biomicroscopic features. Ophthalmology 1994; 101:1030.
40. Tello C, Chi T, Shepps G, et al: Ultrasound biomicroscopy in pseudophakic malignant glaucoma. Ophthalmology 1993; 100:410.
41. Quigley HA: Malignant glaucoma and fluid flow rate. Am J Ophthalmol 1980; 89:879.
42. Fatt I: Hydraulic flow conductivity of the vitreous gel. Invest Ophthalmol Vis Sci 1977; 16:555.
43. Epstein DL, Hashimoto JM, Anderson PJ, Grant WM: Experimental perfusions through the anterior and vitreous chambers with possible relationships to malignant glaucoma. Am J Ophthalmol 1979; 88:1078.
44. Quigley HA, Friedman DS, Congdon VG: Possible mechanisms of primary angle-closure and malignant glaucoma. J Glaucoma 2003; 12:167.
45. Dugel PR, Heuer DK, Thach AB, et al: Annular peripheral choroidal detachment simulating aqueous misdirection after glaucoma surgery. Ophthalmology 1997; 104:439.
46. Liebmann JM, Weinreb RN, Ritch R: Angle-closure glaucoma associated with occult annular ciliary body detachment. Arch Ophthalmol 1998; 116:731.
47. Weiss DI, Shaffer RN, Harrington DO: Treatment of malignant glaucoma with intravenous mannitol infusion: Medical reformation of the anterior chamber by means of an osmotic agent: A preliminary report. Arch Ophthalmol 1963; 69:154.
48. Beckman H, Blau RP: Oral steroid therapy for ciliary (pseudomalignant) glaucoma. Glaucoma 1981; 3:169.
49. Herschler J: Laser shrinkage of the ciliary processes: A treatment for malignant (ciliary block) glaucoma. Ophthalmology 1980; 87:1155.
50. Weber PA, Henry MA, Kapetansky FM, Lohman LF: Argon laser treatment of the ciliary processes in aphakic glaucoma with flat anterior chamber. Am J Ophthalmol 1984; 97:82.
51. Epstein DL, Steinert RF, Puliafito CA: Neodymium-YAG laser therapy to the anterior hyaloid in aphakic malignant (ciliovitreal block) glaucoma. Am J Ophthalmol 1984; 98:137.
52. Little BC, Hitchings RA: Pseudophakic malignant glaucoma: Nd:YAG capsulotomy as a primary treatment. Eye 1993; 7:102.
53. Carasson RG, Bettlin P, Fiori M, Brancato R: Treatment of malignant glaucoma with contact trans-scleral cyclophotocoagulation. Arch Ophthalmol 1999; 117:688.
54. Benedikt O: A new operative method for the treatment of malignant glaucoma. Klin Monatsbl Augenheilkd 1977; 170:665.
55. Chandler PA: A new operation for malignant glaucoma: a preliminary report. Trans Am Ophthalmol Soc 1964; 62:408.
56. Ruben S, Tsai J, Hitchings R: Malignant glaucoma and its management. Br J Ophthalmolol 1997; 81:163.
57. Koerner FH: Anterior pars plana vitrectomy in ciliary and iris block gluacoma. Graefes Arch Clin Exp Ophthalmol 1980; 214:119.
58. Weiss H, Shin DH, Kollarits CR: Vitrectomy for malignant (ciliary block) glaucomas. Int Ophthalmol Clin 1981; 21:113.
59. Momeda S, Hayashi H, Oshima K: Anterior pars plana vitrectomy for phakic malignant glaucoma. Jpn J Ophthalmol 1983; 27:73.
60. Lynch MG, Brown RH, Michels RG, et al: Surgical vitrectomy for pseudophakic malignant glaucoma. Am J Ophthalmol 1986; 102:148.
61. Harbour JW, Rubsamen PE, Palmberg P: Pars plana vitrectomy in the management of phakic and pseudophakic malignant glaucoma. Arch Ophthalmol 1996; 114:1073.
62. Tsai JC, Barton KA, Miller MH, et al: Surgical results in malignant glaucoma refractory to medical or laser therapy. Eye 1997; 11:677.
63. Chen SDM, Salmon JF, Patel CK: Videoendoscopic-guided fluorescein-assisted vitrectomy with phakic malignant glaucoma. Arch Ophthalmol 2005; 123:1419.
64. Lois N, Wong D, Groenewald C: New surgical approach in the management of pseudophakic malignant glaucoma. Ophthalmology 2001; 108:780.
