Elliott M. Kanner,
Peter A. Netland
INTRODUCTION
Posterior segment disorders that are associated with glaucoma may be classified into several categories, including: (1) posterior segment disorders that have an association with glaucoma, and in which underlying glaucoma may play a role in the development of the condition. (2) Posterior segment disorders that result in adhesions of the iris, either posteriorly (pupillary segregation) or anteriorly (angle closure). (3) Anatomic distortion of the angle, from either a posterior (push) or anterior (pull) force. (4) Neovascularization of the angle, with subsequent fibrovascular closure of the angle. (5) Secondary open-angle glaucoma from deposition of materials in the trabecular meshwork, in the absence of gross structural changes in the angle (Tables 216.1 and 216.2).
TABLE 216.1 -- Glaucomas Associated with Disorders of the Retina, Vitreous, and Choroid
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Glaucoma Associated with Ocular Trauma |
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Glaucoma Associated with Orbital and Extraorbital Vascular Factors that Result in Elevated Episcleral Venous Pressure |
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TABLE 216.2 -- Mechanisms of Glaucoma Associated with Disorders of the Retina, Vitreous, and Choroid
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AIDS, acquired immunodeficiency syndrome. |
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Data from Jampol LM: Proliferative retinopathies. Surv Ophthalmol 25:1, 1980. |
Patients with retinal disorders may have an increased intraocular pressure (IOP) with or without glaucoma. Elevated IOP associated with various retinal disorders broadly describes eyes with increased IOP and without glaucomatous optic nerve damage or visual field loss. Eyes with preexisting glaucoma due to other causes may develop elevated IOP associated with retinal disorders. Glaucoma associated with retinal disorders describes eyes with retinal disorders, elevated IOP, and glaucomatous-appearing optic neuropathy or visual field loss. Use of this term implies that the glaucomatous damage is secondary to the retinal disorder. In some instances, patients with elevated IOP without evidence of optic disk changes or visual field loss may be classified a 'glaucoma' because disk and visual field changes are inevitable without appropriate intervention.
The examination of the glaucoma patient with other pathology presents unique challenges. A full baseline initial exam is essential, including biomicroscopy, gonioscopy, a dilated exam, visual field exam and optic nerve pictures and imaging. Refractive error, the presence of a tilted disk, optic nerve drusen, or chorioretinal degeneration can complicate examination of the optic nerves, and mimic visual field defects from glaucoma. In these patients, new visual field deficits may not correlate with changes in the optic nerve since they may be from other causes, and must be investigated even more thoroughly. Unusual increases or decreases in pressure with inflammation may point to a posterior cause and require further investigation.
In many cases the eye that is involved to a lesser extent can assist in the diagnosis. While secondary glaucoma is not as frequently bilateral as primary open-angle glaucoma (POAG), the opposite eye can give a clue about the diagnosis. For example, a patient with neovascular glaucoma secondary to diabetic retinopathy may present with diabetic retinopathy in the fellow eye. Congenital anomalies may be bilateral, although only one eye may be affected with glaucoma.
A retinal detachment may mask underlying glaucoma due to the secondary hypotony, inflammation or media opacification. Glaucoma may limit the visual potential in such eyes with retinal detachment, but is not a contraindication for surgery.[1] However, since eyes with preexisting glaucoma are particularly sensitive to the transient IOP elevations that are common after retinal detachment surgery, the pressure must be more carefully monitored. Also, since the existence of glaucoma may limit the visual recovery, it is important to both identify the problem and counsel the patient as to how much vision to expect to recover. If nystagmus and a miotic pupil limit the view, a direct ophthalmoscope and a Koeppe lens can often be the best examination equipment. If media opacity prevents a view of the posterior segment (which is common with glaucoma), a B-scan can be helpful to rule out retinal pathology.[2] If miotic (cholinergic) drugs are being used as therapy, holding these medications for a few days prior to the examination may improve the view.
If miotic drugs are used, the risk of retinal detachment is increased, so the patient treated with these medications should be questioned for symptoms of flashes and floaters. A dilated exam should be done as soon as possible if the history and symptoms suggests retinal detachment, although this may require discontinuation of the miotic to get good dilation. Flashes and floaters may be due to vitreous separation or other benign causes, but should be investigated.
GLAUCOMA ASSOCIATED WITH CONGENITAL DISORDERS
GLAUCOMA ASSOCIATED WITH NANOPHTHALMOS
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Key Features |
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Nanophthalmos is a disorder with an otherwise normal globe, reduced in overall dimensions by approximately two-thirds, except for the crystalline lens, which is typically normal size.[3-5] For more details about nanopthalmos the reader is referred to Chapter 214. The eye is most commonly hypermetropic (consistent with the short axial length), although emmetropia and myopia have been described.[3,6] The corneal diameter is typically less than normal (microcornea). The axial length should be less than 20.5 mm for diagnosis of nanophthalmos.
Various mechanisms contribute to glaucoma in nanophthalmos. The relatively large lens can cause pupillary block resulting in primary angle-closure glaucoma.[7] The lens in nanophthalmos occupies a disproportionately large percentage of ocular volume (24% vs 4% in a normal eye),[7,8] which causes crowding of the anterior segment, with progressive shallowing of the anterior chamber and narrowing of the angle. Angle closure is most common in the fourth to sixth decades, and frequent gonioscopic examinations are warranted.[7]
Shaffer originally suggested that the abnormal sclera predisposed to choroidal effusion both by impairing drainage through the vortex veins and by reduced permeability to proteins.[9] Subsequent pathological examination has demonstrated that the fibers in nanophthalmic sclera are abnormally arranged.[10-12] This ciliochoroidal thickening and effusion can cause secondary angle-closure glaucoma by an anterior dislocation of the iris.[5,13]
If pupillary block is a factor in angle closure, treatment is initially medical to achieve pressure control, followed by a laser iridotomy.[6] Care must be taken with the use of miotic therapy, since the results are unpredictable, and pupillary block may improve or worsen with use.[6] In cases that do not respond to the above treatment, a choroidal effusion may contribute to the angle closure, and may respond to cycloplegia.[6] Also, in cases not responding to laser iridotomy, a lens-related mechanism (phacomorphic) may predominate rather than pupillary block. When stable, a laser gonioiridoplasty may help open the angle and control IOP, in addition to preventing peripheral anterior synechiae and permanent angle closure.[4,14]
The relative thickening of the sclera can impair drainage of the vortex veins, raising episcleral venous pressure and secondarily causing glaucoma.[5] There is also an increased risk of malignant glaucoma following any intervention such as surgery.[5,6]
The propensity for spontaneous choroidal effusion and nonrhegmatogenous retinal detachment was described by Brockhurst in 1974.[13] One series described 15 patients with nanophthalmos undergoing routine surgery with reduced visual outcome postoperatively from sudden choroidal effusion and retinal detachment (nonrhegmatogenous).[6] Of these patients, 46% were reduced to less than counting fingers vision, and 60% had failure to control IOP. Diagnoses for these patients included choroidal effusion, nonrhegmatogenous retinal detachment, malignant glaucoma and flat anterior chamber.[6] The management and prevention of these intraoperative complications has been controversial. Proposed preventative measures include vortex vein decompression[15,16] and scleral resection.[17] If the ultrasound indicates scleral thickening or active effusion, then elective scleral resection (with or without vortex vein decompression), can be performed 4-6 weeks before the planned anterior surgery.[15-17] Some have had good results with oral steroid as an alternative to posterior segment surgery.[6,15] An anterior sclerectomy has been proposed by Singh and associates, and Simmons either before or during surgery to prevent ciliochoroidal effusion.[4,6,18]
Finally, there is an increased risk of primary open-angle glaucoma in nanophthalmos.[6] All the other mechanisms described above must be considered, but if they are not a factor, the primary mechanism of glaucoma is primary open angle, which responds to conventional therapy. As noted above, surgical intervention has an increased risk of complications.
