Hippocrates made no distinction between cataracts and glaucoma. According to the Greek writings, the term glaucoma defines a “glazed appearance without luster.” In the translation from Greek to Latin, and subsequently into Arabic, this disorder was termed “suffusio.” In the translation of the Arabic teachings back to Latin during the Middle Ages, the term cataract, meaning “waterfall,” was used in reference to suffusio. The term cataract was not known to the Greek writers. Subsequently, the distinctions between the two distinct diseases were first made and accepted during the 17th and 18th centuries. Since that time, they have been treated and approached as two separate but not mutually exclusive causes of human visual impairment.

INFANTILE GLAUCOMA

In infantile glaucoma (without other associated anomalies) there have been notations of cataracts before the patients underwent glaucoma surgery. However, in the majority of patients with infantile glaucoma without anomalies, there are no associated congenital cataracts. When lens opacities do occur, they typically occur after surgical intervention, including both angle and filtering surgery. During the surgery for resistant infantile glaucoma, if fistulizing procedures are necessary, occasionally the crystalline lens is lax and may have a tendency to dislocate; this accounts for the prolapse of the lens into the anterior chamber and the fistula that results in cataractous changes.

Another association of the lens with infantile glaucoma is microphakia. However, this may be a misnomer because of the buphthalmic enlargement of the globe.³ Fortunately, overall, uncomplicated infantile glaucoma without congenital or secondary cataracts is encountered most commonly.

Performing lensectomy during the first 4 weeks of life is associated with a higher risk of subsequent glaucoma than when surgery is performed at a later date. The reason for this association is unknown, but it seems reasonable to delay surgery until the infant is more than 1 month old. These children must undergo regular screenings for glaucoma because it can develop at any time.⁴ A conflicting report suggests that early cataract surgery (within the first 2 weeks of life) is associated with the fewest postoperative complications, including glaucoma, nystagmus, strabismus, and secondary membranes.⁵

Cataracts may be present in a large number of aniridic patients, appearing with advancing age. They are most often developmental and are cortical or polar in location. Cataracts also may be present at birth owing to subluxed or dislocated lenses with adherence to the cornea endothelium. Any surgical procedures performed for aniridia, such as goniotomy for lysis of iris stump adhesions or filtration procedures, also may hasten or cause the development of cataracts. If a child's vision is threatened, cataract formation in aniridia must be treated surgically in an effort to prevent amblyopia. Membranous cataracts and glaucoma formation also have been reported with aniridia.⁹

Axenfeld-Rieger syndrome commonly is associated with glaucoma and occasionally with cataracts as well. It is characterized by posterior embryotoxon (anterior displacement of Schwalbe's line) combined with other ocular findings, such as attached iris strands, iris hypoplasia, and anterior chamber dysgenesis. Fifty percent of these eyes develop glaucoma in late childhood or adulthood.¹¹ Cataracts also are occasionally found in these patients, although not as commonly as glaucoma. When present, lenticular changes vary from nuclear cataracts to anterior polar cataracts. Coloboma of the lens and ectopia lentis also may be present. The glaucoma usually develops before any significant cataract formation in the second or third decade of life. Of note, posterior embryotoxon can be seen as an isolated finding in 15% of normal patients.

Peter's anomaly consists of a posterior corneal defect with opacity of the stroma. In some cases, iris strands adhere to the border of the corneal defect and in severe cases the lens itself adheres to the corneal defect. Peter's anomaly is often the final result of defects such as congenital rubella and the Axenfeld-Rieger's syndrome.¹¹ Peter's anomaly is the most severe of the spectrum of mesodermal dysgeneses, representing difficulties with cataracts and glaucoma often occurring at birth. Because of the severity of the problem, early cataract extraction may be necessary, possibly combined with corneal transplantation. In some instances, only corneal surgery is needed. Goniotomies are difficult to perform in these patients and may be of no benefit. Often the associated glaucoma has to be treated essentially as open-angle glaucoma; fistulizing operations may be necessary. Trabeculotomy for this condition has been associated with secondary cataracts.¹¹

MARFAN'S SYNDROME

Marfan's syndrome is an entity involving the musculoskeletal, cardiovascular, and ocular tissues. Ectopia lentis is seen in up to 70% of those afflicted. The lens also may be globular and have small cortical opacities. Glaucoma can be seen in up to 75% of people with Marfan's syndrome, and often is congenital with anterior chamber anomalies. However, the glaucoma also can be caused by the forward dislocation of the anomalous lens, resulting in secondary angle-closure glaucoma. Miotics have been known to increase pupillary block with such lenses, giving a “paradoxic” angle closure. Treatment may be directed to mydriasis or peripheral iridectomy for this secondary angle-closure glaucoma. If the glaucoma is on the basis of angle anomalies, goniotomies have been attempted. Removal of the lens often results in vitreous loss and should be done only in a vision-threatening situation. Also, any time surgery is performed in a patient with Marfan's syndrome, thromboembolic phenomena associated with anesthesia should be addressed as possible complications.

MARCHESANI'S SYNDROME

Weill-Marchesani's syndrome can be associated with microspherophakia, lens subluxation, and angle anomaly associated with mesodermal dysgenesis.¹² Congenital glaucoma can occur from the angle dysgenesis or a lens dislocation can give rise to a secondary angle closure. Although no reports of cataracts primarily occurring in this syndrome have been described, cataract formation can occur. Capsular tension rings may be a useful adjunct to cataract surgery in these and similar patients.¹³

LOWE'S SYNDROME

The oculocerebrorenal syndrome known as Lowe's syndrome was first described in 1952.¹⁴ It is one of the two major syndromes with naturally occurring cataracts and congenital glaucoma (the other is rubella). The cataracts are bilateral and occur in virtually all reported cases.³ They are present prior to the fifth week of development in utero, with defects of the anterior, equatorial, and posterior subcapsular areas. This is a sex-linked inherited disease. Female carriers exhibit punctate opacities of the lens, which do not cause visual impairment (Fig. 2). Glaucoma, which is present in 60% to 70% of patients, is of an infantile variety with angle anomalies. Systemic manifestations include mental retardation and renal anomalies resulting in aminoaciduria.

Ocular treatment usually is directed toward prevention of amblyopia by aspiration of cataracts and includes goniotomy for the glaucoma. It may be best to do the glaucoma surgery first, followed by lens aspiration. These eyes often respond poorly, with secondary hemorrhages resulting from goniotomies and, despite intensive therapy, blindness may result. Because of the systemic defects, including mental retardation and bone abnormalities resulting from secondary rickets, the overall prognosis is poor.

RUBELLA SYNDROME

The other major common syndrome in which infantile glaucoma is associated with congenital cataracts is rubella, also known as German measles. This is classified as a syndrome and is caused by an in utero rubella virus infection.³

In patients in whom the virus infection occurs during the first trimester of pregnancy, cataracts and glaucoma may both develop. If the infection occurs later, such as during the second trimester, only the glaucoma ensues, because by this time the lens has completed its embryonic capsular development. The glaucoma is frequently attributed to angle maldevelopment. Glaucoma occurs in 10% to 20% of those with rubella, whereas cataracts develop 10 times more frequently. The two may be mutually exclusive in some cases.