65. Azuara-Blanco A, Katz LJ, Grandham SB, Spaeth GL: Pars plana tube insertion of aqueous shunt with vitrectomy in malignant glaucoma. Arch Ophthalmol 1998; 116:808.
66. Tomey KF, Traverso CE: The glaucomas in aphakia and pseudophakia. Surv Ophthalmol 1991; 36:79.
67. McGuigan LJB, Gottsch J, Stark WJ, et al: Extracapsular cataract extraction and posterior chamber lens implantation in eyes with preexisting glaucoma. Arch Ophthalmol 1986; 104:1301.
68. West J, Burke J, Cunliffe I, Longstaff S: Prevention of acute postoperative pressure rises in glaucoma patients undergoing cataract extraction with posterior chamber lens implant. Br J Ophthalmol 1992; 76:534.
69. Meyer MA, Savitt ML, Kopitas E: The effect of phacoemulsification on aqueous outflow facility. Ophthalmology 1997; 104:1221.
70. Kooner KS, Dulaney DD, Zimmerman TJ: Intraocular pressure following extracapsular cataract extraction and posterior chamber intraocular lens implantation. Ophthalmic Surg 1988; 19:471.
71. Kooner KS, Dulaney DD, Zimmerman TJ: Intraocular pressure following secondary anterior chamber lens implantation. Ophthalmic Surg 1988; 19:274.
72. Peräsalo R: Phaco-emulsification of cataract in eyes with glaucoma. Acta Ophthalmol Scand 1997; 75:299.
73. Vu MT, Shields MB: The early postoperative pressure course in glaucoma patients following cataract surgery. Ophthalmic Surg 1988; 19:467.
74. Radius RL, Schultz K, Sobocinski K, Schultz RO, Easom H: Pseudophakia and intraocular pressure. Am J Ophthalmol 1984; 97:738.
75. Suzuki R, Kuroki S, Fugiwara N: Ten-year follow-up of intraocular pressure after phacoemulsification and aspiration with intraocular lens implantation performed by the same surgeon. Ophthalmological 1997; 211:79.
76. Gimbel HV, Meyer D, DeBroff BM, et al: Intraocular pressure response to combined phacoemulsification and trabeculectomy ab externo versus phacoemulsification alone in primary open-angle glaucoma. J Cataract Refract Surg 1995; 21:653.
77. Shingleton BJ, Gamell LS, O'Donoghue MWO, et al: Long-term changes in intraocular pressure after clear corneal phacoemulsification: normal patients versus glaucoma suspect and glaucoma patients. J Cataract Refract Surg 1999; 25:885.
78. Tennen DG, Masket S: Short-term and long-term effect of clear corneal incisions on intraocular pressure. J Cataract Refract Surgery 1996; 22:568.
79. Barnes EA, Murdoch IE, Subramaniam S, et al: Neodymium:yttrium-aluminum-garnet capsulotomy and intraocular pressure in pseudophakic patients with glaucoma. Ophthalmology 2004; 111:1393.
80. Kurata F, Krupin T, Sinclair S, Karp L: Progressive glaucomatous visual field loss after neodymium-YAG laser capsulotomy. Am J Ophthalmol 1984; 98:632.
81. Mitchell PG, Blair NP, Deutsch TA, Hershey JM: The effect of neodymium:YAG laser shocks on the blood-aqueous barrier. Ophthalmology 1987; 94:488.
82. Fourman S, Apisson J: Late onset elevation in intraocular pressure after neodymium-YAG laser posterior capsulotomy. Arch Ophthalmol 1991; 109:511.
83. Wetzel W: Ocular aqueous humor dynamics after photodisruptive laser surgery procedures. Ophthalmic Surg 1994; 25:298.
84. Pollack IP, Brown RH, Crandall AS, et al: Prevention of the rise in intraocular pressure following neodymium-YAGposterior capsulotomy using topical 1% apraclonidine. Arch Ophthalmol 1988; 106:754.
85. Migliori ME, Beckman H, Channell MM: Intraocular pressure changes after neodymium-YAG laser capsulotomy in eyes pretreated with Timolol. Arch Ophthalmol 1987; 105:473.
86. Liesegang TJ: Viscoelastic substances in ophthalmology. Surv Ophthalmol 1990; 34:268.
87. Cherfan GM, Rich WJ, Wright G: Raised intraocular pressure and other problems with sodium hyaluronate and cataract surgery. Trans Ophthalmol Soc UK 1983; 103:277.
