- •Preface
- •Contributors
- •Dedication
- •INFECTIOUS DISEASES
- •ACINETOBACTER
- •BACILLUS SPECIES INFECTIONS
- •ESCHERICHIA COLI
- •GONOCOCCAL OCULAR DISEASE
- •INFECTIOUS MONONUCLEOSIS
- •MICROSPORIDIAL INFECTION
- •MOLLUSCUM CONTAGIOSUM
- •MORAXELLA
- •PROPIONIBACTERIUM ACNES
- •PROTEUS
- •PSEUDOMONAS AERUGINOSA
- •STREPTOCOCCUS
- •VARICELLA AND HERPES ZOSTER
- •PARASITIC DISEASES
- •PEDICULOSIS AND PHTHIRIASIS
- •NUTRITIONAL DISORDERS
- •INFLAMMATORY BOWEL DISEASE
- •DISORDERS OF CARBOHYDRATE METABOLISM
- •MUCOPOLYSACCHARIDOSIS IH
- •MUCOPOLYSACCHARIDOSIS IH/S
- •MUCOPOLYSACCHARIDOSIS II
- •MUCOPOLYSACCHARIDOSIS III
- •MUCOPOLYSACCHARIDOSIS IV
- •MUCOPOLYSACCHARIDOSIS VI
- •MUCOPOLYSACCHARIDOSIS VII
- •DISORDERS OF LIPID METABOLISM
- •HEMATOLOGIC AND CARDIOVASCULAR DISORDERS
- •CAROTID CAVERNOUS FISTULA
- •DERMATOLOGIC DISORDERS
- •ERYTHEMA MULTIFORME MAJOR
- •CONNECTIVE TISSUE DISORDERS
- •PSEUDOXANTHOMA ELASTICUM
- •RELAPSING POLYCHONDRITIS
- •UVEITIS ASSOCIATED WITH JUVENILE IDIOPATHIC ARTHRITIS
- •WEGENER GRANULOMATOSIS
- •WEILL–MARCHESANI SYNDROME
- •SKELETAL DISORDERS
- •PHAKOMATOSES
- •NEUROFIBROMATOSIS TYPE 1
- •STURGE–WEBER SYNDROME
- •NEUROLOGIC DISORDERS
- •ACQUIRED INFLAMMATORY DEMYELINATING NEUROPATHIES
- •CREUTZFELDT–JAKOB DISEASE
- •NEOPLASMS
- •JUVENILE XANTHOGRANULOMA
- •LEIOMYOMA
- •ORBITAL RHABDOMYOSARCOMA
- •SEBACEOUS GLAND CARCINOMA
- •SQUAMOUS CELL CARCINOMA
- •MANAGEMENT OF SCLERAL RUPTURES 871.4 AND LACERATIONS 871.2
- •IRIS LACERATIONS 364.74, IRIS HOLES 364.74, AND IRIDODIALYSIS 369.76
- •ORBITAL IMPLANT EXTRUSION
- •SHAKEN BABY SYNDROME
- •PAPILLORENAL SYNDROME
- •ANTERIOR CHAMBER
- •CHOROID
- •ANGIOID STREAKS
- •CHOROIDAL DETACHMENT
- •SYMPATHETIC OPHTHALMIA
- •CONJUNCTIVA
- •ALLERGIC CONJUNCTIVITIS
- •BACTERIAL CONJUNCTIVITIS
- •LIGNEOUS CONJUNCTIVITIS
- •OPHTHALMIA NEONATORUM
- •CORNEA
- •BACTERIAL CORNEAL ULCERS
- •CORNEAL MUCOUS PLAQUES
- •CORNEAL NEOVASCULARIZATION
- •FUCHS’ CORNEAL DYSTROPHY
- •KERATOCONJUNCTIVITIS SICCA AND SJÖGREN’S SYNDROME
- •LATTICE CORNEAL DYSTROPHY
- •NEUROPARALYTIC KERATITIS
- •PELLUCID MARGINAL DEGENERATION
- •EXTRAOCULAR MUSCLES
- •ACCOMMODATIVE ESOTROPIA
- •CONVERGENCE INSUFFICIENCY
- •MONOFIXATION SYNDROME
- •NYSTAGMUS
- •EYELIDS
- •BLEPHAROCHALASIS
- •BLEPHAROCONJUNCTIVITIS
- •EPICANTHUS
- •FACIAL MOVEMENT DISORDERS
- •FLOPPY EYELID SYNDROME
- •MARCUS GUNN SYNDROME
- •SEBORRHEIC BLEPHARITIS
- •XANTHELASMA
- •GLOBE
- •BACTERIAL ENDOPHTHALMITIS
- •FUNGAL ENDOPHTHALMITIS
- •INTRAOCULAR PRESSURE
- •ANGLE RECESSION GLAUCOMA
- •GLAUCOMA ASSOCIATED WITH ELEVATED VENOUS PRESSURE
- •GLAUCOMATOCYCLITIC CRISIS
- •NORMAL-TENSION GLAUCOMA (LOW-TENSION GLAUCOMA)
- •IRIS AND CILIARY BODY
- •ACCOMMODATIVE SPASM
- •LACRIMAL SYSTEM
- •LACRIMAL HYPOSECRETION
- •DISLOCATION OF THE LENS
- •LENTICONUS AND LENTIGLOBUS
- •MICROSPHEROPHAKIA
- •MACULA
- •CYSTOID MACULAR EDEMA
- •EPIMACULAR PROLIFERATION
- •OPTIC NERVE
- •ISCHEMIC OPTIC NEUROPATHIES