Heart anomalies, mental retardation, and hearing abnormalities are associated along with the ocular problems. These have to be considered in determining the time of surgical intervention. The cataracts are usually nuclear in location, but the cortical fibers often become involved secondarily. There have been reports of persistence of the virus in the lens, and this should be considered when performing aspiration of the lens in the infant.³ Spherophakia has been noted histologically and could conceivably result in pupillary block in rare instances. Continued development of the angle after birth could account for some of the reported cases of spontaneous resolution of the infantile glaucoma. An interesting observation of specks or pigmentation of the angle has been described in infantile glaucoma.¹⁵ This is in addition to the typical mottled pigmentation of the retinal posterior pole. A concomitant keratitis may complicate the picture when one is attempting to make a determination as to whether the pressure is elevated in infancy. This keratouveitis may rarely cause a secondary form of glaucoma. When cataracts and glaucoma occur together, the glaucoma usually should be treated before the cataract surgery.¹⁶ Secondary glaucoma can occur after cataract surgery. Despite modern surgical techniques, visual acuity after cataract extraction still remains poor in many of these patients.¹⁷

HOMOCYSTINURIA

Homocystinuria is caused by an autosomal recessive enzymatic defect, resulting in increased blood concentrations of homocysteine and methionine. Inability to metabolize homocystine is apparently caused by the absence of cystathionine beta-synthase.¹⁸ Aminoaciduria, mental retardation, a fair appearance, malar flush, and a stature similar to Marfan's syndrome are possible systemic findings. The ocular findings include dislocated lenses in 90% of patients and often a pupillary block with secondary glaucoma.¹⁹ Cataracts are seen in 20% of patients, and glaucoma on a secondary or congenital basis is seen in approximately 10% of patients. A nonsurgical treatment consisting of a low methionine diet and supplementary vitamin B6 during the early weeks of infant life has been shown to significantly reduce the risk of ocular complications associated with this disease.^19,20 Any surgical treatment must take into account the tendency for thromboembolic phenomena under general anesthesia in those with this disease.

CHROMOSOMAL ANOMALIES

Many chromosomal anomalies have been associated with ophthalmic disorders, including cataracts and glaucoma. These and other eye findings usually are seen together with other systemic signs such as deafness, heart defects, mental retardation, polydactyly, seizures, and cleft lip. Three of the more common chromosomal anomalies are trisomy 21, 18, and 13 (Down's, Edward's and Patau's syndromes, respectively), which all can have ophthalmic manifestations.

Trisomy 21 affects approximately 1.69 in 1000 live births, making it the most common major chromosomal abnormality.²¹ Ophthalmic disorders are encountered in 60% of these patients, with congenital cataracts seen in approximately 3%, according to one source.²² A majority of Down's syndrome patients have acquired lens opacities by adulthood as a complication of the premature senescence commonly seen.²³

Trisomy 18 and 13 occur at much lower incidences than trisomy 21. Both have poor 1-year survival rates and only rarely do patients live into their teen years. Patients with these two disorders often suffer from a variety of physical developmental problems, including microphthalmia. If the microphthalmia is severe enough, it can lead to primarily nuclear cataract formation and persistent hyperplastic primary vitreous (PHPV), the latter sometimes associated with glaucoma. Surgical intervention for cataracts and glaucoma must be weighed in view of the overall poor prognosis of these and the many other chromosomal syndromes.²⁴

PIERRE ROBIN'S SYNDROME

This syndrome of micrognathia, cleft palate, and glossoptosis has varied ocular anomalies, including congenital glaucoma and cataracts.²⁵ Retinal detachment, high myopia, microphthalmia, and esotropia also are noted. Failure of the lower jaw to come forward with normal development at approximately the fourth month of fetal life could be associated with concomitant angle anomalies, resulting in angle maldevelopment at the same stage of embryogenesis. The cataracts consist of posterior subcapsular opacities. The glaucoma may require surgical intervention. When surgery is necessary, any heart defects must be considered when assessing risk. The prognosis is not poor, however, and attempts to prevent visual deprivation or blindness often are rewarding.

PERSISTENT HYPERPLASTIC PRIMARY VITREOUS

Persistent hyperplastic primary vitreous is a congenital anomaly in which the primary vitreous adheres to the posterior capsule of the lens, resulting in cataract formation. Glaucoma is not on the basis of angle anomalies, but usually is secondary to angle closure, because of either intumescence of the lens or hemorrhage from the persistent vessels on the posterior aspect of the lens. The glaucoma usually is approached as a secondary angle-closure glaucoma, with iridectomy or lens aspiration as the treatment of choice.

Retinopathy of Prematurity

In advanced retinopathy of prematurity, tissue from the retinal periphery can extend to the retrolental area, and this fibrovascular tissue can form a pseudotumor. As this progresses, total retinal detachment, secondary hemorrhage, swelling and edema of the mass, and the development of posterior synechia can occur. The anterior chamber can become shallow, resulting in secondary angle-closure glaucoma. This has been noted to occur in approximately 2% of patients. Lens aspiration may be performed to relieve the forward displacement of the iris-lens diaphragm (Fig. 3), and iridectomy usually is necessary. This is often done for cosmetic purposes to prevent enucleation, as vision is usually poor because of the underlying retinal problems.

Angle-closure glaucoma after photocoagulation for retinopathy of prematurity has been reported.²⁶ Confluent laser photoablation also has been associated with cataracts and other complications,²⁷ mostly related to anterior chamber ischemia.²⁸ Overall, the incidence of cataract formation in patients who have undergone argon laser photocoagulation for retinopathy of prematurity is approximately 1%. The occurrence of cataracts may be higher when persistent hyaloidal vessels are present on the lens.²⁶

OTHER SYNDROMES

For a complete list of all the associated syndromes of lenticular opacities with infantile glaucoma, several other syndromes would have to be included that are beyond the scope of this text.

There are many possible causes, including lens remnants with swelling, postoperative uveitis with occlusion of the pupil and peripheral anterior synechiae, and postsurgical flat anterior chambers with resultant synechia of the angle. Blockage of the pupil by vitreous may occur. Hyphema and, rarely, epithelial invasion of the anterior chamber have been noted. The uveitis may result from the presence of virus (as in the rubella syndrome), the surgical procedure itself, or retained lens particles. Measures directed toward each of these etiologies can be instituted. One report³¹ indicates that even though the angle remains completely free of any debris or inflammation, glaucoma may ensue after congenital cataract surgery. This glaucoma may result from underlying angle anomalies and could represent the coexistence of congenital glaucoma and cataracts. The postoperative appearance of the angle with an anterior iris insertion and prominent uveal scleral meshwork supports this. The time interval between the original cataract surgery and the onset of glaucoma is variable, with glaucoma occasionally occurring many years later.³² Thus, patients should be followed indefinitely for pressure stability, even if this requires examination under anesthesia.

Interestingly, aphakia may be a risk factor for open-angle glaucoma. Research suggests that placing a posterior-chamber intraocular lens during congenital cataract surgery significantly decreases the incidence of postoperative glaucoma, although the mechanism for this is unclear.³³

Treatment for postcataract surgery glaucoma is usually the same as that for open-angle glaucoma, with medications being the initial modality of choice. Surgical intervention is shown to have limited success.³⁴

If the lens anomaly is the cause of the glaucoma or visual impairment resulting from cataractous changes is present, removal of the lens may be indicated. A peripheral iridectomy in the presence of a subluxated clear lens may relieve the glaucoma. The treatment of angle-contusion glaucoma is essentially the same as for open-angle glaucoma, regardless of age.