GLAUCOMA ASSOCIATED WITH RETINOPATHY OF PREMATURITY, FAMILIAL EXUDATIVE VITREORETINOPATHY, AND COATS' DISEASE
Retinopathy of prematurity (ROP), initially called retrolental fibroplasia, has increased in incidence as the survival of premature, low-birth weight children has increased.[19] As the role of oxygen supplementation became clear, lower levels have been used, and protocols developed for proper screening and treatment in order to reduce vision loss.[20,21] While in 1981 it was estimated that 30% of low-birth weight infants (<1000 g) would develop severe ROP, and 8% would be blind, aggressive screening and early treatment has reduced these numbers substantially.[22] Long-term follow-up is required, since glaucoma is likely to develop in about a quarter to a third of cases with severe ROP.[23] Although the rates of development of glaucoma for milder cases is unclear, long-term follow-up is still advised.
ROP can result in glaucoma by multiple mechanisms, both early during the initial diagnosis and treatment phase and long-term. In addition to the effects of advanced ROP, a variety of other mechanisms in the anterior segment can predispose to glaucoma. Hartnett and associates prospectively analyzed 27 eyes of 17 premature infants with stage IV and V ROP to describe the range of anterior segment anomalies.[24] They found hypopigmentation of the iris root in 73%, a translucent or Barkan's-type membrane in 69%, detectable posterior synechiae in 62%, prominent iris convexity in 58%, visible angle or iris vessels in 46%, pigment clumping in the angle recess in 46%, a prominent Schwalbe's line in 15% and greater than 180° of angle closure in 12%.[24]
Advanced ROP with a full detachment (stage V) can cause anterior displacement of the lens-iris diaphragm (and angle-closure glaucoma) both from disruption of the posterior architecture and from contraction of the retrolental membranes. This usually occurs from ages 3 to 6 months, but can occur later, even in adulthood.[25,26] Angle closure can also be caused by ciliary block[27] and neovascularization of the anterior segment.[25,27] The inflammation that can occur in eyes with ROP can result in glaucoma by the same mechanisms in conventional uveitic glaucoma, with synechiae formation resulting in partial or complete pupillary block, or PAS resulting in partial to complete closure of the angle.[27] Treatment with iridectomy, lensectomy, topical steroids. and cycloplegics, is often insufficient to regain control of IOP.[24,27,28] The contraction of retrolental membranes may eventually result in decreased IOP if the centripetal traction detaches the ciliary body.[24] There are reports of familial exudative vitreoretinopathy causing angle closure without neovascularization.[29]
After invasive intervention such as reattachment of the retina in stage V, initial IOP control does not predict long-term control.[24] As in any case of childhood eye surgery, long-term follow-up is required to monitor late-developing glaucoma. Similar to ROP, other congenital disorders can cause retinal ischemia resulting in neovascularization and closed-angle glaucoma. Familial exudative vitreoretinopathy[30]and Coat's disease[31] can cause this problem in children and adolescents. These and other retinal ischemia disorders are discussed in more detail in Chapter 213.
GLAUCOMA ASSOCIATED WITH PERSISTENT HYPERPLASTIC PRIMARY VITREOUS
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Synonym |
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Persistent hyperplastic primary vitreous (PHPV) is an older term and persistent fetal vasculature (PFV) is a newer term for a congenital disorder that usually affects normal birth weight children and is unilateral (90%).[32] A developmentally required vascular system consisting of the hyaloid artery, vasa hyaloidea propria, and anterior ciliary vessels fail to undergo complete regression. The disease is classified as anterior or posterior based on the location of the retained vessels (see Figure 216.1).[33]
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FIGURE 216.1 Persistent hyperplastic primary vitreous. Left panel: Fluorescein angiography of PHPV shows vascular tuft posterior to the crystalline lens, which retains optical clarity at this stage. Right panel: Color photograph of PHPV with intralenticular hemorrhage, which can contribute to lens swelling and angle closure. |
The anterior form is associated with microphthalmos, shallow anterior chamber, elongated ciliary processes, engorged iris vessels, and leukocoria. Since the posterior capsule of the lens is often absent, the metabolism of the lens is disrupted, resulting in opacification, and swelling of the lens, which can precipitate secondary angle-closure glaucoma by forwards displacement of the lens and iris, or by causing pupillary block. A retrolenticular membrane may contract, causing anterior movement of the lens and iris with subsequent angle closure. In addition, bleeding from the vessels can cause a vitreous hemorrhage and result in inflammatory or ghost-cell glaucoma.[33] In rare instances, intralenticular hemorrhage may occur, causing swelling of the lens and resulting in angle closure. As a developmental disorder, the changes are not completely isolated to the affected eye, since the contralateral (uninvolved eye) is at risk for open-angle glaucoma.[34]
In posterior PHPV, there is an association with mircrocornea, embryonic filtration angle abnormalities, vitreous membranes, stalks, retinal folds and tractional retinal detachment. Although there are no clear mechanisms for angle-closure glaucoma as in anterior PHPV, the involved eye is at increased risk for open-angle glaucoma.[33]
If there is progressive cataract formation, surgical intervention is indicated, since the lens will shallow the anterior chamber likely resulting in glaucoma, in addition to the likelihood of amblyopia.[35] A vitrector is used to remove the cataract, and any fibrovascular membranes. Surgery is less successful with coexisting microphthalmos, longstanding intractable glaucoma, or hemorrhage.[35] Careful evaluation is required, since some cases of PHPV with minimal changes to the lens are better observed for progression.
GLAUCOMA ASSOCIATED WITH RETINITIS PIGMENTOSA
Reports in the literature indicate a rate of glaucoma in retinitis pigmentosa of between 2% and 12%,[36] mostly angle-closure glaucoma. Retinitis pigmentosa is a heterogeneous disease, as demonstrated by the number of different causative mutations that have been identified, and the reason for the potential association with glaucoma has not been described. Since these patients already suffer from a disease that negatively impacts their visual potential, it is important to not overlook a potentially treatable cause of vision loss. This can be complicated by the fact that visual field changes in retinitis pigmentosa may mimic those in glaucoma (and the reverse).[36,37] Diagnosis of glaucoma may depend much more strongly on careful analysis of the nerve for notching, focal hemorrhages, and overall thinning.
GLAUCOMA ASSOCIATED WITH STICKLER'S SYNDROME
Stickler's syndrome is an autosomal dominant connective tissue disorder that includes ocular, orofacial, and generalized skeletal findings.[38] Major ocular features include myopia, open-angle glaucoma, cataract, vitreoretinal degeneration, perivascular pigmentary retinopathy, and retinal detachment that is resistant to repair.[39] Orofacial findings include midfacial flattening and the Pierre Robin malformation complex (micrognathia, cleft palate, and glossoptosis). Skeletal abnormalities include joint enlargement, hyperextensibility, arthritis, and mild spondyloepiphyseal dysplasia.[39] Clinically the vitreoretinal degeneration manifests as an 'optically empty vitreous cavity'.[40]
Patients known to be affected by Stickler's syndrome should be examined periodically, which should allow treatment of glaucoma, and retinal breaks or detachment (if properly detected). Some recommend avoiding miotic therapy to reduce the risk of retinal detachment.[41] Most glaucoma in Stickler's syndrome presents with elevated IOP that can be treated medically.[41] The degree of myopia may complicate the evaluation of the optic nerve, and retinal changes can complicate the analysis of visual field changes. Newer optic nerve analysis can be helpful in characterizing any changes in the optic nerve.