- •TRAUMATIC OPTIC NEUROPATHY
- •ORBIT
- •EXTERNAL ORBITAL FRACTURES
- •INTERNAL ORBITAL FRACTURES
- •OPTIC FORAMEN FRACTURES
- •RETINA
- •ACQUIRED RETINOSCHISIS
- •ACUTE RETINAL NECROSIS
- •DIFFUSE UNILATERAL SUBACUTE NEURORETINITIS
- •RETINOPATHY OF PREMATURITY
- •SCLERA
- •SCLEROMALACIA PERFORANS
- •VITREOUS
- •VITREOUS WICK SYNDROME
- •Index
S E CT I O N
23 Intraocular Pressure
258 ANGLE RECESSION GLAUCOMA
921.3
Sarwat Salim, MD, FACS
Memphis, Tennessee
Raghu Mudumbai, MD
Seattle, Washington
Spaeth et al showed that approximately 50% of patients with traumatic glaucoma developed open angle glaucoma in the unaffected, nontraumatized eye, suggesting that patients who develop angle recession glaucoma may have an underlying predisposition to developing glaucoma, which may be accelerated by the additional insult of trauma.
Since angle recession glaucoma may not occur for months or years after the original trauma, these patients need to be followed regularly.
ETIOLOGY
Angle recession glaucoma is one of the manifestations of blunt ocular trauma. The contusion leads to shearing forces between the anterior uvea and its various attachments. Damage can occur to the iris, trabecular meshwork (TM), or ciliary body. Angle recession involves rupture of the face of the ciliary body, resulting in a tear between the longitudinal and circular fibers of the ciliary muscle. Initially, this may be masked by the concomitant presence of hyphema, a common clinical presentation that occurrs after anterior segment trauma. Although a large percentage of patients may exhibit some level of angle recession on gonioscopy, only 4%–10% of these patients will develop angle recession glaucoma. The term angle recession glaucoma is somewhat misleading because the resultant glaucoma is not secondary to angle recession, but due to the initial trauma to the trabecular meshwork. Tears in the trabecular meshwork, along with degenerative changes and scarring, can lead to obstruction of aqueous outflow.
COURSE
Acutely, patients may have elevated intraocular pressure (IOP) from associated co-morbidities, such as hyphema, iridocyclitis, or pupillary block resulting from ectopia lentis with or without vitreous prolapse. In some cases, the IOP may be low secondary to decreased production of aqueous humor from associated inflammation, transient increase in outflow facility from disruption of structures in the angle, or due to the presence of a cyclodialysis cleft.
As previously mentioned, only a small minority of these patients develop late glaucoma. The risk of glaucoma appears to be related to the extent of angle recession. Usually, angle recession greater than 180º is deemed a considerable risk. In addition to the aforementioned changes described in the TM, another mechanism leading to chronic IOP elevation is due to formation of a Descemet’s-like membrane lined by endothelial cells over the drainage angle.