88. Naeser K, Thim K, Hansen TE, et al: Intraocular pressure in the first days after implantation of posterior chamber lenses with the use of sodium hyaluronate (Healon). Acta Ophthalmol 1986; 64:330.
89. Alpar JJ, Alpar AJ, Baca J, Chapman D: Comparison of Healon and Viscoat in cataract extraction and intraocular lens implantation. Ophthalmic Surg 1988; 19:636.
90. Barron BA, Busin M, Page C, et al: Comparison of the effects of Viscoat and Healon on postoperative intraocular pressure. Am J Ophthalmol 1985; 100:377.
91. Caporossi A, Baiocchi S, Sforzi C, Frezzotti HE: Healon GV versus Healon in demanding cataract surgery. J Cataract Refract Surg 1995; 21:710.
92. Schwenn O, Dick HB, Krummenauer F, et al: Healon 5 versus Viscoat during cataract surgery: intraocular pressure, laser flare and corneal changes. Graefes Arch Clin Exp Ophthalmol 2000; 238:861.
93. Arshinoff SA, Albiani DA, Taylor-Laporte J: Intraocular pressure after bilateral cataract surgery using Healon, Healon 5 and Healon GV. J Cataract Refract Surg 2002; 28:617.
94. Aron-Rosa D, Cohn HC, Aron JJ, Bouquety C: Methylcellulose instead of Healon in extracapsular surgery with intraocular lens implantation. Ophthalmology 1983; 90:1235.
95. Fry LL: Postoperative intraocular pressure rises: A comparison of Healon, Amvisc, and Viscoat. J Cataract Refract Surg 1989; 15:415.
96. Jurgens I, Matheu A, Castilla M: Ocular hypertension after cataract surgery. A comparison of three surgical techniques and two viscoelastics. Ophthalmic Surg 1997; 28:30.
97. Lane SS, Naylor DW, Kullerstrand LJ, et al: Prospective comparison of the effects of Occucoat, Viscoat, and Healon on intraocular pressure and endothelial cell loss. J Cataract Refract Surg 1991; 17:21.
98. MacRae SM, Edelhauser HF, Hyndiuk RA, et al: The effects of sodium hyaluronate, chondroitin sulfate, and methylcellulose on the corneal endothelium and intraocular pressure. Am J Ophthalmol 1983; 95:332.
99. Glasser DB, Matsuda M, Edelhauser HF: A comparison of the efficacy and toxicity of and intraocular pressure response to viscous solutions in the anterior chamber. Arch Ophthalmol 1986; 104:1819.
100. Wiles SB, MacKenzie D, Ide CH: Control of intraocular pressure with apraclonidine hydrochloride after cataract extraction. Am J Ophthalmol 1991; 111:184.
101. Hollands RH, Drance SM, Schulzer M: The effect of acetylcholine on early postoperative intraocular pressure. Am J Ophthalmol 1987; 103:749.
102. Ruiz RS, Wilson CA, Musgrove KH, Prager TC: Management of increased intraocular pressure after cataract extraction. Am J Ophthalmol 1987; 103:487.
103. Hollands RH, Drance SM, Schulzer M: The effect of intracameral carbachol on intraocular pressure after cataract extraction. Am J Ophthalmol 1987; 104:225.
104. Biedler B, Rothkoff L, Blumenthal M: The effect of acetazolamide on early intraocular pressure after cataract extraction. Am J Ophthalmol 1977; 83:565.
105. Ostbaum JA, Galin MA: The effects of timolol on cataract extraction and intraocular pressure. Am J Ophthalmol 1979; 88:1017.
106. West DR, Lischwe TD, Thompson VM, Ide CH: Comparative efficacy of the ?-blockers for the prevention of increased intraocular pressure after cataract extraction. Am J Ophthalmol 1988; 106:168.
107. Swan KC: Hyphema due to wound vascularization after cataract extraction. Arch Ophthalmol 1973; 89:87.
108. Jarstad JS, Hardwig PW: Intraocular hemorrhage from wound neovascularization years after anterior segment surgery (Swan syndrome). Can J Ophthalmol 1987; 22:271.
109. Petrelli EA, Wiznia RA: Argon laser photocoagulation of inner wound vascularization after cataract extraction. Am J Ophthalmol 1977; 84:58.