GLAUCOMA ASSOCIATED WITH INFECTION/INFLAMMATION
GLAUCOMA ASSOCIATED WITH ACQUIRED IMMUNODEFICIENCY SYNDROME
Some of the major ocular manifestations of acquired immune deficiency syndrome (AIDS) are opportunistic infections and neoplasms secondary to the loss of immune function and surveillance.[42,43]Common diseases include cytomegalovirus (CMV) retinitis, retinal phlebitis, cotton wool spots (HIV retinopathy), and conjunctival Kaposi's sarcoma.[42] In AIDS, retinitis may be caused by a member of the herpesvirus family, and the resulting acute retinal necrosis, uveitis, rhegmatogenous, and nonrhegmatogenous retinal detachments can drastically reduce vision. Some other less common infectious agents include cryptococcal choroiditis, choroidal Mycobacterium avium intracellulare, Histoplasma capsulatum chorioretinitis, toxoplasmosis, syphilis, and Pneumocystis carinii retinitis.[43]
These infections and the inflammation associated with them can cause glaucoma by forming synechiae (anterior or posterior), by clogging the trabecular meshwork with inflammatory material, or by causing angle closure due to ciliochoroidal effusion and detachment.[44-46] AIDS-related ciliochoroidal effusions may cause secondary angle closure, not relieved by surgical iridectomy. In this situation, cycloplegia and topical aqueous inhibitors to improve or temporize the problem until resolution.[46] Topical steroids may be helpful, but a careful examination of the retina is required to rule out infectious retinitis prior to use, or to cover with antiviral therapy if necessary.[47,48]
GLAUCOMA ASSOCIATED WITH UVEITIS
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The goal of treatment in uveitic glaucoma is twofold. First and most importantly, diagnose the inflammatory cause and treat (see Table 216.3), and secondly, control the IOP while waiting for response to therapy for uveitis. Various studies have shown that in acute uveitis, between 8% and 26% will develop increased IOP, and with chronic uveitis between 11% and 46%.[49-54] Medical therapy can be started immediately based on the degree of IOP rise. If there is a component of pupillary block then a laser peripheral iridectomy is indicated if the eye is not uncontrollably inflamed.
TABLE 216.3 -- Uveitic Conditions Associated with Glaucoma
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Modified from Netland PA and Denton N. Uveitic glaucoma. Contemp Ophthalmol, 2006; 5:1-6.
If infectious uveitis can be ruled out or covered with appropriate antibiotics, then topical or systemic steroids, systemic nonsteroidal antiinflammatory drugs, and systemic immunosuppressive agents can then be used to control the inflammation. Since steroid medications can independently raise IOP in susceptible individuals, minimizing the steroid use may be considered when IOP is difficult to control.[55,56]
Ongoing inflammation can result in reduced aqueous production, which will result in lower IOP. As uveitis is controlled, there may be a rise of IOP, before a likely steroid pressure response, which must be managed medically until the inflammation has been brought under control.
Although systemic administration of corticosteroids may be effective for controlling ocular inflammation, they can be associated with significant systemic side effects, including suppression of the hypothalamic-pituitary-adrenal axis, osteoporosis, Cushing's syndrome, cataracts, glaucoma, secondary diabetes, peptic ulcer disease, and psychosis.[57] Systemic immunomodulation and immunosuppression with other drugs besides steroids is now emerging as an increasingly useful therapy for difficult to control inflammation. However, these immunomodulatory drugs should be used with caution, and in conjunction with an internist, oncologist or rheumatologist.[58,59]
Immunomodulatory drugs vary in their efficacy for uveitis in different inflammatory diseases.[60] Behçet's disease (also known as Adamantiades-Behçet[61] disease discussed in Chapter 173), responds to cyclosporine both during the acute attack and for controlling the chronic disease. Due to the potential for side effects associated with use of cyclosporine, including renal toxicity, the dosing and monitoring should be reviewed with a specialist familiar with this medication.[61] Wegener's granulomatosis may respond to the application of chronic low-dose cyclophosphamide and alternate-day prednisone therapy. The long-term remission rates were 93% (70 of 85 patients) over a 21-year study with the mean duration of remission being 48.2 (±3.6 months). Common side effects of cyclophosphamide include bone marrow suppression, leukopenia, and consequent infectious disease resulting from impaired immune function, hemorrhagic cystitis, hair loss, and gonadal dysfunction.[59] Rheumatoid arthritis may respond to immunosuppressive therapy in the form of high-dose pulse intravenous steroid therapy combined with once-a-week methotrexate therapy.[62] Common side effects of methotrexate therapy include stomatitis, alopecia, gastrointestinal intolerance, and bone marrow toxicity usually associated with renal insufficiency.[63]
Nonsteroidal antiinflammatory agents are used to treat postoperative inflammation and prevent or treat pseudophakic and aphakic cystoid macular edema.[64] Available topical ophthalmic cyclooxygenase inhibitors include flurbiprofen (Ocufen), suprofen 1% (Profenal), diclofenac 1% (Voltaren), nepafenac 0.1% (Nevanac), and ketorolac tromethamine (Acular). Although these agents may be useful to suppress postoperative inflammation, there is no evidence to support their efficacy in the treatment of endogenous uveitis.[64]
Inflammation in the eye may cause glaucoma by a variety of mechanisms. Gonioscopic examination of the angle is important, especially to distinguish open from closed angle mechanisms. Inflammatory cells and debris can deposit in the trabecular meshwork, resulting in open-angle glaucoma.[65,66] In some cases, inflammatory precipitates can occur in the trabecular meshwork, causing significant elevation in IOP with minimal overall inflammation. However it is clear that the primary process is inflammatory since it responds well to intensive corticosteroid therapy with some conventional pressure reducing medications to control IOP.[65] Inflammation affecting the trabecular meshwork itself may contribute to this effect in some cases. Peripheral anterior synechiae (PAS) can form and close off the angle, causing angle-closure glaucoma. Posterior synechiae can seclude the pupil resulting in partial or complete papillary-block and angle-closure glaucoma. This papillary-block glaucoma can also progress to permanent closure of the angle as the inflamed iris, apposed to angle structures, forms PAS as well. Inflammation can also result in ciliochoroidal effusions, which can rotate the lens and iris forward to cause angle closure glaucoma.
When the angle and/or trabecular meshwork is severely compromised, medical therapy will likely fail to control the IOP, and surgical intervention will be required to bypass the nonfunctioning trabecular meshwork. Both trabeculectomy (with and without adjunctive antifibroblast medications) and aqueous drainage implants have been used to control IOP.[60] Glaucoma drainage implants are helpful in patients with extensive conjunctival scarring, in patients with active or recurrent uveitis, or after failed trabeculectomy. The results of drainage implant surgery in uveitic glaucoma are improved with effective treatment of uveitis.[60,67-70]
Uveitis has been identified as an important mechanism contributing to glaucoma in Schwartz's syndrome,[71] iris retraction syndrome,[72] ROP,[24] and others that feature long-standing retinal detachment with possible formation of posterior and anterior synechiae. Other disorders affecting the posterior segment that have been associated with secondary glaucoma due to uveitis include but are not limited to toxoplasmosis,[73] Vogt-Koyanagi-Harada syndrome,[74,75] toxocariasis,[76] cytomegalic inclusion disease retinitis,[77] mumps,[78] coccidioidomycosis,[79] onchocerciasis,[80] leprosy,[81] tuberculosis,[82] and AIDS-related opportunistic infections.[48]
GLAUCOMA ASSOCIATED WITH ACQUIRED RETINAL DISEASE
GLAUCOMA ASSOCIATED WITH CENTRAL RETINAL VEIN OCCLUSION
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Glaucoma and ocular hypertension (OHT) are risk factors for the development of central retinal vein occlusion (CRVO).[83-85] After the development of CRVO, different types of glaucoma may occur, including secondary angle closure[86,87] and primary angle closure.[87,88] Another major glaucoma entity associated with CRVO is neovascular glaucoma, which is much more common with the ischemic form of CRVO. Ischemic CRVO is defined as having at least 10 disk areas of nonperfused capillary bed (based on fluorescein angiography). Ischemic CRVO patients were often given prophylactic panretinal photocoagulation (PRP); however, prospective studies by the CRVO study group found very limited protection unless anterior segment neovascularization developed. Therefore, the CRVO study group recommended close follow-up of patients with ischemic CRVO, and prompt PRP if anterior segment neovascularization develops.[89-91] Furthermore, data from the CRVO study group and others have shown that angle neovascularization can occur without iris neovascularization, so gonioscopic screening is recommended (see Fig. 216.2).[89,90,92,93]
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FIGURE 216.2 Iris and angle neovascularization in patients with central retinal vein occlusion (CRVO) and diabetes mellitus. In two different studies (left and right figures), while no diabetic patients presented with angle neovascularization only, a significant number of CRVO patients did, emphasizing the need for gonioscopic screening. |
On initial examination, the anterior chamber may be shallow compared to the fellow eye. This may occur ?3 days after the event, although onset as much as 2 years after the vascular even have been reported.[94] If the fellow eye has an occludable angle, pupillary block should be considered as a factor in the angle narrowing. A prophylactic laser peripheral iridectomy may be indicated. The CRVO may be classified based on fluorescein angiography as noted above, and the patient seen at least monthly for evaluation for possible pan retinal photocoagulation.