If hyphema is present, a secondary glaucoma may result. This is more commonly seen in the eight-ball or total anterior chamber hemorrhage. In these patients, cataracts, either of posterior subcapsular or anterior subcapsular location, often are seen. Treatment is directed toward control of the bleeding. If blood staining of the cornea or intractable intraocular pressure ensues, irrigation of the chamber may be attempted. Various methods, including diathermy, fibrinolysis, and cryoextraction of the clot, have been tried in the treatment of this difficult problem.³¹ Essentially, treatment has to be individualized because there is no commonly accepted mode of therapy.

If the cataract is of such a nature to decrease vision significantly, the treatment is cataract removal and iridectomy. It is well known that treatment with parasympathomimetic agents, such as pilocarpine, has been implicated in the formation of lens opacities,⁴⁰ although this may be related to older studies of its previous long-term use in open-angle glaucoma rather than short-term use in angle-closure glaucoma. Miotic therapy is discussed in further detail later in this chapter.

A peripheral iridectomy is the treatment of choice for pupillary block glaucoma. Most iridectomies today are performed by laser, although surgical iridectomies are still performed in many parts of the world. The incidence of lens opacities after surgical peripheral iridectomy is increased, usually related to direct injury from a surgical instrument. Meticulous care at the time of surgery may decrease the incidence of direct traumatic cataracts.³⁸ Prolonged flat anterior chambers occurring after peripheral iridectomy also may lead to a higher incidence of cataracts.

Although the advent of laser iridotomy has greatly decreased the incidence of cataract development compared to surgical iridotomy, laser iridotomy (Fig. 4) also can cause lenticular changes. Several reports have demonstrated small lens opacities appearing at the site of the laser beam after laser iridotomy (Fig. 5),^36,41,42 but no progression of these opacities has been described. Zonular rupture can occur from the laser as well.⁴³ One case report describes an “exploding” cataract with posterior capsular rupture and release of cortical material into the vitreous following a YAG laser peripheral iridectomy.³⁷

Regardless of whether cataracts are associated with iridectomies, this intervention is still the treatment of choice in primary angle-closure glaucoma in which the cataract causes reversible visual loss, but glaucomatous damage to the nerve is irreversible.

OCULAR HYPERTENSION

An extensive review of currently published literature fails to find a correlation between open-angle glaucoma itself and cataracts. However, surgeries for either glaucoma or cataracts can lead to formation of the other. Some medical therapies for glaucoma can be associated with cataract formation, but most of these have been replaced with noncataractogenic medications.

Visual field testing may be altered by the presence of cataracts, potentially leading to the false interpretation of glaucomatous damage (Fig. 6).⁴⁵ When both the optic nerve and visual field cannot be evaluated because of lenticular opacities, then the clinician must rely most heavily on the binocular status of the patient, the level of intraocular pressure, and the results of the last reliable examination. Lens extraction generally is justified if management of the glaucoma is hindered by the cataract, such as in unreliable visual field results or poor visualization of the optic nerve.

  Prostaglandin analogues
  Beta-adrenergic antagonists
  Carbonic anhydrase inhibitors
  Adrenergic agents (nonselective and selective alpha-2 agonists)

An extensive review of the literature found no association between glaucoma medications from the listed categories and cataract formation.

Miotic therapy itself, in addition to reducing the visual acuity in those with pre-existing cataracts, has been noted to be cataractogenic.^40,46 The most common association is with the anticholinesterases.⁴⁷ Lens opacities have been noted in more than 50% of patients treated for a long period with strong anticholinesterases. The exact mechanism of cataract formation after the use of anticholinesterases has not been elucidated, and articles even argue against a causal relationship.⁴⁸ Other reports, however, implicate the long-term use of anticholinesterases in concentrations greater than 0.06%. Whether the cataracts are reversible is debatable and seems to depend on the age of the patient being treated. Lens opacities in younger people are more likely to be reversible.⁴⁹

The bottom line is that miotic therapy can be both cataractogenic and visually disturbing because of pupillary constriction. Luckily, miotic therapy has been largely replaced with therapies that are neither cataractogenic nor cause pupillary constriction; therefore, miotic therapy should generally be reserved as a last-line agent for open-angle glaucoma.

EXFOLIATION SYNDROME

In the exfoliation syndrome (pseudoexfoliation), fibrillar material is scattered throughout the anterior chamber of the eye. Histochemically the material is similar to amyloid. It has been found in and on the lens epithelium and capsule, lens zonular fibers, ciliary epithelium, pupillary margin, iris pigment epithelium, iris stroma, iris blood vessels, corneal epithelium, and subconjunctival tissue (Fig. 7).^50,51 On the anterior lens capsule, a peripheral zone of exfoliative material is separated from a central zone by a clear area, presumably from the iris rubbing away the material. The source of the material is not yet known, but it appears unlikely that the lens is the sole source of the particles as deposits of material persist after cataract extraction. It is assumed that multiple sources contribute as part of a generalized basement membrane disorder. Exfoliation syndrome is a systemic disease, as fibrillar material has been found in connective tissue portions of various visceral organs.⁵² This syndrome is most commonly found in elderly patients.

The anterior chamber angle in pseudoexfoliation exhibits a heavily pigmented trabecular meshwork and an inferior pigmented deposition anterior to Schwalbe's line (Sampoelesi's line). Often the angle is narrow, presumably from anterior displacement of the lens secondary to zonular weakness. Exfoliation syndrome is the most common cause of glaucoma identified. It can cause both open-angle and angle-closure glaucoma in all populations, and accounts for the majority of cases in some countries.⁵²

Cataract and glaucoma filtering surgery are both complicated by the presence of pseudoexfoliation. In cataract surgery, zonular weakness can lead to an increased risk of vitreous loss, among other possible complications.⁵³ Some experts argue that cataract extraction ought to be performed earlier in patients with pseudoexfoliation, when lenses are softer and zonules are stronger. The advent of capsular tension rings is a major advance for cataract surgeons in dealing with lens instability from pseudoexfoliation, with studies showing decreased complications from zonular separation, with an increase in capsular fixation of intraocular lenses and improved final visual acuity.⁵⁴ Interestingly, in one study patients with pseudoexfoliative glaucoma exhibited a 2 mm Hg greater decrease in intraocular pressure (IOP) at 6 months following cataract surgery when compared to patients with primary open-angle glaucoma. However, this difference became small after the 6-month period.⁵⁵

RETINAL DETACHMENT

Retinal detachments often produce hypotony rather than glaucoma. As a result of inflammation, trauma, pigment debris, or other unknown factors, glaucoma may ensue, but can often be cured by the successful reattachment of the retina.⁵⁶ Detachments can be associated with posterior subcapsular opacities, and these may progress to dense cataracts. When the cataract matures, it cannot be distinguished from other types of senile cataracts.

Retinal detachment can occur after either cataract surgery or Nd:YAG laser capsulotomy. The estimated risk of retinal detachment in patients who undergo cataract surgery is 1% to 3%.⁵⁷ Detailed ophthalmic examination and repair of any lesion that can contribute to a retinal tear is advised before cataract surgery or Nd: YAG laser capsulotomy.