DIAGNOSIS
Clinical signs and symptoms
Acutely, the eye may be difficult to examine because of inflammation and hyphema. Once the view has cleared, attention should be paid to anterior chamber depth. The affected eye may appear deeper. On gonioscopy, characteristic findings of angle recession include widening of the ciliary body band, torn iris processes with resultant whitening of the scleral spur, and irregular and darker pigmentation in the angle. Peripheral anterior synechiae may be present. It is prudent to compare the angle appearance between the two eyes to evaluate subtle differences. Also, different quadrants within the same eye should be inspected carefully.
Other angle abnormalities from trauma such as iridodialysis (tear of the iris root) or cyclodialysis cleft (separation of the ciliary body from the scleral spur) may be detected.
Corneal blood staining, cataract, lens subluxation or dislocation, vitreous hemorrhage, retinal commotion, and retinal dialysis may be concomitantly present and accompany glaucoma.
Differential diagnosis
Acutely, many factors may contribute to elevated intraocular pressure. The trabecular meshwork may be overwhelmed by red blood cells and their byproducts or by inflammatory cells from iridocyclitis. Later, ghost cell glaucoma may develop. Chronic treatment with steroids can lead to steroid-induced glaucoma. Other differential diagnoses for unilateral glaucoma should be entertained, including pseudoexfoliative glaucoma and neovascular glaucoma. Unrelated open angle glaucoma and uveitic glaucoma should also be considered.
TREATMENT
In the acute setting, treatment should be directed at lowering intraocular pressure and controlling inflammation.
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Pressure Intraocular • 23 SECTION
Ocular
Topical steroids with cycloplegic agents may be helpful for both inflammation and pain control. Aqueous suppressants, including beta blockers, carbonic anhydrase inhibitors, and alpha agonist agents should be used to control IOP. Osmotic agents, by reducing vitreous volume, may provide acute but transient pressure reduction.
Medical
With chronic IOP elevation, medical therapy with aqueous suppressants should be attempted first. Miotics are usually ineffective in these cases and can actually cause paradoxical rise in pressure. Prostaglandin analogs may provide the benefit of bypassing the compromised trabecular meshwork and increase the uveoscleral outflow.
Salmon JF, Mermoud A, Ivey A, et al: The detection of post-traumatic angle recession by gonioscopy in a population-based glaucoma survey. Ophthalmology 101:1844, 1994.
Shields MB: Textbook of glaucoma. 4th ed. Baltimore, Williams & Wilkins, 1997:339–344.
Spaeth GL: Traumatic hyphema, angle recession, dexamethasone hypertension and glaucoma. Arch Ophthalmol 78:714–721, 1967.
Tumbocon JA, Latina MA: Angle recession glaucoma. Int Ophthalmol Clin 42:69–78, 2002.
259CORTICOSTEROID-INDUCED GLAUCOMA 365.31
John R. Samples, MD
Portland, Oregon
Surgical
Laser trabeculoplasty is usually not successful due to distortion of the angle anatomy and TM scarring. Filtration surgery with the use of antimetabolites is the most effective surgical procedure in these cases. Glaucoma drainage devices play a role in cases of failed filtering surgery or in patients who are not candidates for trabeculectomy due to excessive scarring from the initial trauma. In eyes with limited visual potential, a cyclodestructive procedure may be an alternative option.
COMPLICATIONS
The clinician should be mindful of complications associated with medical and surgical intervention. These include worsening of asthma and heart failure with beta blockers, allergic reactions to alpha2 agonists, and paresthesias, acidosis, fatigue, renal stones, and other adverse effects of carbonic anhydrase inhibitors. Filtration surgery poses risks of late onset bleb leaks with hypotony maculopathy and infection. Drainage implants can present a different set of problems, including corneal decompensation, tube retraction and erosion, and strabismus. Proper instruction ofpatients combined with a good clinical exam and frequent follow-up visits can, we hope, detect or prevent these problems.
COMMENTS
The clinician should be cognizant of both the short-term and long-term risks of glaucoma in patients who have suffered blunt ocular trauma. Patients presenting with hyphema should be evaluated with gonioscopy at an appropriate time to check for the presence of angle recession and other abnormalities. Usually, angle involvement of greater than 180º confers approximately a 10% risk for development of angle recession glaucoma. Since glaucoma can occur at any time after injury, regular follow-up examinations are mandatory for these patients, with particular attention to tonometry, gonioscopy, and optic nerve examination.