Mechanisms proposed to explain the anterior chamber shallowing after CRVO are transudation of fluid from the retinal vessels, which increases the volume of the vitreous cavity, and choroidal edema with resultant effusion and ciliary body detachment.[86,87] Both of these mechanisms involve forward displacement of the lens-iris diaphragm and secondary angle closure. Hyams and Neumann[88] invoked angle closure on the basis of pupillary block, but several cases reported by Grant failed to respond to peripheral iridectomy.[86]
The angle closure usually widens gradually over a period of several weeks. Treatment with topical cycloplegic agents helps resolve the condition by relaxing the ciliary muscle, tightening the zonules, and moving the lens and iris posteriorly. Pressure reduction may be achieved by topical ?2-adrenergic agonists, ?-blockers, carbonic anhydrase inhibitors, and hyperosmotic agents, as needed. When inflammation is controlled, prostaglandin analogs may be useful. Topical steroid preparations may help resolve the inflammatory component of the choroidal effusion and thus assist in resolving the angle closure on this basis.[95]
GLAUCOMA ASSOCIATED WITH HEMORRHAGIC COMPLICATIONS OF AGE-RELATED MACULAR DEGENERATION
This is a rare syndrome with a massive hemorrhage causing retinal and/or choroidal detachment from a disciform macular degeneration lesion. The angle may be closed by an anterior displacement of the iris and lens, and concomitant rotation of the ciliary body.[96-98] Risk factors include systemic hypertension and a clotting disorder.[97-100] Anticoagulant use has been implicated with these large hemorrhages.[99-101] The presentation is usually abrupt vision loss, with pain, nausea, and vomiting. At presentation, the pressure can be as high as 60-70 mmHg, often accompanied with corneal edema and shallowing of the anterior chamber (Fig. 216.3). The aqueous may have a reddish or wine-colored appearance, presumably due to blood-breakdown products. If visible, the angle is usually closed.[97] The posterior segment is seldom visible, and must be examined with ultrasound. The fellow eye typically has an open, nonoccludable angle and signs of age related macular degeneration. Other causes of nonsurgical suprachoroidal hemorrhage should be ruled out, such as a melanoma of the ciliary body or choroid.[102]
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FIGURE 216.3 Angle closure secondary to spontaneous hemorrhage due to age-related macular degeneration in a patient treated with anticoagulants. Left panel: The anterior chamber is shallowed due to massive subretinal and suprachoroidal hemorrhage. The iris and aqueous have a darkened and slightly reddish hue due to blood-breakdown products. Right panel: fellow eye, with a lighter (normal) iris and deeper chamber. Examination of the fundus of the normal eye showed signs of age-related macular degeneration. Note the heterochromia and shallowing of the anterior chamber of the affected eye. |
On ultrasound, hemorrhagic choroidal detachment is evident, often with a 'kissing choroidal' pattern. The absence of a regular structure and low internal reflectivity melanoma will usually exclude that possibility.[102] However, enucleation my still be required if melanoma is a possibility or if the visual prognosis is very poor. In one series, two of 17 eyes retained any light perception, and 10 of 17 eyes required enucleation for pain.[97]
Initial medical therapy for pressure reduction includes topical ?2-adrenergic agonists, ?-blockers, carbonic anhydrase inhibitors, and hyperosmotic agents as tolerated. When inflammation is controlled, prostaglandin analogs may be useful. Topical cycloplegics and steroids may help reduce discomfort and inflammation. In the event of a blind and painful eye, medical therapy commonly fails, and retrobulbar alcohol or thorazine injections may be required for relief of pain. Other treatments for absolute glaucoma and pain, including cyclophotocoagulation and enucleation or evisceration, may be helpful for some individuals.
If the fellow eye is affected by age-related macular degeneration in the form of a disciform lesion and the patient is taking oral anticoagulant therapy, consultation with the internist is recommended. The possibility of discontinuing anticoagulants to reduce the risk of a similar hemorrhagic episode in the fellow eye may be considered.[97]
GLAUCOMA ASSOCIATED WITH COMPLICATIONS OF INTRAOCULAR HEMORRHAGE (HEMOLYTIC, GHOST CELL, HEMOSIDEROTIC, AND SICKLE CELL HEMOGLOBINOPATHY)
Hemorrhage without neovascularization can cause glaucoma through several mechanisms, which are subclassified as hemolytic,[103] ghost cell,[104] and hemosiderotic[105] glaucomas. Each can cause persistent IOP elevations. Both hemolytic and ghost cell glaucoma result from deposits of red cell breakdown products in the trabecular meshwork. In the case of hemolytic glaucoma, the material consists of fragments of hemolyzed red blood cells and hemoglobin filled macrophages. The presentation is typically 5-7 days after the hemorrhage. Ghost cell glaucoma is associated with tan- or khaki-colored hyphema, typically presenting 11-14 days after the hemorrhage. In ghost cell glaucoma, red blood cell outer membranes, with very little hemoglobin, accumulate in the trabecular meshwork and obstruct aqueous flow. These ghost cells are usually from blood in the vitreous that is sequestered, and presumably enters the anterior of the eye through a disruption in the vitreous face. Hemosiderotic glaucoma is caused by longstanding or recurrent hemorrhage, in which hemoglobin breakdown products accumulate in the trabecular meshwork and possibly the deeper endothelial cell layer. This causes degenerative changes along with the pressure increase, which may not be reversible.
The first line is medical therapy for each of these, but surgical evacuation of the anterior chamber or even vitrectomy may be required. The management of hyphema is more complex if the patient has known or suspected sickle-cell hemoglobinopathy (or trait) since optic nerve damage and corneal blood staining may occur even with mild to moderate elevation of IOP.[106] Red blood cells in the anterior chamber can sickle due to the more acidic and hypoxic conditions (compared to the plasma). Sickled red blood cells can obstruct the trabecular meshwork, causing elevated IOP. The increased pressure can cause posterior and anterior chamber hypoxia, further exacerbating the problem. Unlike other typical cases of elevated IOP, carbonic anhydrase inhibitors should not be used since they cause metabolic acidosis, which worsens sickling. Systemic hyperosmotic agents can cause systemic hyperviscosity syndrome with blockage of small end arterioles, although these drugs are generally safe in limited doses (e.g., one dose in a 24-h period).[106] Patients with sickle cell hemoglobinopathy experiencing persistent pressure elevations of more than 24 mmHg for longer than 24 h are at significant risk for visual loss secondary to optic nerve ischemia. Surgical intervention in the form of anterior chamber washout or filtration surgery, or both, may be indicated.[107]
GLAUCOMA ASSOCIATED WITH NEOVASCULARIZATION
Neovascular glaucoma is the common final pathway of many different kinds of eye disease. In the literature, there are more than 40 well-documented causes of iris neovascularization.[108] The distribution in descending incidence is retinal venous obstructive disease (36.1%), diabetic retinopathy (32.2%), carotid artery obstructive disease (12.9%), central retinal artery obstruction (3.8%), combined retinal artery and vein obstructive disease (3.8%), rhegmatogenous retinal detachment (1.5%), and anterior uveitis (1.5%).[109] For a full discussion of the causes of neovascularization, see Chapter 213.