Retinal detachment repair procedures may be associated with subsequent glaucoma and cataract formation. This is discussed in the section on secondary glaucoma.

RETINITIS PIGMENTOSA

Retinitis pigmentosa is associated with open-angle glaucoma⁵⁸ and cataracts of a posterior subcapsular type. The incidence of glaucoma has been reported from 3% to 12%,^39,59 and the incidence of cataracts may be higher.⁵⁶ Treatment for glaucoma is the same as for traditional open-angle glaucoma. The cataract can be approached conventionally if vision is threatened.

HIGH MYOPIA

In high myopia (> −5.00 diopters), there is an increased incidence of open-angle glaucoma, with an estimated occurrence rate from 5% to 18%.⁶⁰ In addition, cataracts of the posterior cortex may complicate high myopia but do not occur until after middle age.⁶⁰

The treatment of the glaucoma is the same for open-angle glaucoma. In removal of the cataract, the thin and weakened scleral shell and retina must be approached cautiously. There is a much higher risk of retinal detachment after cataract surgery in highly myopic eyes, even with modern surgical techniques.⁶⁰

Implantation of a phakic implantable contact lens for high myopia may lead to several complications, including pigmentary dispersion, angle-closure glaucoma, and cataract formation.⁶¹

FUCHS' DYSTROPHY

Open-angle glaucoma may occur in up to 15% of patients with Fuchs' endothelial dystrophy.³⁹ Patients with already narrow angles can develop angle closure with thickening of the cornea from edema.⁶² There is no increased incidence of cataracts in this disease over that found in the general population, although cataract formation can follow keratoplasty.⁶³ This is in contrast to Fuchs' heterochromic-iridocyclitic syndrome, in which glaucoma and cataracts are essential features.

The therapeutic approach for glaucoma in these patients is the same as in traditional open-angle glaucoma. Because of the corneal findings and often concomitant cataracts, combined keratoplasty with cataract extraction frequently is needed in these eyes. The dystrophic changes in the endothelium (Fig. 8) must be estimated when glaucoma and cataract surgery are planned. If the endothelium is not severely damaged and cataract is present, it may be possible to obtain good pressure control and visual results for a long period of time with combined cataract-glaucoma procedures, when necessary.

DIABETES MELLITUS

Both open-angle glaucoma and cataracts may occur more commonly in those with diabetes mellitus.⁶⁴ Furthermore, the presence of diabetic retinopathy may affect perimetric results.⁶⁵ The management of the patient with open-angle glaucoma, diabetes mellitus, and cataracts is the same as for a patient with uncomplicated open-angle glaucoma. Clinical progression or aggravation of diabetic retinopathy may occur after cataract extraction or filtration surgery. Medical and surgical management of patients with these three diseases must be tailored to suit the needs of each individual. Luckily, modern surgical techniques of phacoemulsification have greatly reduced the risk of ocular complications in diabetics. Macular edema before surgery is the diabetic ocular condition most likely to limit postoperative visual recovery. Laser photocoagulation of preproliferative or early proliferative diabetic retinopathy is recommended before cataract extraction.⁶⁶

PSEUDOPHAKIA/PUPILLARY BLOCK

The insertion of an intraocular lens in patients with ocular hypertension or glaucoma does not appear to negatively affect pressure control in most cases.⁶⁷ Pupillary block can occur in both pseudophakic and aphakic eyes. When this occurs, the anterior chamber generally shallows with the formation of iris bombé (Fig. 9). As opposed to typical angle-closure situations where miotics are used, pupillary block is treated with mydriatic agents to re-establish aqueous flow through the pupil. Peripheral laser iridotomy is curative in most cases, although often it has to be repeated because of a tendency to lose patency.⁶⁸

Pupillary block occurs quite frequently after the placement of an anterior chamber intraocular lens subsequent to cataract surgery (Fig. 10). Thus it is generally recommended to create a peripheral iridectomy at the time of surgery when placing an anterior chamber intraocular lens. Although rare, pupillary block glaucoma also can occur after posterior chamber intraocular lens implantation, even years after the original surgery.⁶⁸

IRIDOCYCLITIS

Iridocyclitis can occur in a wide spectrum of systemic diseases. Juvenile rheumatoid arthritis is a common systemic cause of a chronic anterior uveitis complicated by cataracts and glaucoma.⁶⁹ These patients often are asymptomatic; thus, regular comprehensive ophthalmologic examinations are essential.

Another common cause of iridocyclitis is sarcoidosis, for which granulomatous iridocyclitis is the most frequent ocular manifestation.⁷⁰ Up to 72% of patients may have either acute or chronic iridocyclitis. Macular edema, cataract, and glaucoma are other ocular complications seen in this disease. In one study of Japanese patients, 15% of the participants with sarcoid uveitis eventually demonstrated a poor visual outcome because of ocular complications.⁷¹

Treatment of iridocyclitis includes attempts to control the inflammatory process with steroids, mydriatics, and cycloplegics, in addition to the standard antiglaucoma therapy. Miotic agents usually are avoided because they can worsen inflammation and lead to posterior synechiae of the iris to the lens. The response often is disappointing. An important factor to consider in the treatment of patients with iridocyclitis is the side effects of topical steroids, especially the hastening or aggravating of the underlying secondary glaucoma or cataractogenesis.

FUCHS' HETEROCHROMIC IRIDOCYCLITIS

Open-angle glaucoma occurs in 20% of the involved (hypochromic) eye in heterochromic iridocyclitis.³⁹ Despite the fact that small neovascular twigs are seen on the iris root, neovascularization does not complicate the glaucoma. Low-grade iritis, an underlying defect in the trabecular meshwork, and hyaline membrane proliferation are factors in the glaucoma.¹⁵ Although depigmentation of the iris occurs, little pigmentation is noted in the trabecular meshwork.⁷² The incidence of cataracts is high, ranging from 17% to 70%.⁷³ The cataracts usually begin as fine punctate opacities and progress to maturity.

The glaucoma is treated using the medical and surgical approaches generally used for traditional open-angle glaucoma. Glaucoma and endothelial difficulties make cataract extraction more hazardous,³⁹ but most patients fare well after surgery.⁷⁴ There is some literature pointing to the benefits of using heparin surface–modified intraocular lenses in patients with heterochromic uveitis.^75,76

TUMORS

Tumors can cause secondary glaucoma in a variety of ways: inflammation from necrotic tumors, direct angle invasion, peripheral synechiae as a result of inflammation,⁷⁷ and mechanical shallowing of the anterior chamber. Cataracts occasionally occur as a result of a tumor and usually consist of posterior cortical opacities resembling those seen in posterior segment disease. In the presence of a cataract, secondary glaucoma, and retinal detachment, an underlying tumor should be suspected and evaluation with the appropriate ultrasound and scanning procedures must be undertaken.

INTERSTITIAL KERATITIS

Secondary open-angle glaucoma is seen in 10% of patients with interstitial keratitis in later life.¹⁵ The etiology of the glaucoma varies. Angle closure has been seen, but the angle appears open in the majority of those examined gonioscopically. Iris cysts,⁷⁸ irregular peripheral anterior synechiae, and the possibility of a membrane covering the angle⁷⁹ are reported as causes of the secondary open-angle glaucoma. Cataracts of various types, ranging from posterior cortical opacities to mature types,² may occur. In late cases of interstitial keratitis now quiescent, it is difficult to determine if earlier treatment of the anterior segment inflammation with steroids played a role in the formation of glaucoma and cataract.