ETIOLOGY/INCIDENCE
Corticosteroids may cause elevated intraocular pressure (IOP) through any route of administration, including oral, inhaled, topical, and periocular. Individuals vary a great deal in sensitivity to corticosteroids. Pulmonologists are sometimes skeptical that inhaled steroids will raise pressure, and it may be best to recommend that the patient get checked two weeks after this medication is started. Approximately one-third of otherwise healthy individuals will have some type of IOP elevation in response to the use of corticosteroids. Age may be an important factor in determining this; children may be particularly susceptible. Steroid-induced glaucoma in children has been reported, and in some instances, congenital glaucoma may be corticosteroid related.
The popularity of intravitreal corticosteroid injections by retinal specialists has increased the occurrence of steroidinduced glaucoma. It may be warranted to check such patients two or three weeks after an injection. Patients with already compromised optic nerves should be followed especially closely.
In addition to the age of the patient, the magnitude and duration of IOP elevation is determined by dose, route of administration, frequency, duration of exposure, and predisposition of the individual to respond to corticosteroids. (The time of onset suggests a biochemical mechanism.) Because most individuals have normal optic nerves, patients with elevated IOP secondary to corticosteroid therapy may not have glaucomatous damage.
The elevation of IOP is related to biochemical abnormality in the trabecular meshwork. Several specific hypotheses have been put forward. Impaired outflow may be related to impaired enzymes in the trabecular meshwork.
COURSE
The course remits with discontinuation of corticosteroid and may be altered with decreased potency of drug. In some instances where the response to the intravitreal injection of steroid is aromatically effective, it may be best just to continue the injections and treat the glaucoma.
REFERENCES
Girkin CA, McGwin G, Jr, Long C, et al: Glaucoma after ocular contusion: a cohort study of the United States Eye Injury Registry. J Glaucoma 14:470–473, 2005.
Kaufman JH, Tolpin DW: Glaucoma after traumatic angle recession: a tenyear prospective study. Am J Ophthalmol 78:648–654, 1974.
Mermoud A, Salmon JF, Barron A, et al: Surgical management of posttraumatic angle recession glaucoma. Ophthalmology 100:634, 1993.
DIAGNOSIS
Clinical signs and symptoms
Ocular or periocular
●Eyelids: slight ptosis.
●Lens: cataracts, particularly posterior subcapsular cataracts.
●Other: increased intraocular pressure; visual field loss.
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TREATMENT
Ocular
●Discontinue the use of corticosteroids when steroid-induced glaucoma is suspected if the underlying condition permits. Whether the IOP falls will depend on the concurrent presence of uveitis or other conditions that raise the IOP. Most pressure reductions occur two weeks after steroid is discontinued.
●Alteration in the trabecular cells and in the cellular events surrounding outflow may occur as a result of corticosteroid use. Patients with corticosteroid-induced IOP elevations
respond to the usual antiglaucoma medications, including miotics, epinephrine, dipivefrin, β-adrenergic antagonists, and carbonic anhydrase inhibitors. As with ocular hypertension, there may be no need to treat mildly elevated pressure if the optic nerve is normal.
●Corticosteroid glaucoma generally does not respond to laser trabeculoplasty.
●If a topical ocular steroid is needed, it is sometimes useful to use a weaker synthetic steroid, such as fluorometholone or loteprednol etabonate, which will cause less pressure elevation for a given amount of antiinflammatory effect.
●Topical nonsteroidal anti-inflammatory drugs that are sufficiently potent to penetrate the eye and have significant anti-inflammatory action are available.
●Topical nonsteroidal anti-inflammatory drugs may have significant potency as well as a useful anti-inflammatory effect when used four times a day in lieu of a corticosteroid.
●The metabolism of steroids in systemic tissues, as well as the eye, seems to be a major determinant of steroid effects and side effects.
●A major part of the increased potency of steroids, such as dexamethasone, systemically is due to substitutions occurring on the cortisol molecule, some of which decrease degradation and others of which increase binding to steroid receptors. In direct contrast, steroids that are synthesized using progesterone rather than cortisol as the foundation molecule, such as fluorometholone and medrysone, seem to be particularly susceptible to degradation. In the eye, both medrysone and fluorometholone have a lesser tendency to raise the IOP, but they are not considered as efficacious, probably because of the inactivation due to metabolism.