Iris neovascularization is a sign of ischemia of the posterior segment of the eye, which results in the release of vasculogenic factors, which act on the responsive vasculature in the anterior segment (Fig. 216.4). In addition to having neovascularization of the iris, the neovascularization invades the angle. With the new vessels comes fibrovascular tissue, which matures and contracts, resulting in angle closure. Early in the process, reduction of these factors will cause the new blood vessels to regress, stopping the process prior to the stage of angle closure.[110] The standard treatment for neovascularization is panretinal photocoagulation of the retina.[111] Newer therapies being currently developed include antivascular endothelial growth factor (anti-VEGF) agents, which have been effective in reversing neovascularization of the iris and angle.[112,113]
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FIGURE 216.4 Neovascular glaucoma. The left panel shows iris neovascularization and posterior synechiae. The right panel shows advanced neovascular glaucoma with neovascularization of the iris and a glaucoma drainage implant tube. Note the inflammatory fibrin reaction in the anterior chamber. |
If panretinal photocoagulation is not possible due to vitreous hemorrhage or cataract, surgery may be required, consisting of lensectomy, or pars plana vitrectomy, or both, with endolaser or indirect laser application in the operating room. If the pressure is not medically controlled, filtration surgery or glaucoma drainage implant surgery may also be required.[114] During pars plana vitrectomy, endophotocoagulation of the ciliary body can be performed to reduce aqueous production directly.[115] Ciliary body endophotocoagulation is generally reserved for intractable glaucoma or eyes with a poor visual prognosis, because of the risk of hypotony and phthisis.[115] Other methods of achieving IOP control of refractory glaucoma include contact or noncontact cyclophotocoagulation,[103-105] therapeutic ultrasound,[116] and cyclocryotherapy.[117] Although these methods do not require direct visualization of intraocular tissues, they may be associated with a higher incidence of decreased vision, postoperative pain, and inflammation because of increased damage to ocular tissues.
Neovascular glaucoma may occur after posterior segment surgery. The incidence after pars plana vitrectomy ranges in the literature from 11% to 28%.[118-120] Many authors have noted an increase in postoperative rubeosis iridis after intraocular surgery in diabetics with either aphakia, or a posterior capsular compromise ranging from 32% to 40%.[120,121] This is likely due increased communication between the posterior and anterior chamber under these circumstances. The removal of the vitreous likely also contributes to anterior movement of molecules that stimulate neovascularization. High risk eyes may benefit from prophylactic panretinal photocoagulation.
GLAUCOMA ASSOCIATED WITH SYSTEMIC DISEASES
GLAUCOMA ASSOCIATED WITH DIABETES MELLITUS
Several investigators have noted an increased prevalence of POAG, ranging from 6% to 11%, in patients with diabetes compared with the control population.[122-125] Becker found a significant correlation between elevated IOP (?20 mmHg) and lack of proliferative retinopathy in a clinical comparison of diabetic patients older than 40 years of age, thus supporting a protective effect of elevated IOP against the development of proliferative diabetic retinopathy.[123] Others have suggested that the relationship of POAG and diabetic retinopathy involves many variables and that no simple relationship can be implied.[126]In a large study of risk factors for glaucoma, diabetes emerged as a protective factor, possibly due to the exclusion criteria, which only allowed diabetics with no retinopathy.[127] As noted elsewhere, if proliferative diabetic retinopathy develops, there is risk for anterior segment neovascularization, and subsequent neovascular glaucoma.
GLAUCOMA ASSOCIATED WITH AMYLOIDOSIS
Primary familial amyloidosis is an autosomal dominantly inherited systemic disorder that may have neurologic, cardiac, and renal involvement.[128] Ocular manifestations of primary familial amyloidosis include bilateral secondary open-angle glaucoma, progressive vitreous opacities, and lattice corneal dystrophy type II.[128,129]
Open-angle glaucoma associated with amyloidosis develops earlier than POAG, with incidence highest in the third through fifth decades. Electron microscopy shows amyloid fibrils in the trabecular meshwork. Other findings include pigment on the corneal endothelium and iris transillumination. Vision may be further reduced by amyloid opacification of the vitreous, which may interfere with visual field testing. Conventional medical and surgical therapy is effective, although trabeculectomy failure from amyloid fibers have been described.[128]
GLAUCOMA ASSOCIATED WITH NEOPLASIA
GLAUCOMA ASSOCIATED WITH TUMORS OF THE POSTERIOR SEGMENT (MELANOMA, RETINOBLASTOMA, AND CHOROIDAL HEMANGIOMA)
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Glaucoma can be an important indicator of posterior segment neoplasia. Fraser and Font found that 3% of eyes with vitreous hemorrhage harbored a choroidal melanoma (Fig. 216.5).[130] Yanoff found that 20% of eyes diagnosed with choroidal malignant melanoma presented clinically with glaucoma.[131] In 37% of these eyes with glaucoma, media opacification prevented detection of the tumors before enucleation. Ultrasonographic evaluation is recommended for eyes with opaque media to aid in the detection of choroidal melanoma or retinal detachment before invasive action is taken.[131]
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FIGURE 216.5 Iris melanoma invading the angle. In the left panel a gonioscopic view of an iris melanoma is shown that involves the angle. The right panel shows a slit lamp view of an iris melanoma, with feeder vessels in the area affected by the tumor. |
Several mechanisms of glaucoma associated with choroidal melanoma have been identified.[131] Tumors may obstruct the outflow pathway by direct extension (usually with ciliary body and iris melanomas), or obstruct the trabecular meshwork with melanoma cells or macrophages with melanin (melanomalytic glaucoma).[131] Alternatively, inflammation caused by the tumor may cause angle-closure glaucoma similar to uveitic glaucoma. Also, choroidal and subretinal fluid, or the tumor itself, may cause the iris and lens to shift anteriorly, resulting in angle closure.
Neovascular glaucoma is considered to be the most common mechanism by which secondary angle closure with formation of peripheral anterior synechiae occurs in association with choroidal melanoma and retinal detachment.[131] Neovascular glaucoma is also common with retinoblastoma.[132] If a retinoblastoma tumor cases a retinal detachment, then glaucoma can be caused by angle closure. Finally the angle can become obstructed secondary to the direct involvement of neoplastic cells and inflammatory cells containing necrotic debris.[132] Neovascular glaucoma caused by tumors is more difficult to treat than from other causes, so most that have progressed to this stage require enucleation.[133]
Two mechanisms have been proposed to explain glaucoma occurring in patients with choroidal hemangiomas associated with Sturge-Weber syndrome. Early-onset glaucoma is thought to be related to a developmental abnormality of the anterior chamber angle similar to primary congenital glaucoma,[134] whereas glaucoma that occurs later in life may be explained by elevated episcleral venous pressure caused by small arteriovenous fistulas occurring in episcleral vessels.[135]
GLAUCOMA ASSOCIATED WITH OCULAR METASTATIC DISEASE (METASTASES ORIGINATING FROM PRIMARY CARCINOMA OF THE LUNG, BREAST, KIDNEY, RECTUM, LEUKEMIA, AND RETICULUM CELL SARCOMA)
Like most areas of the body with a blood supply that is greater than its metabolic need, the posterior segment of the eye is involved more frequently as a site of metastatic disease than is the anterior segment.[136] Metastases to the anterior segment tend to occur along the horizontal meridians of the iris or ciliary body, consistent with the blood supply through two long posterior ciliary arteries that are located at the 3 and 9 o'clock positions.[136] Since metastasis in the anterior segment has a more direct mechanism for interfering with aqueous dynamics, glaucoma is reported more frequently as a symptom of ocular metastatic disease affecting the anterior segment (56%) compared with the posterior segment (1%).[136,137]
Secondary open-angle glaucoma may occur in anterior segment metastatic disease due to obstruction of the anterior chamber angle by tumor cells that infiltrate the trabecular meshwork and emissary vessels. Secondary angle closure may occur from tumor-related obstruction of the angle, peripheral anterior synechiae formation, and the development of neovascular glaucoma.[136] Mechanisms of glaucoma occurring in posterior segment metastatic disease are secondary angle closure resulting from increased posterior segment volume and ciliochoroidal effusion, retinal and choroidal detachment, and neovascular glaucoma.[137]
In order of decreasing frequency, the sites of primary carcinoma responsible for ocular metastatic disease are the lung, breast, kidney, and rectum.[136] Posterior segment metastases usually appear clinically as small, multifocal, grayish elevations.[136] Glaucoma arising from ocular metastatic disease is treated with pressure-reducing agents (prostaglandin analogs, topical ?2-adrenergic agonists, ?-blockers, oral carbonic anhydrase inhibitors, and systemic hyperosmotic agents, as needed). Secondary angle-closure glaucoma on the basis of suspected ciliochoroidal effusion is treated with topical cycloplegic agents, corticosteroids, and aqueous suppressants, as needed.