Treatment depends on the type of glaucoma present: peripheral iridectomy is used for angle closure glaucoma and the usually medical-surgical regimen is followed for the open-angle glaucomas. The surgeon must take into account the presence of corneal disease when planning cataract surgery.

LENS-INDUCED GLAUCOMAS

Phacolytic Glaucoma

Phacolytic glaucoma usually is seen in eyes with open angles, with a mature or hypermature cataract, and anterior chamber inflammation (Fig 11). The events leading to elevated pressures are: (a) lens material leaks through the lens capsule, (b) macrophages engulf the material, and (c) lens substance, macrophages, and other inflammatory material are carried by the aqueous currents to the angle, clogging the trabecular meshwork and obstructing the outflow passages.

Clinically, phacolytic glaucoma usually presents in an elderly patient with worsening vision, pain, conjunctival injection, elevated IOP of 30 to 50 mm.⁸⁰

LENS PARTICLE GLAUCOMA

An inflammatory reaction to retained lens material can occur any time from days to years after cataract surgery. Elevated IOP occurs along with anterior chamber cellular reaction. Free cortical material sometimes can be seen in the anterior chamber and microcystic corneal edema, posterior, and peripheral anterior synechiae may develop. Medical therapy aimed at decreasing aqueous formation, corticosteroids to reduce inflammation, and mydriatics to help prevent formation of posterior synechiae are mainstays of treatment. Surgical removal of the lens material is required in some cases refractory to medical therapy.⁸⁰

PHACOANAPHYLAXIS

In phacoanaphylaxis, patients become immune-sensitized to their own lens protein after surgery or trauma. Although this results in a granulomatous reaction, glaucoma is rare. This disorder is differentiated from phacolytic glaucoma by the presence of keratic precipitates. Treatment is the same as for lens particle glaucoma.⁸⁰

GLAUCOMATOCYCLITIC CRISIS (POSNER-SCHLOSSMAN'S SYNDROME)

Glaucomatocyclitic crisis is characterized by a recurrent cycle of unilateral bouts of mild, nongranulomatous iritis with elevated IOP. Studies have shown that as many as 45% of patients with this syndrome also have primary open-angle glaucoma.^81,82 Posner-Schlossman's syndrome itself also can cause glaucomatous damage; therefore, these patients need to be monitored as if they had glaucoma.⁸³ Treatment is usually medical and includes the use of topical steroids. Some of these patients develop posterior cortical opacities, but whether these are caused by steroid treatment or the underlying anterior segment inflammation is not clear.

STEROID-INDUCED GLAUCOMA

Nearly all forms of steroid use have been associated with ocular side effects, including topical, oral, inhaled, and intravenous.⁸⁴ To date, nasal steroids have not been associated with any significant ocular side effects.⁸⁵ Even periorbital topical steroid use has been linked to ocular complications, such as in a case report of bilateral glaucomatous damage in a 29-year-old woman using topical steroids around her eyes.⁸⁶ Glaucoma can develop at any time during the use of corticosteroids.

Steroid-induced glaucoma, which was recognized as early as 1950,⁸⁷ resembles open-angle glaucoma in many aspects: The normal angle appears open by gonioscopy, the facility of outflow decreases, the optic nerve is damaged, and visual fields decrease as a result of increased IOP.

Topical steroid use shows the greatest incidence of IOP elevation. The incidence of a rise in IOP induced by the use of topical steroids in a normal population is between 6% and 30%,⁸⁸ above 30% in those cases with a family history of glaucoma,³⁹ and 75% to 90% in patients with glaucoma.⁸⁹ In different studies, different criteria for separating responders from nonresponders have been used. Hence, the percentages listed vary from study to study. The results depend on the type of steroids used and the pressure levels chosen for responsiveness or nonresponsiveness. There is no doubt, however, despite the wide ranges and results, that topical steroid use can significantly raise the IOP leading to permanent visual damage if left untreated.

The reason for steroid-induced elevation of IOP is unclear. Cells of the trabecular meshwork contain steroid-specific receptors, and it is theorized that corticosteroids may alter the expression of trabecular meshwork genes by activating these receptors, eventually leading to increased resistance of aqueous humor outflow. Other theories have been published, but no conclusive findings have been elicited.^90–92

Treatment may consist of medications aimed at lowering IOP, discontinuing or reducing the frequency of the corticosteroid, or substituting the corticosteroid for a weaker one. Intraocular pressure often returns to baseline within 2 to 4 weeks after cessation of topical steroids.⁹³ Some patients may require surgical intervention.

Nearly all forms of corticosteroids have been linked to cataract formation as well. They are usually posterior subcapsular in location. Cataracts induced by topical steroids are noted in 21% to 36% of cases studied.⁹⁴ The relationship of systemic corticosteroid use and cataract formation was first described in 1960.⁹⁵ The overall incidence of cataract formation with systemic corticosteroid use ranges from 6% to 38%. Although quite variable, increased dosage and duration of corticosteroid use generally is related to increased incidence of cataract formation.⁹⁶ Diabetic patients treated with topical steroids are more prone to develop these opacities.⁹⁷ As with corticosteroid-induced glaucoma, the pathophysiology of cataract formation with steroid use is not clear.

Management of steroid-induced cataracts is similar to other adult cataract types, except that in cases of steroid use for intraocular inflammation it is generally recommended to control the inflammation as much as possible before cataract extraction.

TRAUMA

Secondary open-angle glaucoma and cataracts may occur as a result of trauma. In nonpenetrating injuries of the eye, contusion angle deformity or recession of the angle can cause secondary glaucoma, either acutely or chronically. Mechanisms include disinsertion of the ciliary muscle from the scleral spur, meshwork sclerosis or fibrosis, or hyaline membrane formation. Cataracts may occur in 24% of patients with contusion injuries, varying from hypermature to cortical types.⁹⁸

The open-angle glaucoma is treated medically or surgically, with the realization that some treatments, such as miotics, may be ineffective because of disruption of the normal ciliary muscle–scleral spur relationship. Cataract surgery is approached as adult cataract surgery, keeping in mind that subluxation of the lens and vitreous loss may complicate the lens extraction. Capsular tension rings may be useful in these cases.

LENS-INDUCED SECONDARY ANGLE-CLOSURE GLAUCOMA

In lens-induced (phacomorphic) secondary angle-closure glaucoma, a swollen, cataractous lens, because of its shape and size, induces a pupillary block and closes the angle. Comparison of the involved eye with the contralateral eye often helps distinguish this form of induced glaucoma from that of narrow-angle glaucoma with pupillary block, in which both eyes are anatomically similar. Removal of the lens is the treatment of choice. Mydriatics and cycloplegics, as well as steroids, may help prepare the patient's eye for surgery.

In ectopia lentis, anterior displacement of the lens can cause pupillary block, resulting in an acute attack or chronic angle-closure glaucoma. Common causes of ectopia lentis include trauma, Marfan's syndrome, homocystinuria, Weill-Marchesani's syndrome, and microspherophakia. Laser iridectomy is the treatment of choice. Often, after direct trauma that results in a subluxated lens and angle closure, a cataract forms, and removal of the lens is indicated. Furthermore, if iridectomy does not relieve the pupillary block, then lens extraction is indicated. Capsular tension rings, perhaps with scleral fixation, may be useful in these cases.