Surgical
●Corticosteroid-induced glaucomas may require filtering surgery if they do not remit. Any decision to perform surgery must be based on the appearance of the visual field, as well as that of the optic nerve. Occasionally, corticosteroidinduced glaucomas are observed in the presence of a functioning filter or a Seton procedure.
●Glaucomatologists vary in their opinions on whether steroid-induced pressure elevations can be a significant
problem when an outflow-enhancing procedure, such as trabeculectomy or a Seton procedure, has been performed.
●The diagnosis of steroid-induced IOP elevation after filtration should include consideration of other causes of bleb failure, such as closure of the internal aspect of the filtering fistula and subconjunctival scarring.
COMPLICATIONS
Whenever a patient undergoes corticosteroid therapy, a baseline examination and close follow-up are mandatory. Patients who are treated with oral prednisone on a long-term basis or who have recurrent intravitreal corticosteroid injections may be particularly at risk and should have an eye examination to ensure that they have not developed steroid-induced glaucoma.
In addition to the side effects of corticosteroids, steroid injections can also cause problems due to the preservatives used and due to the direct toxicity of high steroid concentration on certain cell types. Periocular methyl prednisone preparations may causesteroid-related effects for longer than is generally appreciated.
COMMENTS
Many corticosteroid-induced glaucomas result from the inappropriate use of corticosteroids for minor conditions, such as eye irritation or contact lens discomfort. Also, it is not uncommon for patients who have been treated with oral steroids to have pressure elevations. The failure of a physician to recognize corticosteroid-induced glaucoma may lead to needless visual loss and difficult medicolegal problems.
REFERENCES
Agrawal S, Agrawal J, Agrawal TP: Management of intractable glaucoma following intravitreal triamcinolone acetonide.[comment]. [Comment. Letter] Am J Ophthalmol 139(3):575–576, author reply 576, 2005.
Armaly MF: Effect of corticosteroids on intraocular pressure and fluid dynamics. I. The effect of dexamethasone in the normal eye. Arch Ophthalmol 70:482, 1963.
Armaly MF: Effect of corticosteroids on intraocular pressure and fluid dynamics. II. The effect of dexamethasone in the glaucomatous eye. Arch Ophthalmol 70:492, 1963.
Armaly MF: Statistical attributes of steroid hypertensive response in the clinically normal eye. Invest Ophthalmol Vis Sci 4:187, 1965.
Jampol LM. Yannuzzi LA. Weinreb RN. Glaucoma and intravitreal steroids. [Editorial] Ophthalmology 112(8):1325–1326, 2005.
260 EXFOLIATION SYNDROME 365.52
(Pseudoexfoliation Syndrome,
Pseudoexfoliation Glaucoma,
Exfoliative Glaucoma, Capsular
Glaucoma)
Andrew G. Iwach, MD
San Francisco, California
Ümit Aykan, MD
Istanbul, Turkey
H. Dunbar Hoskins, Jr., MD
San Francisco, California
ETIOLOGY/INCIDENCE
The exfoliation syndrome occurs when ocular tissues synthesize an abnormal protein, which may obstruct the trabecular
Glaucoma260 CHAPTERRecession Angle •
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Pressure Intraocular • 23 SECTION
meshwork. Exfoliation syndrome with glaucoma appears to be a secondary glaucoma in which exfoliation material and pigment obstruct the trabecular meshwork, with an associated elevation in intraocular pressure
●Once thought to occur primarily in Scandinavia, exfoliation syndrome is now known to occur throughout the world.
●There is a higher prevalence in certain areas of the world.
●Prevalence increases with age.
●Exfoliation syndrome occurs equally in both sexes.
●This syndrome presents unilaterally in one-third to one half of cases; however, as many as 43% of cases become bilateral in 5 to 10 years.
●As many as 7% of patients with exfoliation syndrome are initially diagnosed with glaucoma, but an additional 15% are found to have only elevated IOPs without optic nerve damage.