110. McDonnell PJ, Champion R, Green WR: Location and composition of haptics of posterior chamber intraocular lenses. Ophthalmology 1987; 94:136.
111. Johnson SH, Kratz RP, Olson PF: Iris transillumination defect and microhyphema syndrome. Am Intraocul Implant Soc J 1984; 10:425.
112. Hutton WL, Snyder WB, Vaiser A: Management of surgically dislocated intravitreal lens fragments by pars plana vitrectomy. Ophthalmology 1978; 85:176.
113. Layden NW: Pseudophakia and glaucoma. Ophthalmology 1982; 89:875.
114. Apple DJ, Brems RN, Park RB, et al: Anterior chamber lenses. Part I: Complications and pathology and a review of designs. J Cataract Refract Surg 1987; 13:157.
115. Miyake K, Asakura M, Kobayashi H: Effect of intraocular lens fixation on the blood-aqueous barrier. Am J Ophthalmol 1984; 98:451.
116. Piette S, Canlas OA, Tran HV, et al: Ultrasound biomicroscopy in uveitis-glaucoma-hyphema syndrome. Am J Ophthalmol 2002; 133:839.
117. Kirsch RE: Glaucoma following cataract extraction associated with use of alpha-chymotrypsin. Arch Ophthalmol 1964; 72:612.
118. Podos SM, Krupin T, Assef C, Becker B: Topically administered corticosteroid preparations: Comparison of intraocular pressure effects. Arch Ophthalmol 1971; 86:251.
119. Jonas JB, Kreissig I, Degenring R: Intraocular pressure after intravitreal injection of triamicinlone acetonide. Br J Ophthalmol 2003; 87:24.
120. Epstein DL: Diagnosis and management of lens-induced glaucoma. Ophthalmology 1982; 89:3.
121. Rosenbaum JT, Samples JR, Seymour B, et al: Chemotactic activity of lens proteins and the pathogenesis of phacolytic glaucoma. Arch Ophthalmol 1987; 105:1582.
122. Campbell DG, Simmons RJ, Grant WM: Ghost cells as a cause of glaucoma. Am J Ophthalmol 1976; 81:441.
123. Summers CG, Lindstrom RL, Cameron JD: Phase contrast microscopy: Diagnosis of ghost cell glaucoma following cataract extraction. Surv Ophthalmol 1984; 28:342.
124. Summers CG, Lindstrom RL: Ghost cell glaucoma following lens implantation. Am Intraocul Implant Soc J 1983; 9:429.
125. Brucker AJ, Michels RG, Green WR: Pars plana vitrectomy in the management of blood-induced glaucoma with vitreous hemorrhage. Ann Ophthalmol 1978; 10:1427.
126. Ballin N, Weiss DM: Pigment dispersion and intraocular pressure elevation in pseudophakia. Ann Ophthalmol 1982; 14:627.
127. Brandt JD, Mockovak ME, Chayet A: Pigmentary dispersion syndrome induced by a posterior chamber phakic refractive lens. Am J Ophthalmolol 2001; 131:260.
128. Samples JR, Van Buskirk EM: Pigmentary glaucoma associated with posterior chamber intraocular lenses. Am J Ophthalmol 1985; 100:385.
129. Woodhams T, Lester JC: Pigmentary dispersion glaucoma secondary to posterior chamber intraocular lenses. Ann Ophthalmol 1984; 16:852.
130. Grant WM: Open-angle glaucoma associated with vitreous filling the anterior chamber. Trans Am Ophthalmol Soc 1963; 61:197.
131. Sugar SH: Pupillary block and pupil-block glaucoma following cataract extraction. Am Ophthalmol 1966; 61:435.
132. Anderson DR, Forster RK, Lewis ML: Laser iridotomy for aphakic pupillary block. Arch Ophthalmol 1975; 93:343.
133. Chandler PA: Glaucoma from pupillary block in aphakia. Arch Ophthalmol 1962; 67:14.
134. Van Buskirk EM: Pupillary block after intraocular lens implantation. Am J Ophthalmol 1983; 95:55.
135. Werner D, Kaback M: Pseudophakic pupillary-block glaucoma. Ophthalmology 1977; 61:329.
136. Weinreb RN, Wasserstrom JP, Forman JS, Ritch R: Pseudophakic pupillary block with angle-closure glaucoma in diabetic patients. Am J Ophthalmol 1986; 102:325.
137. Samples JR, Bellows AR, Rosenquist RC, et al: Pupillary block with posterior chamber intraocular lenses. Arch Ophthalmol 1987; 105:335.