Ocular involvement in leukemia most frequently affects the choroid and retina with retinal and vitreous hemorrhages, but anterior segment involvement with iris infiltration, hyphema, and glaucoma may rarely occur as the initial manifestation.[138] After diagnostic anterior chamber paracentesis, irradiation usually promotes resolution of the ocular findings, and pressure reduction is achieved by aqueous suppressants and topical corticosteroids.
Intraocular reticulum cell sarcoma (intraocular B-cell lymphoma) is a rare cause of uveitis that is usually recalcitrant to conventional corticosteroid therapy.[139,140] It characteristically manifests in patients older than 40 years of age with symptoms of uveitis affecting the posterior segment (vitritis) to a greater degree than the anterior segment (iridocyclitis), with choroidal or retinal infiltrates. It may be unilateral or bilateral in occurrence. Secondary glaucoma and corneal edema may preclude adequate fundus examination. Pars plana vitrectomy is diagnostic and therapeutic in terms of obtaining a cytologic diagnosis and in clearing the visual axis. A search for central nervous system involvement is indicated through computed tomography or magnetic resonance imaging, especially in the setting of neurologic symptoms. Treatment may include irradiation to the eye, brain, and spinal chord. Patients with central nervous system involvement may be treated with intrathecal chemotherapeutic agents such as methotrexate. It is uncertain whether reticulum cell sarcoma represents a primary or metastatic tumor of the eye, central nervous system, or other site.[139,140]
GLAUCOMA ASSOCIATED WITH RETINAL DETACHMENT
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Although most patients with retinal detachment present with low or normal IOP, 4-13% will have elevated IOP.[141] The causes of elevated IOP when a patient presents with retinal detachment are varied (Table 216.4). Patients with retinal detachment and elevated IOP may have previously unrecognized glaucoma, present prior to retinal detachment. In other patients, the IOP elevation is secondary to the retinal detachment, as in Schwartz's syndrome (Fig. 216.6).
TABLE 216.4 -- Causes of Elevated IOP at Presentation with Retinal Detachment
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Modified from Netland PA, Mukai S, Covington HI. Elevated intraocular pressure secondary to rhegmatogenous retinal detachment. Surv Ophthalmol 1994; 39:234.
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FIGURE 216.6 Prevalence of Schwartz's syndrome in patients presenting with retinal detachment. In this series of 817 patients, 7.3% had glaucoma as a preexisting condition. Upon presentation with retinal detachment, 4.4% had ocular hypertension, 2.1% had clinical evidence of Schwartz's syndrome, with normalization of intraocular pressure with repair of the retinal detachment. |
ROLE OF MIOTIC THERAPY OF GLAUCOMA IN RELATION TO RETINAL DETACHMENT
Retinal detachment associated with miotic therapy is uncommon and is unlikely to occur in patients who are free of retinal pathology.[142-147] Nonetheless, the risks and benefits of miotic therapy and retinal detachment precautions should be explained to patients prior to initiating miotic therapy. Patients with flashes or floaters or any other risk factor for retinal detachment should have a dilated fundus examination and peripheral retinal evaluation prior to initiating mitotic therapy. Patients with any retinal pathology or predisposing conditions should be offered prophylactic treatment. Also, any patient on miotic therapy who develops new symptoms (flashes/floaters) should be dilated and examined, even if miotic therapy has not been recently initiated or increased.
POAG ASSOCIATED WITH RHEGMATOGENOUS RETINAL DETACHMENT
IOP after retinal detachment may be reduced, unchanged, or elevated compared with the fellow eye. Decreased IOP may result from fluid flow through a retinal break and absorbtion by the retinal pigment epithelium. A study involving 604 patients with uncomplicated unilateral retinal detachment identified relative hypotony of 1.3 mmHg in 40% of the eyes compared with the normal fellow eye.[147] In eyes with unilateral retinal detachment, the IOP was lower in 64.2%, equal in 26%, and higher in 9.8%, compared with the unaffected fellow eye.[147]
Several investigators have noted a higher prevalence of POAG occurring in patients with nontraumatic, rhegmatogenous retinal detachments compared with the general population.[148-152] In 1955, Becker reported bilateral tonographic and clinical data from 530 patients with retinal detachment and found that POAG was present in 5.8%.[151] In 1977, Phelps and Burton evaluated 817 patients undergoing primary retinal detachment repair and found that POAG was present in 4.4%, while 86.2% had normal to low pressure (Fig. 216.4).[152] Langham and Regan found reduced IOPs, decreased outflow facilities, and decreased rates of aqueous humor formation in eyes with retinal detachment, compared with a control population.[153] Evidence to support the genetic association of POAG and retinal detachment on a multiple allelic basis is derived from a study involving 30 patients with nontraumatic retinal detachment.[154] Two factors predisposing to POAG, large cup:disk ratio[155] and topical steroid responsiveness[156], were found to be significantly correlated with nontraumatic, rhegmatogenous retinal detachment, compared with the nonglaucomatous population.
GLAUCOMA ASSOCIATED WITH SCHWARTZ'S SYNDROME
An unusual open-angle glaucoma secondary to rhegmatogenous retinal detachment was described by Schwartz in 1973.[71] He presented 11 patients with unilateral glaucoma in which an untreated retinal detachment preceded a secondary open-angle glaucoma. The cases were unusual for the age of onset of glaucoma, and half of the cases had a history of direct ocular trauma. The affected eyes had IOP ranging from 29 to 55 mmHg, with normal contralateral eyes. Most of the cases had concomitant iridocyclitis and glaucoma, both of which were poorly responsive to medical management including corticosteroids. When the longstanding retinal detachment was repaired, the pressure resolved within days to weeks.
Several theories have been postulated to explain the reduced aqueous outflow facility and glaucoma associated with Schwartz's syndrome (or Schwartz-Matsuo syndrome).[71,157,158] Schwartz hypothesized that iridocyclitis could cause a reduction in outflow facility, which could contribute to an elevated IOP in the presence of normal or reduced aqueous production.[71] Davidorf proposed that retinal breaks could release retinal pigment epithelial cells that could then migrate anteriorly with the aqueous humor to obstruct the trabecular meshwork.[157] However, based upon microscopic evidence, the predominant mechanism is obstruction of the trabecular meshwork by photoreceptor outer segments.[146,147] These photoreceptor outer segments pass through the retinal break and gain access to aqueous outflow pathways, thus producing outflow obstruction. Microscopic analysis of aqueous revealed isolated photoreceptor outer segments and variable levels of inflammatory cells in patients who met the criteria for Schwartz's syndrome.[158,159] In Figure 216.7, electron micrographs show photoreceptor outer segments in various stages of degeneration from aqueous humor aspirate from a patient with Schwartz's syndrome.[159]
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FIGURE 216.7 Electron micrograph analysis of anterior segment samples in Schwartz's syndrome. Shown are outer segments (top left), partially degraded outer segments (top right), degraded outer segments (bottom left), and ghost outer segments (bottom right). |
In Schwartz's syndrome, the elevation of IOP may be so prominent that the underlying treatable cause of retinal detachment may be overlooked. Although glaucoma medications may be helpful prior to definitive treatment, repair of the retinal detachment is the surgical therapy for Schwartz's syndrome. The IOP promptly becomes normal following retinal reattachment.