●Causes are related to mechanical obstruction by exfoliative material of exotrabecular origin, apparent production of exfoliative material by trabecular cells, and abnormal regulation of elastin synthesis, degradation, or both in the optic nerve.
●In eyes with exfoliation syndrome, a small optic disk does not predispose to glaucoma. The optic disk does not show pathognomonic features for exfoliation.
●Fluorescein angiography of the iris reveals a decreased number of vessels, neovascularization, and leakage from the vessels.
●The extensive blood-aqueous barrier breakdown in eyes with exfoliation syndrome after intraocular surgery is a risk factor for early or late postoperative complications. Resulting alterations in the blood-aqueous barrier should be considered in the medical and surgical treatment.
Differential diagnosis
Significant fluctuation in the diurnal curve of the IOP distinguishes exfoliative glaucoma from primary open-angle glaucoma and may be an important factor in predicting any subsequent poor response to medical therapy.
TREATMENT
The treatment of glaucoma associated with exfoliation syn-
●The main risk factor for glaucoma is the degree of drome is similar to that for primary open-angle glaucoma.
chamber angle pigmentation rather than the amount of exfoliation.
●Exfoliation may be a risk factor for angle-closure glaucoma.
●Exfoliation syndrome is a risk factor in the evolution and treatment of exfoliative glaucoma and cataract.
●A poorer functional outcome and an increased incidence of preoperative and postoperative complications and senile cataract should be anticipated after surgery.
●The severity of glaucoma is related to the amount of exfoliative material present in the cribriform region.
DIAGNOSIS
Clinical signs and symptoms
●Patients with exfoliation syndrome present with a pattern on the anterior lenticular surface consisting of a central translucent disk surrounded by a clear zone, which in turn is surrounded by a granular gray-white area with scalloped edges that is best seen after pupillary dilation.
●Dandruff-like flakes of exfoliative material are deposited on the conjunctiva, corneal endothelium, trabecular meshwork, iris, pupillary margin, ciliary processes, zonules, and anterior hyaloid face in aphakic eyes.
●The amount of angle pigmentation is moderate, and distribution is patchy.
●Transillumination defects of the iris and reduced response to mydriatics are associated with exfoliation syndrome.
●The amount of exfoliative material correlates with the IOP and is inversely correlated with the number of axons in the optic nerve.
●Quantification may be achieved with flare measurement and biochemical protein determination, which affect pharmacologic and surgical treatment.
●Expect greater visual field loss and more difficulty in gaining control of IOP on presentation than with primary openangle glaucoma.
●Expect a higher mean range of IOP, a higher maximum IOP, and a higher minimum IOP.
More aggressive management is warranted.
●IOP is typically high in exfoliative glaucoma, so the response to medical treatment is less favorable.
●The glaucoma in exfoliation syndrome tends to be less responsive to medical therapy than in primary open-angle glaucoma, and a higher percentage of exfoliative glaucoma patients require surgical intervention.
●Laser trabeculoplasty has its highest initial success rate in exfoliative glaucoma, although the IOP may rise again within a few years.
●Filtering surgery has a high success rate.
●Expect a higher incidence of vitreous loss during cataract surgery in exfoliation syndrome.
●Patients respond well to timolol initially but then have a higher IOP and significant fluctuation in the diurnal curve.
●Latanoprost causes a marked and sustained IOP reduction in eyes also being treated with timolol.
●Although the initial response to argon laser trabeculoplasty in exfoliative patients is greater, the long-term outcome is similar to that of primary open-angle glaucoma.
●Phacoemulsification can be well tolerated if a careful preoperative protocol is followed, including pupillary dilatation, wide capsulorhexis, and total nucleus hydrodisection.
●Trabecular aspiration is a new proposed mode to treat exfoliation glaucoma.
COMPLICATIONS
●Exfoliation syndrome is a risk factor for retinal vein thrombosis.
●Exfoliative glaucoma is a risk factor for accelerated cataract progression after trabeculectomy.
●Abnormal extracellular matrix production and vascular abnormalities may cause degenerative tissue changes, and atrophy of muscle cells might potentiate the reduction in dilating properties of the iris.
●There is an increased incidence of the intraoperative and postoperative complications, including insufficient dilata-
482
tion of the pupil, tearing of the posterior capsule, loss of the vitreous, modifications of the corneal endothelium, increased postoperative IOP, and more frequent opacification of the posterior capsule.