138. Sathish S, MacKinnon JR, Atta HR: Role of ultrasound biomicroscopy in managing pseudophakic pupillary block glaucoma. J Cat Refract Surg 2000; 26:1836.
139. Evans RB: Peripheral anterior synechia overlying the haptics of posterior chamber lenses. Occurrence and natural history. Ophthalmology 1990; 97:415.
140. Yeo JH, Jakobiec FA, Pukorny K: The ultrastructure of anterior intraocular lens "cocoon membrane.". Ophthalmology 1983; 90:410.
141. Bomer TG, Lagréze WD, Funk J: Intraocular pressure rise after phacoemulsification with posterior chamber lens implantation: effectof prophylactic medication, wound closure, and surgeon's experience. Br J Ophthalmol 1995; 79:809.
142. Willes SB, MacKenzie D, Ide CH: Control of intraocular pressure with apraclonidine hydrochloride after cataract extraction. Am J Ophthalmol 1991; 111:184.
143. Schwenn O, Xia N, Krummenauer F, Dick HB: Prevention of early postoperative increase in intraocular pressure after phacoemulsification: comparison of different antiglaucoma drugs. Ophthalmologe 2001; 98:934.
144. Arcieri ES, Santana A, Rocha FN, et al: Blood-aqueous barrier changes after the use of prostaglandin analogues in patients with pseudophakia and aphakia: a 6-month randomized trial. Arch Ophthalmol 2005; 123:186.
145. Halpern DL, Pasquale LR: Cystoid macular edema in aphakia and pseudophakia after use of prostaglandin analogs. Semin Ophthalmol 2002; 17:181.
146. Wand M, Gaudio AR, Shields MB: Latanoprost and cystoid macular edema in high-risk aphakic or pseudophakic eyes. J Cataract Refract Surg 2001; 27:1397.
147. Asaria RHY, Salmon JF, Skinner AR, et al: Electron microscopy findings on an intraocular lens in the uveitis, glaucoma, hyphaema syndrome. Eye 1997; 11:827.
148. Peyman GA, Sanders DR, Minatoya H: Pars plana vitrectomy in the management of pupillary block glaucoma following irrigation and aspiration. Br J Ophthalmol 1978; 62:336.
149. Bellows AR, Johnstone MA: Surgical management of chronic glaucoma in aphakia. Ophthalmology 1983; 90:807.
150. Schultz JS, Slamovits TL, Rockwood EJ, Coleman AL: Surgical management of glaucoma associated with pseudophakia. Surv Ophthalmol 2001; 46:275.
151. Lee LC, Pasquale LR: Surgical management of glaucoma in pseudophakic patients. Semin Ophthalmol 2002; 17:131.
152. Thomas JV, Simmons RJ, Belcher CD: Argon laser trabeculoplasty in the pre-surgical glaucoma patient. Ophthalmology 1982; 89:187.
153. Schwartz AL, Wilson MC, Schwartz LW: Efficacy of argon laser trabeculoplasty in aphakic and pseudophakic eyes. Ophthalmic Surg Lasers 1997; 28:215.
154. Gross RL, Feldman RM, Spaeth GL, et al: Surgical therapy of chronic glaucoma in aphakia and pseudophakia. Ophthalmology 1988; 95:1195.
155. Shingleton BJ, Alfano C, O'Donoghue MW, Rivera J: Efficacy of glaucoma filtration surgery in pseudophakic patients with or without conjunctival scarring. J Cataract Refract Surg 2004; 30:2504.
156. Fontana H, Nouri-Mahdavi K, Caprioli J: Trabeculectomy with mitomycin C in pseudophakic patients with open-angle glaucoma: outcomes and risk factors for failure. Am J Ophthalmol 2006; 141:652.
157. The Fluorouracil Filtering Surgery Study Group: Three year follow-up of the Fluorouracil Filtering Surgery Study. Am J Ophthalmol 1993; 115:82.
158. Lamping KA, Belkin JK: 5-Fluorouracil and mitomycin C in pseudophakic patients. Ophthalmology 1995; 102:70.
159. Prata JA, Minckler DS, Baerveldt G, et al: Trabeculectomy in pseudophakic patients: postoperative 5-fluorouracil versus intraocular mitomycinC antiproliferative therapy. Ophthalmic Surg 1995; 26:73.