For patients with both cataracts and glaucoma requiring surgical intervention, the various approaches are: (a) filtration surgery with possible cataract extraction later, (b) cataract extraction alone with possible filtration surgery later, and (c) a combination of filtration surgery and cataract extraction. Whether or not to combine cataract and glaucoma surgery is a topic of great controversy among ophthalmic surgeons, and is probably most dependent on the patient's individual situation.

Combined phacoemulsification and trabeculectomy (phacotrabeculectomy) has a better IOP-lowering effect than phacoemulsification alone.¹⁰² However, numerous studies suggest that trabeculectomy alone has superior IOP-lowering effects than combined phacoemulsification and trabeculectomy in lowering IOP, although the reason is unclear.^103,104 One hypothesis is that phacoemulsification increases trauma to the wound. When phacotrabeculectomy is performed, the concomitant use of mitomycin C leads to a significantly lower IOP of 2 to 4 mm Hg.¹⁰⁵

There are conflicting reports on the effect of phacoemulsification on IOP and bleb performance after trabeculectomy. Some studies have reported improved IOP, whereas others have shown worsening IOP. However, it is not clear if elevated IOP is simply the natural course of glaucoma, unrelated to the cataract surgery. Overall, it seems that phacoemulsification with clear corneal incision does not affect IOP, but increases 3-year bleb failure rates.¹⁰⁶ Cataract surgery performed within 6 months of trabeculectomy, iris manipulation, and age younger than 50 years all seem to be risk factors for failure of a filtering bleb.¹⁰⁷

Perhaps patients with open-angle glaucoma can benefit from cataract extraction alone. Some studies have demonstrated that phacoemulsification alone can reduce IOP long-term by 2 to 4 mm Hg.¹⁰² However, it is also known that some patients demonstrate a long-term increase in IOP after cataract extraction.^99,108 Early postoperative spikes in IOP also are common, although these tend to resolve quickly and may be diminished by the postoperative use of pressure-lowering medications.^109,110 The most commonly encountered clinical scenario for concomitant glaucoma and cataracts is a patient with well-controlled glaucoma, and a cataract for which isolated cataract surgery is currently the most common therapy.

For angle-closure glaucoma, cataract surgery alone significantly improves IOP regulation, with one study reporting an IOP reduction of 7 mm Hg 2 years after surgery.¹⁰⁸ Therefore, a patient with angle-closure glaucoma with even mild lenticular opacities should undergo cataract extraction before any other surgical intervention is considered. In the event of total synechial angle closure, 180-degree goniosynechialysis and peripheral diode laser iridoplasty could be performed at the time of phacoemulsification.¹¹¹

It is certain that the topic of combined versus separate procedures for glaucoma and cataracts will continue to be a controversial topic. Hopefully, as new studies are published the “rules” will become clearer. Table 1 provides some general guidelines from one major meta-review, although each patient's individual situation must be considered and discussed.¹⁰⁶

TABLE 1. Guidelines for Glaucoma and Cataract Treatment

1. Wstat Inc: Summary and critique of available data on the prevalence and economic and social costs of visual disorders and disabilities. Vision Res 1:27, 1978

2. Duke-EIder S: System of Ophthalmology, Vol 11, Diseases of the Lens and Vitreous: Glaucoma and Hypotony. St. Louis: Mosby, 1969

3. Kwitko ML: Glaucoma in Infants and Children. New York: Appleton-Century-Crofts, 1973

4. Vishwanath M, Cheong-Leen R, Taylor D, Russell-Eggitt I, Rahi J: Is early surgery for congenital cataract a risk factor for glaucoma? Br J Ophthalmol 88(7):905, 2004

5. Watts P, Abdolell M, Levin AV: Complications in infants undergoing surgery for congenital cataract in the first 12 weeks of life: Is early surgery better? J AAPOS 7(2):81, 2003

6. Nelson LB, Spaeth GL, Nowinski TS, et al: Aniridia: A review. Surv Ophthalmol 28:621, 1984

7. Swanner JC, Walton DS, Chen TC: Prevention of aniridic glaucoma with goniosurgery. Int Ophthalmol Clin 44(1):67, 2004

8. Young TL: Ophthalmic genetics/inherited eye disease. Curr Opin Ophthalmol 14(5):296, 2003

9. Yoshikawa K, Asakage H, Inoue Y: Membranous cataract in association with aniridia. Jpn J Ophthalmol 37(3):325, 1993

10. Brandt JD, Casuso LA, Budenz DL: Markedly increased central corneal thickness: An unrecognized finding in congenital aniridia. Am J Ophthalmol 137(2):348, 2004

11. Mullaney P, al-Awad A: Cataract formation in Peter's anomaly after trabeculotomy. Ophthalmic Surg 26(3):267, 1995

12. Kanski JJ: Clinical Ophthalmology: A Systemic Approach, 4th ed. Oxford: Butterworth Heinemann, 1999

13. Groessl SA, Anderson CJ: Capsular tension ring in a patient with Weill-Marchesani syndrome. J Cataract Refract Surg 24(8):1164, 1998

14. Lowe CU, Terrey M, MacLachlan EA: Organic-aciduria, decreased renal ammonia production, hydrophthalmos and mental retardation: A clinical entity. Am J Dis Child 83:164, 1952

15. Chandler PA, Grant WM: Lectures on Glaucoma. Philadelphia: Lea & Febiger, 1965

16. Boniuk M: Glaucoma in the congenital rubella syndrome. Int Ophthalmol Clin 12:121, 1972

17. Vijayalakshmi P, Srivastava KK, Poornima B, Nirmalan P: Visual outcome of cataract surgery in children with congenital rubella syndrome. J AAPOS 7(2):91, 2003

18. Refsum H, Fredriksen A, Meyer K, Ueland PM, Kase BF: Birth prevalence of homocystinuria. J Pediatr 144(6):830, 2004

19. Burke JP, O'Keefe M, Bowell R, Naughten ER: Ocular complications in homocystinuria—early and treated. Br J Ophthalmol 73(6):427, 1989

20. Mudd SH, Skovby F, Levy HL, et al: The natural history of homocystinuria due to cystathionine beta synthase deficiency. Am J Hum Genet 37(1):1, 1985

21. Nielsen J, Wohlert M, Fauborg-Anderson J, et al: Incidence of chromosome abnormalities in newborn children: Comparison between incidence in 1969–1974 and 1980–1982 in the same area. Hum Genet 61:98, 1982

22. Roizen NJ, Mets MB, Blondis TA: Ophthalmic disorders in children with Down syndrome. Devel Med Child Neurol 36:594, 1994

23. Catalano RA: Down syndrome. Surv Ophthalmol 34:385, 1990

24. Levin AV: Congenital eye anomalies. Pediatr Clin North Am 50(1):55, 2003

25. Smith JL, Cavanaugh JJ, Stowe FC: Ocular manifestations of the Pierre Robin syndrome. Arch Ophthalmol 63:784, 1960

26. Lee GA, Lee LR, Gole GA: Angle-closure glaucoma after laser treatment for retinopathy of prematurity. J AAPOS 2(6):383, 1998