●Comorbidity with acute cerebrovascular disease is more common with exfoliative glaucoma than with primary open-angle glaucoma.
SUPPORT GROUP
Glaucoma Research Foundation
490 Post Street, Suite 1427
San Francisco, CA 94102
REFERENCES
Henry JC, Krupin T, Schmitt M, et al: Long-term follow-up of pseudoexfoliation and the development of elevated intraocular pressure. Ophthalmology 94:545, 1987.
Jonas JB, Papastathopoulos KI: Optic disk appearance in pseudoexfoliation syndrome. Am J Ophthalmol 123:174–180, 1997.
Konstas AG, Stewart WC, Stroman GA, Sine CS: Clinical presentation and initial treatment patterns in patients with exfoliation glaucoma versus primary open-angle glaucoma. Ophthalmic Surg Lasers 28:111–117, 1997.
Layden WE, Shaffer RN: Exfoliation syndrome. Am J Ophthalmol 78:835, 1974.
Ritland JS, Egge K, Lydersen S, et al: Exfoliation glaucoma and primary open-angle glaucoma: associations with death causes and comorbidity. Acta Ophthalmol Scand 82(4):397–400, 2004.
●The increased protein content of the aqueous humor with the inflammatory reaction can result in compromise of aqueous outflow.
●Damage to trabecular cells after engulfing inflammatory debris may reduce outflow.
●Corticosteroids can cause IOP elevation.
CLOSED ANGLE
●The angle can be closed by extensive peripheral anterior synechiae or neovascularization.
●Posterior synechiae can lead to pupillary-block angle closure.
●Ciliary body swelling can cause forward rotation of the iris-lens diaphragm, leading to angle closure.
DIAGNOSIS
Laboratory findings
●Signs of acute iridocyclitis include ciliary flush, slight miosis, varying degrees of aqueous flare and cell, and frequent keratic precipitates.
●Chronic anterior uveitis often produces few or no symptoms but is particularly prone to cause secondary glaucoma.
●The IOP may vary in uveitic glaucoma due to variations in aqueous secretion, amount of outflow obstruction, and dose of corticosteroids being used at the time.
●A variety of noninvasive and invasive studies can be used to determine the cause of the uveitis, including serology, skin tests, chest radiographs, conjunctival biopsy, and anterior chamber paracentesis.
261 GLAUCOMA ASSOCIATED WITH
ANTERIOR UVEITIS 365.62
Leon W. Herndon, MD
Durham, North Carolina
ETIOLOGY
Increased intraocular pressure (IOP) can occur with any type of ocular inflammation, and it can be acute, transient, or chronic. Anterior uveitis influences IOP through a delicate balance between aqueous humor production and resistance to aqueous outflow. Usually, the production of aqueous is diminished in anterior uveitis; if this reduction is greater than the increase in resistance to outflow, the IOP will be low. In other cases, the increased resistance to aqueous outflow may be sufficiently greater than aqueous production, leading to pressure elevation.
The causes of glaucoma associated with anterior uveitis can be divided into two categories, depending on whether the angle is open or closed.
OPEN ANGLE
●Inflammatory cells (polymorphonuclear leukocytes and macrophages) can infiltrate the trabecular meshwork, leading to IOP elevation.
TREATMENT
Systemic
●Carbonic anhydrase inhibitors can be administered orally or intravenously.
●Systemic hyperosmotic agents are used to rapidly lower IOP and include oral glycerin, oral isosorbide, and intravenous mannitol.
Ocular
●Treatment should be directed at the underlying cause of the ocular inflammation.
●Inflammation can be treated with topical and systemic nonsteroidal anti-inflammatory agents; topical, periocular, and systemic corticosteroids; and systemic immunosuppressive agents.
●Ocular hypertension and glaucoma can be treated with topical β-blockers, alpha agonists, and carbonic anhydrase inhibitors.
●Miotics should be avoided because they may lead to increased inflammation.
●Prostaglandin analogs should probably be avoided because they may have a deleterious effect on the inflammatory cascade.
Surgical
Closed-angle glaucoma
●Laser iridotomy should be performed to reestablish communication between the posterior and anterior chambers.
Uveitis Anterior261withCHAPTERAssociated Glaucoma •
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