160. Lamping KA, Belkin JK: 5-Fluorouracil and mitomycinC in pseudophakic patients. Ophthalmology 1995; 102:70.
161. Assaad MH, Baerveldt G, Rockwood EJ: Glaucoma drainage devices: pros and cons. Curr Opin Ophthalmol 1999; 10:147.
162. Broadway DC, Iester M, Schulzer M, Douglas GR: Survival analysis for success of Molteno tube implants. Br J Ophthalmol 2001; 85:689.
163. Heuer DK, Lloyd MA, Abrams DA, et al: Which is better? One or two? A randomized clinical trial of single-plate versus double-plate Molteno implantation for glaucomas in aphakia and pseudophakia. Ophthalmology 1992; 99:1512.
164. Shields MB, Shields SE: Noncontact transscleral Nd:YAG cyclophoto-coagulation: a long-term follow-up of 500 patients. Trans Am Ophthalmol Soc 1994; 92:271.discussion 283.
165. Bloom PA, Tsai JC, Sharma K, et al: "Cyclodiode": trans-scleral diode laser cyclo photogoagulation in the treatment of advanced refractory glaucoma. Ophthalmology 1997; 104:1508.
166. Collins ET, Cross FR: Two cases of epithelial implantation cyst in the anterior chamber after extraction of cataract. Trans Ophthal Soc UK 1892; 12:175.
167. Perera C: Epithelium in the anterior chamber of the eye after operation and injury. Trans Am Acad Ophthal Otol 1937; 42:142.
168. Weiner MJ, Trentacoste J, Pon DM, Albert DM: Epithelial downgrowth: a 30-year clinicopathological review. Br J Ophthalmol 1989; 73:6.
169. Regan LF: Epithelial invasion of the anterior chamber. Trans Am Ophthalmol Soc 1957; 55:741.
170. Maumenee AE, Paton D, Morse PH, Butner R: Review of 40 histologically proven cases of epithelial downgrowth following cataract extraction and suggested surgical management. Am J Ophthalmol 1970; 69:598.
171. Smith RE, Parrett C: Specular microscopy of epithelial downgrowth. Arch Ophthalmol 1978; 96:1222.
172. Smith MF, Doyle JW: Glaucoma secondary to epithelial and fibrous downgrowth. Semin Ophthalmol 1994; 9:248.
173. Swan KC: Fibroblastic ingrowth following cataract extraction. Arch Ophthalmol 1973; 89:445.
174. Dunnington JH: Healing of incisions for cataract extraction. Am J Ophthalmol 1951; 34:36.
175. Cameron JD, Flaxman BA, Yanoff M: In vitro studies of corneal wound healing: Epithelial endothelial interactions. Invest Ophthalmol 1974; 12:575.
176. Henderson T: A histological study of the normal healing of wounds after cataract extraction. Ophthalmol Rev 1907; 26:127.
177. Stark WJ, Michels RG, Maumenee AE, Cupples H: Surgical management of epithelial ingrowth. Am J Ophthalmol 1978; 85:772.
178. Peyman GA, Peralta E, Ganiban GJ, Kraut R: Endoresection of the iris and ciliary body in epithelial downgrowth. J Cataract Refract Surg 1998; 1998:130.
179. Friedman AH: Radical anterior segment surgery for epithelial invasion of the anterior chamber. Report of three cases. Trans Am Acad Ophthalmol Otolaryngol 1977; 83:216.
180. Brown SI: Treatment of advanced epithelial downgrowth. Trans Am Acad Ophthalmol Otol 1973; 77:618.
181. Naumann GOH, Rummelt V: Block excision of cystic and diffuse epithelial ingrowth of the anterior chamber. Arch Ophthalmol 1992; 110:223.
182. Shaikh AA, Damji KF, Mintsiolis G, et al: Bilateral epithelial downgrowth managed in one eye with intraocular 5-fluorouracil. Arch Ophthalmol 2002; 120:1396.
183. Loane ME, Weinreb RN: Glaucoma secondary to epithelial downgrowth and 5-fluorouracil. Ophthalmic Surg 1990; 21:704.
184. Fish LA, Heuer DK, Baerveldt G, et al: Molteno implantation for secondary glaucoma associated with advanced epithelial downgrowth. Ophthalmology 1990; 97:557.
185. Costa VP, Katz LJ, Cohen EJ, Raber IM: Glaucoma secondary to epithelial downgrowth and 5-fluorouracil. Ophthalmic Surg 1990; 21:704.