27. Fallaha N, Lynn MJ, Aaberg TM Jr, Lambert SR: Clinical outcome of confluent laser photoablation for retinopathy of prematurity. J AAPOS 6(2):81, 2002

28. Lambert SR, Capone A Jr, Cingle KA, Drack AV: Cataract and phthisis bulbi after laser photoablation for threshold retinopathy of prematurity. Am J Ophthalmol 129(5):585, 2000

29. Asrani S, Freedman S, Hasselblad V, et al: Does primary intraocular lens implantation prevent “aphakic” glaucoma in children? J AAPOS 4(1):33, 2000

30. Mandal AK, Netland PA: Glaucoma in aphakia and pseudophakia after congenital cataract surgery. Indian J Ophthalmol 52(3):185, 2004

31. Phelps CD, Arafat NI: Open-angle glaucoma following surgery for congenital cataracts. Arch Ophthalmol 95:1985, 1977

32. Ariturk N, Oge I, Mohajery F, Erkan D, Turkoglu S: Secondary glaucoma after congenital cataract surgery. Int J Ophthalmol 22(3):175, 1998-99

33. Asrani S, Freedman S, Hasselblad V, et al: Does primary intraocular lens implantation prevent “aphakic” glaucoma in children? J AAPOS 4(1):33, 2000

34. Mandal AK, Bagga H, Nutheti R, Gothwal VK, Nanda AK: Trabeculectomy with or without mitomycin-C for paediatric glaucoma in aphakia and pseudophakia following congenital cataract surgery. Eye 17(1):53, 2003

35. Shaffer RN, Weiss DI: Congenital and Pediatric Glaucomas. St. Louis: Mosby, 1970

36. Wollensak G, Eberwein P, Funk J: Perforation rosette of the lens after Nd:YAG laser iridotomy. Am J Ophthalmol 123(4):555, 1997

37. Lin JC, Katz LJ, Spaeth GL, Klancnik JM Jr: An “exploding cataract” following Nd:YAG laser iridectomy. Ophthal Surg Lasers Imag 34(4):310, 2003

38. Gitter KA, Harris LS, Galin MA, et al: The post-congestive triad of angle-closure glaucoma. Am J Ophthalmol 67:540, 1969

39. Kolker AE, Hetherington J: Becker-Shaffer's Diagnosis and Therapy of the Glaucomas, 4th ed. St. Louis: Mosby, 1976

40. Levene RZ: Uniocular miotic therapy. Trans Am Acad Ophthalmol Otolaryngol 79:OP376, 1975

41. Abraham RK, Miller GL: Outpatient argon laser iridectomy for angle closure glaucoma: A two-year study. Trans Am Acad Ophthalmol Otolaryngol 79:OP529, 1975

42. Zadok D, Chayet A: Lens opacity after neodymium: YAG laser iridectomy for phakic intraocular lens implantation. J Cataract Refract Surg 25(4):592, 1999

43. Berger CM, Lee DA, Christensen RE: Anterior lens capsule perforation and zonular rupture after Nd:YAG laser iridotomy. Am J Ophthalmol 107(6):674, 1989

44. Ritch R, Tham CC, Lam DS: Long-term success of argon laser peripheral iridoplasty in the management of plateau iris syndrome. Ophthalmology 111(1):104, 2004

45. Tanna AP, Abraham C, Lai J, Shen J: Impact of cataract on the results of frequency-doubling technology perimetry. Ophthalmology 111(8):1504, 2004

46. Axelsson U, Holmberg A: The frequency of cataract after miotic therapy. Acta Ophthalmol 44:421, 1966

47. Pietsch RL, Bobo CB, Finklea JF, et al: Lens opacities and organophosphate cholinesterase-inhibiting agents. Am J Ophthalmol 73:236, 1972

48. Thoft RA: Incidence of lens changes in patients treated with echothiophate iodide. Arch Ophthalmol 80:317, 1968

49. Axelsson U: Miotic-induced cataract. In The Human Lens: In Relation to Cataract, Ciba Foundation Symposium. Amsterdam: Associated Scientific, 1973

50. Cantor L, et al: Basic and Clinical Science Course: Glaucoma. San Francisco: American Academy of Ophthalmology, 2003:81

51. Ringvold A: Electron microscopy of the limbal conjunctiva in eyes with pseudo-exfoliation syndrome (PE syndrome). Virchows Arch 355:275, 1972

52. Ritch R, Schlotzer-Schrehardt U, Konstas AG: Why is glaucoma associated with exfoliation syndrome? Prog Retin Eye Res 22(3):253, 2003

53. Conway RM, Schlotzer-Schrehardt U, Kuchle M, Naumann GO: Pseudoexfoliation syndrome: Pathological manifestations of relevance to intraocular surgery. Clin Exp Ophthalmol 32(2):199, 2004

54. Bayraktar S, Altan T, Kucuksumer Y, Yilmaz OF: Capsular tension ring implantation after capsulorrhexis in phacoemulsification of cataracts associated with pseudoexfoliation syndrome. Intraoperative complications and early postoperative findings. J Cataract Refract Surg 27(10):1620, 2001

55. Merkur A, Damji KF, Mintsioulis G, et al: Intraocular pressure decrease after phacoemulsification in patients with pseudoexfoliation syndrome. J Cataract Refract Surg 27:528, 2001

56. Schwartz A: Chronic open-angle glaucoma secondary to rhegmatogenous retinal detachment. Am J Ophthalmol 75:205, 1973

57. Banker AS, Freeman WR: Retinal detachment. Ophthalmol Clin North Am 14(4):695, 2001

58. Kogbe OI, Follman P: Investigations into the aqueous humour dynamics in primary pigmentary degeneration of the retina. Ophthalmologica 171:165, 1975

59. Duke-EIder S: Diseases of the Retina. St. Louis: Mosby, 1967

60. Ripandelli G, Scassa C, Parisi V, et al: Cataract surgery as a risk factor for retinal detachment in very highly myopic eyes. Ophthalmology 110(12):2355, 2003

61. Pineda-Fernandez A, Jaramillo J, Vargas J, et al: Phakic posterior chamber intraocular lens for high myopia. J Cataract Refract Surg 30(11):2277, 2004

62. Cantor LB: Basic and Clinical Science Course: Glaucoma. San Francisco: American Academy of Ophthalmology, 2003

63. Price MO, Price FW Jr: Cataract progression and treatment following posterior lamellar keratoplasty. J Cataract Refract Surg 30(6):1310, 2004

64. Centers for Disease Control and Prevention (CDC): Prevalence of visual impairment and selected eye diseases among persons aged ≥50 years with and without diabetes—United States, 2002. MMWR Morb Mortal Wkly Rep 53(45):1069, 2004

65. Realini T, Lai MQ, Barber L: Impact of diabetes on glaucoma screening using frequency-doubling perimetry. Ophthalmology 111(11):2133, 2004

66. Menchini U, Cappelli S, Virgili G: Cataract surgery and diabetic retinopathy. Semin Ophthalmol 18(3):103, 2003

67. Smith JA, Anderson DR: Effect of the intraocular lens on intraocular pressure. Arch Ophthalmol 94:1291, 1976

68. Gaton DD, Mimouni K, Lusky M, Ehrlich R, Weinberger D: Pupillary block following posterior chamber intraocular lens implantation in adults. Br J Ophthalmol 87(9):1109, 2003