GLAUCOMA ASSOCIATED WITH THE IRIS RETRACTION SYNDROME
In 1984, Campbell reported nine patients with traumatic rhegmatogenous retinal detachment, hypotony, seclusion of the pupil, and retraction of the peripheral iris.[72] Other associated findings were ciliochoroidal detachment, inflammation, progressive cataract formation, and proliferative vitreoretinopathy.[72] Two types of clinical manifestations were identified: (1) angle closure secondary to iris bombé with elevation of IOP, which could revert to (2) iris retraction with deep anterior chamber and relative hypotony under the influence of pharmacologic aqueous suppressants. Several investigators have noted the association of hypotony with retinal detachment[153,160,161] and have proposed the existence of a subretinal fluid pump.[161,162] In the iris retraction syndrome, in patients with an occluded or secluded pupil, the subretinal fluid removal mechanism apparently equals or exceeds aqueous production after the addition of an aqueous suppressant. In Campbell's series, only two patients underwent successful reattachment and six of nine cases were considered to be inoperable because of proliferative vitreoretinopathy. Preoperatively, posterior synechiae may be broken pharmacologically, and glaucoma may be controlled by administration of topical glaucoma medications, when necessary.
PIGMENTARY DISPERSION SYNDROME GLAUCOMA AND ITS ASSOCIATION WITH RETINAL DETACHMENT
It has been suggested that there is an increased prevalence of pigmentary glaucoma with rhegmatogenous retinal detachment, although this has never been proved. Bracket and Chermet suggested an association of pigmentary dispersion-related glaucoma and retinal detachment in their presentation of 19 patients affected by both disorders, but they offered no statistical analysis.[163] In a retrospective study of 407 patients, Scheie and Cameron found an approximately equal incidence of retinal detachment in glaucomatous (6%) and nonglaucomatous (6.6%) patients with pigmentary dispersion.[164]
Eyes with rhegmatogenous retinal detachment have been found to have pigmentation of the angle structures in several studies, but no association with preexisting glaucoma has been proved statistically. Sebestyen and associates prospectively examined 160 eyes with preoperative rhegmatogenous retinal detachment but no prior history of glaucoma and found that 22.5% had marked pigmentation of the trabecular meshwork or peripheral anterior synechiae, or both, associated with postoperative pressure elevations.[165] Syrdalen conducted a prospective gonioscopic evaluation of 267 patients diagnosed with rhegmatogenous retinal detachment and found no significant difference in the degree of pigmentation when compared with the fellow eyes, when complicated detachments were excluded from consideration.[166]
GLAUCOMA ASSOCIATED WITH OCULAR TRAUMA
Ocular trauma may cause glaucoma and retinal detachment.[166,167] In this setting, multiple mechanisms may be responsible for glaucoma (discussed in Chapter 206) and for retinal abnormalities. The retinal problems and glaucoma may or may be causally related, or may be unrelated mechanisms resulting from the original trauma. Patients with Schwartz's syndrome, for example, often have a history of antecedent trauma, with the retinal abnormality causally related to the development of elevated IOP. Choroidal and subretinal hemorrhage may cause secondary angle closure.
GLAUCOMA ASSOCIATED WITH ORBITAL AND EXTRAORBITAL VASCULAR FACTORS THAT RESULT IN ELEVATED EPISCLERAL VENOUS PRESSURE
Fluid that leaves the eye through the conventional pathway drains from Schlemm's canal to the episcleral venules, so any increase of pressure in the episcleral veins will alter aqueous flow and potentially increase IOP (discussed in Chapter 211). Abnormalities in the orbit or cranium or even in the venous return system at the heart, can affect the IOP.[168] Increased venous pressure can also cause choroidal effusions and even choroidal hemorrhage, especially when IOP is surgically lowered (Fig. 216.8).
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FIGURE 216.8 Elevated episcleral venous pressure with engorged, tortuous veins and secondary glaucoma. |
GLAUCOMA RESULTING FROM THE TREATMENT OF DISORDERS OF THE RETINA, VITREOUS, AND CHOROID
GLAUCOMA RESULTING FROM ANGLE CLOSURE SECONDARY TO THE REPAIR OF RETINAL DETACHMENT BY SCLERAL BUCKLE
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A scleral buckle works on the principle of closing a retinal break by applying force to the sclera so that it becomes directly apposed to the detached retina. This, however, can distort the rest of the eye by direct force. In addition, an encircling band may impair normal venous drainage. In reported cases, narrowing of the anterior chamber from a buckle ranged from 14.4% to 50%.[169-171] The rate of angle closure has been lower, ranging from 2.1% to 14.4%.[171-174] The mechanism of angle closure is postulated to occur from anterior rotation of the ciliary body at the scleral spur as a result of ciliochoroidal effusion and detachment.[175,176] Fluid accumulation in the suprachoroidal space may result from surgical manipulation, inflammation, relative ischemia, and impedance of vortex venous outflow.[45,171,177,178]Pupillary block is not usually a mechanism and can be excluded by history and clinical examination.
The immediately post operative eye is difficult to examine, and is normally tender, with conjunctival injection and chemosis. Corneal edema may or may not be present, anterior chamber examination may reveal mild cell and flare, and IOP can be measured by Goldmann or Perkins applanation. Treatment may be required if the IOP is markedly elevated.[179,180] If pupillary block remains a possibility, laser iridotomy may be both diagnostic and therapeutic.[180] Angle closure without pupillary block can be treated by laser gonioplasty, as shown in Figure 216.9. Posterior segment evaluation by indirect or direct ophthalmoscopy, or ultrasonography, may not reveal clinically detectable ciliochoroidal detachment, but this does not eliminate this possibility because effusion is rarely detected clinically.[179,180]
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FIGURE 216.9 Gonioscopic view of angle several months after scleral buckle. This patient developed angle closure after scleral buckle, which was treated with laser gonioplasty. With longer term follow-up, the angle continued to deepen. Note the chronic appearance of the iridoplasty in the peripheral iris. |
Since the risk of an increased pressure is high during the immediate postoperative period, frequent pressure checks are indicated, to detect elevation of IOP (>30 mmHg) that could damage the optic nerve. Most cases resolve spontaneously within 1-3 days.[181,182] However, if the IOP is too high, then medical treatment with topical glaucoma medications and cycloplegic drugs can be helpful. Topical and oral steroids may help reduce the inflammatory component but should be used with caution because of the possibility of side effects, including untoward psychotropic reactions, physiologic disturbances, and steroid-induced glaucoma in susceptible individuals.[55] Cycloplegic medications may improve patient comfort and reduce angle closure. However, miotic drugs have not been effective and may actually exacerbate the angle closure by increasing congestion and anterior movement of the lens and iris.
If angle closure persists for more than 4 days, with failure of medical therapy, loosening of the buckle or surgical drainage of ciliochoroidal effusions may be warranted.[182] If the closure persists, permanent damage to angle structures may occur, with the development of peripheral anterior synechiae. In contrast, a narrowed angle without closure can be tolerated for several weeks until resolution.[182] In some cases of secondary angle narrowing or closure that are unresponsive to medical therapy, laser gonioplasty can be used to open the angle. Other indications for drainage of choroidal effusion or re-formation of the anterior chamber include flat anterior chamber with lenticular-corneal endothelial touch and the presence of 'kissing choroidal' effusions.