69. Paroli MP, Speranza S, Marino M, Pirraglia MP, Pivetti-Pezzi P: Prognosis of juvenile rheumatoid arthritis-associated uveitis. Eur J Ophthalmol 13(7):616, 2003

70. Ryan SJ, Maumenee AE: Ocular sarcoidosis. In Selected Topics in the Eye in Systemic Disease. New York: Grune & Strutton, 1974

71. Uyama M: Uveitis in sarcoidosis. Int Ophthalmol Clin 42(1):143, 2002

72. Shaffer RN: Pigment and glaucoma. In Symposium on Glaucoma: Transactions of the New Orleans Academy of Ophthalmology. St. Louis: Mosby, 1975

73. Smith RE, O'Connor RG: Cataract extraction in Fuchs' syndrome. Arch Ophthalmol 91:39, 1974

74. Milazzo S, Turut P, Borhan M, Kheireddine A: Intraocular lens implantation in eyes with Fuchs' heterochromic iridocyclitis. J Cataract Refract Surg 22 Suppl 1:800, 1996

75. Budak K, Akova YA, Yalvac I, et al: Cataract surgery in patients with Fuchs' heterochromic iridocyclitis. Jpn J Ophthalmol 43(4):308, 1999

76. Jones NP: Cataract surgery using heparin surface-modified intraocular lenses in Fuchs' heterochromic uveitis. Ophthalmic Surg 26(1):49, 1995

77. Yanoff M: Glaucoma mechanisms in ocular malignant melanomas. Am J Ophthalmol 70:898, 1970

78. Lichter PR, Shaffer RN: Interstitial keratitis and glaucoma. Am J Ophthalmol 68:241, 1969

79. Grant WM: Late glaucoma after interstitial keratitis. Am J Ophthalmol 79:87, 1975

80. Cantor L, et al: Basic and Clinical Science Course: Glaucoma. San Francisco: American Academy of Ophthalmology, 2003

81. Raitta C, Vannas A: Glaucomatocyclitic crisis. Arch Ophthalmol 95:608, 1977

82. Kass MA, Becker B, Kolker AE: Glaucomatocyclitic crisis and primary open-angle glaucoma [case report]. Am J Ophthalmol 75:668, 1973

83. Jap A, Sivakumar M, Chee SP: Is Posner Schlossman syndrome benign? Ophthalmology 108(5):913, 2001

84. Carnahan MC, Goldstein DA: Ocular complications of topical, peri-ocular, and systemic corticosteroids. Curr Opin Ophthalmol 11(6):478, 2000

85. Ozturk F, Yuceturk AV, Kurt E, Unlu HH, Ilker SS: Evaluation of intraocular pressure and cataract formation following the long-term use of nasal corticosteroids. Ear Nose Throat J 77(10):846, 850, 1998

86. Sahni D, Darley CR, Hawk JL: Glaucoma induced by periorbital topical steroid use: A rare complication. Clin Exp Dermatol 29(6):617, 2004

87. McLean JM: Use of ACTH and cortisone [discussion of paper by Woods AC]. Tr Am Ophthalmol Soc 48:293, 1950

88. Francois François J: Corticosteroid glaucoma. Ann Ophthalmol 9:1075, 1977

89. Wilensky JT, Podos SM: Prognostic parameters in primary open-angle glaucoma. In Symposium on Glaucoma: Transactions of the New Orleans Academy of Ophthalmology. St. Louis: Mosby, 1975

90. Hernandez MR, Wenk EJ, Weinstein BI: Glucocorticoid target cells in human outflow pathway: Autopsy and surgical specimens. Invest Ophthalmol Vis Sci 24:1612, 1983

91. Clark AF: Steroids, ocular hypertension, and glaucoma. J Glaucoma 4:354, 1995

92. Clark AF, Wilson K, de Kater AW, et al: Dexamethasone-induced ocular hypertension in perfusion-cultured human eyes. Invest Ophthalmol Vis Sci 36:478, 1995

93. Tripathi RC, Parapuram SK, Tripathi BJ, et al: Corticosteroids and glaucoma risk. Drugs Aging 15:439, 1999

94. Spaeth GL, Von Sallman L: Corticosteroids and cataracts. Int Ophthalmol Clin 6:915, 1966

95. Black RL, Oglesby RB, von Sallman L, et al: Posterior subcapsular cataracts induced by corticosteroids in patients with rheumatoid arthritis. JAMA 174:166, 1960

96. Hanania NA, Chapman KR, Kesten S: Adverse effects of inhaled corticosteroids. Am J Med 98:196, 1995

97. Yablonski ME, Burde RM, Kolker AE, Becker B: Cataracts induced by topical dexamethasone in diabetics. Arch Ophthalmol 9:474, 1978

98. Palmer E, Lieberman TW, Burns S: Contusion angle deformity in prizefighters. Arch Ophthalmol 94:225, 1976

99. Pohjalainen T, Vesti E, Uusitalo RJ, et al: Phacoemulsification and intraocular lens implantation in eyes with open-angle glaucoma. Acta Ophthalmol Scand 79:313, 2001

100. Frankelson EN, Shaffer RN: The management of coexisting cataract and glaucoma. Can J Ophthalmol 9:298, 1974

101. Jerndal T, Lundstrom Lundström M: 330 trabeculectomies: A follow-up study through 1/2–3 years. Acts Ophthalmol 55:52, 1977

102. Friedman DS, Jampel HD, Lubomski LH, et al: Surgical strategies for coexisting glaucoma and cataract: An evidence-based update. Ophthalmology 109:1902, 2002

103. Caprioli J, Park HJ, Weitzman M: Temporal corneal phacoemulsification combined with superior trabeculectomy: A controlled study. Trans Am Ophthalmol Soc 94:45; discussion: 463, 1996

104. Lochhead J, Casson RJ, Salmon JF: Long term effect on intraocular pressure of phacotrabeculectomy compared to trabeculectomy. Br J Ophthalmol 87:850, 2003

105. Jampel HD, Friedman DS, Lubomski LH, et al: Effect of technique on intraocular pressure after combined cataract and glaucoma surgery: An evidence-based review. Ophthalmology 109:2215, 2002

106. Vass C, Menapace R: Surgical strategies in patients with combined cataract and glaucoma. Curr Opin Ophthalmol 15(1):61, 2004

107. Chen PP, Weaver YK, Budenz DL, et al: Trabeculectomy function after cataract extraction. Ophthalmology 105:1928, 1998

108. Hayashi K, Hayashi H, Nakao F, et al: Effect of cataract surgery on intraocular pressure control in glaucoma patients. J Cataract Refract Surg 27:1779, 2001

109. Rainer G, Menapace R, Schmetterer K, et al: Effect of dorzolamide and latanoprost on intraocular pressure after small incision cataract surgery. J Cataract Refract Surg 25:1624, 1999

110. Rainer G, Menapace R, Findl O, et al: Randomised fellow eye comparison of the effectiveness of dorzolamide and apraclonidine on intraocular pressure following phacoemulsification cataract surgery. Eye 14:757, 2000

111. Lai JS, Tham CC, Lam DS: The efficacy and safety of combined phacoemulsification, intraocular lens implantation, and limited goniosynechialysis, followed by diode laser peripheral iridoplasty, in the treatment of cataract and chronic angle-closure glaucoma. J Glaucoma 10:309, 2001