GLAUCOMA RESULTING FROM ANGLE CLOSURE SECONDARY TO PANRETINAL PHOTOCOAGULATION
When neovascularization develops in the retina, iris, or anterior chamber angle, panretinal photocoagulation is the standard treatment.[183] Experiments in rabbit eyes have demonstrated pronounced IOP spikes of 0.3 s duration during laser pulses using the xenon and ruby laser.[184,185] One early study found a rate of 33% for angle closure and 66% for angle narrowing after PRP, which resolved in 3-4 days.[186] The argon laser has demonstrated lower complication rates. Reported complication rates after argon laser PRP include 81% with choroidal detachment, 38% with anterior chamber shallowing, 12% with exudative retinal detachment, and 7% with increased IOP.[187-190]
During PRP, light energy converted to thermal energy creates an inflammatory process, resulting in disruption of the blood-retinal barrier.[184,185] This promotes ciliochoroidal effusion and detachment, which allows anterior rotation of the ciliary body, forward displacement of the lens and iris, and angle narrowing or closure. Pupillary block usually does not contribute to this problem.[188]
Initially patients report little or no ocular discomfort or visual disturbance, and a clear cornea is found on examination. If the IOP increases corneal edema may develop. Applanation pressure may be normal or elevated in the range of 20-50 mmHg. Biomicroscopy may show a shallow or closed angle with anterior annular ciliochoroidal detachment.[188]
Unless there is a component of pupillary block, medical treatment with topical cycloplegic therapy will relax the ciliary muscle and move the lens-iris diaphragm posteriorly, thus opening the angle.[188] If the pressure rises acutely (e.g., >30 mmHg), treatment with aqueous suppressants and hyperosmotic drugs may be helpful. Topical steroid application may enhance resolution of the effusion by reducing the inflammatory component. Most cases resolve spontaneously over a period of 4-14 days.[188,189]
GLAUCOMA RESULTING FROM SECONDARY ANGLE CLOSURE ASSOCIATED WITH INTRAVITREAL GAS TAMPONADE
The use of intravitreal gas injection for repair of retinal detachment was introduced in 1911 by Ohm and later used in conjunction with diathermy and subretinal fluid drainage in 1938 by Rosengren.[191,192]Longer acting sulfur hexafluoride (SF6) was introduced in 1973 by Norton.[193] Octofluorocyclopropane (C3F8) was introduced in 1973 by Vygantas and Peyman.[194,195] Both SF6 and C3F8 are inert, lipid-soluble gases that expand and increase their volume within the vitreous cavity. Their volume expansion occurs as a result of nitrogen diffusion from body tissues and blood into the gas pocket until equilibrium is achieved.[191,194-196] These gases provide superior tamponade to air since they are long-lasting (plain air absorbs in 4 days) and expand in the vitreous cavity.[193] SF6 (molecular weight 146) expands to twice its original volume over the first 24-36 h and lasts for 14 days.[197] C3F8 (molecular weight 200) expands to four times its original volume over the first 18-36 h and lasts 4-6 weeks.[198]
With injection of gas for tamponade, the IOP can rise to 80 mmHg for several minutes, before increased outflow can compensate.[199] Some complications of expandable intravitreal gas tamponade include central retinal artery occlusion, acute open-angle glaucoma, and acute pupillary-block glaucoma.[200] Published reports showed a higher incidence of ocular hypertension with the use of 100% SF6 compared with lesser gas concentrations.[200] Twenty-six of 101 eyes developed transient fibrinous exudation (with a greater incidence noted in diabetic patients), which contributed to pupillary block and angle closure, 10 eyes developed elevated IOP, and one eye had total loss of vision on the first postoperative day.[200]
While the transient pressure elevations from intraocular gasses have been well tolerated overall, patients with vulnerable optic nerves, tentative vascular supply to the retina, or reduced aqueous outflow capacity may be at increased risk of complications. Expandable gasses should be used with caution in such patients.[201]
Until the gas is at equilibrium, the pressure should be frequently monitored using Goldmann, Perkins, or MacKay-Marg tonometry.[196,202] Abrupt increases in IOP may require vitreous tap to reduce pressure. Medical therapy can temporarily achieve pressure control. Once the gas has fully expanded, daily pressure checks should be sufficient if stable. Caution is advised concerning air travel for patients harboring intravitreal gases. A prospective study of simulated air travel with monkeys containing intravitreal gas volumes as small as 0.25 mL after vitrectomy and air-fluid exchange showed an average IOP elevation of 42 mmHg associated with complications of central retinal artery occlusion and visual loss.[202] Some recommend that air travel be postponed until all intraocular gas has resorbed or that precautions be taken to ensure that cabin pressure is maintained at 2000 ft (706 mmHg).[200,201] Others recommend that patients who harbor greater than or equal to 1 mL of expansile gas should avoid air travel completely.[196]
GLAUCOMA ASSOCIATED WITH INTRAVITREAL SILICONE INJECTION
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More complex retinal detachments not amenable to repair with gasses can require silicone oil, introduced by Cibis and associates in 1962.[203] It has been commonly used with vitrectomy, membrane peeling, endophotocoagulation and scleral buckling.[204-206] In early studies, elevated IOP associated with silicone oil injection often resulted from secondary angle closure. Silicone oil can occlude the pupil, causing pupillary block.[207] In aphakic patients, an inferior peripheral iridectomy is now routinely performed to maintain communication between the anterior and posterior chambers. This has greatly reduced the incidence of pupillary block in eyes containing silicone oil. One study showed over half (56%) had an IOP elevation of at least 10 mmHg at some point between 6 h and 60 days postoperatively.[208] Of these, about half resolved spontaneously or with medical therapy, while about a quarter required removal of oil, and the other quarter required extensive medical management. Figure 216.10 shows silicone oil in the anterior chamber of an eye with a glaucoma drainage implant.
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FIGURE 216.10 Silicone oil in the anterior chamber. The inferiorly located glaucoma drainage implant tube is shown, with silicone oil adhering to the tip but not occluding it. Inferior location of the tube reduces the chance of occlusion of the tube and loss of silicone oil through the tube. |
A more recent study of glaucoma in eyes with silicone oil found only an 11% incidence of increased IOP, which was managed medically in 78% of cases, with only 12% requiring surgery.[209] In Figure 216.11 the time course of elevation of IOP during the postoperative period after injection of silicone oil is shown, indicating an early onset of increased IOP.[209] Pupillary block is uncommon or avoided altogether when aphakic patients are treated with iridectomy in an inferior location.[209] Recent formulations of silicone oil for retinal surgery have increased purity compared with earlier formulations, which may reduce the incidence of glaucoma.[209] Presumably this increased purity will reduce the incidence of other long term complications of silicone oil, such as keratitis, and uveitis.
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FIGURE 216.11 Mean intraocular pressure in eyes that developed elevated intraocular pressure after pars plana vitrectomy and silicone oil injection. The peak mean IOP was 26 mmHg at 3 months after pars plana vitrectomy and silicone oil injection, which was significantly higher than the baseline IOP of 12 mmHg (P < 0.001). |
Anatomic success rates in reattaching the retina have been reported between 64% and 66%, and complications associated with silicone oil placement over a 1- to 3-year period of follow-up include cataract (60%), glaucoma (17%), and keratopathy (12.3%).[205] Histopathologic findings in eyes enucleated after intravitreal silicone oil for 5-12 years have shown blockage of the trabecular meshwork by macrophages that contained phagocytized silicone. Silicone was also present in the vitreous, preretinal membranes, optic disk, iris, and choroid.[210,211] The most common cause of enucleation after silicone placement was for intractable secondary glaucoma.[212]
RETINAL ABNORMALITIES RESULTING FROM TREATMENT OF GLAUCOMA
Choroidal effusion or hemorrhage and retinal detachment may be observed after glaucoma surgery (Fig. 216.12). In eyes that have been treated with filtration surgery, treatment of the fellow eye with beta-blockers[213] or carbonic anhydrase inhibitors[214] may promote formation of choroidal effusions, which can be reversed by discontinuation of the drug. Patients with low IOP after filtration surgery may develop hyptotony maculopathy (Fig. 216.13).
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FIGURE 216.12 Hypotony with choroidal effusions. Large effusions are shown, which do not meet centrally. |
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FIGURE 216.13 Hypotony maculopathy. Fluorescein angiograph image showing choroidal folds inferiorly and diffuse leakage of dye into the retina indicating edema. The hypofluorescent areas are blocking defects secondary to hemorrhage. |
Decompression retinopathy may be observed when the IOP is rapidly lowered after glaucoma surgery. This is characterized by diffuse retinal hemorrhages, which may be superficial or deep, and may contain white centers.[215] IOP and visual results are generally not affected by the hemorrhages, and resolve without special treatment. Retinal hemorrhages are most often a benign occurrence in the setting of ocular decompression.
CONCLUSION
Glaucoma associated with disorders of the retina, vitreous, and choroid glaucoma encompasses a variety of primary and secondary diseases, ranging from congenital anomalies to acquired retinal abnormalities. Any surgical treatments of the retina can increase the risk of glaucoma, and conversely, glaucoma treatment can affect the retina. Although glaucoma and retinal problems may overlap without any causal association, in many instances, the problems are interrelated. The relationships between glaucoma and retinal abnormalities can influence patient management.
Information from The Code of Ethics of the American Academy of Ophthalmology has been reproduced with permission from the AAO.
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