Ординатура / Офтальмология / Английские материалы / Oxford American Handbook of Ophthalmology_Tsai, Denniston, Murray_2011

286 CHAPTER 10 Glaucoma

Other secondary open-angle glaucomas

Steroid-induced

Exogenous and occasionally endogenous steroids may decrease outflow facility, leading to increased IOP after days, weeks, or months. In the normal population, 5% will have an IOP increase of >15 mmHg and 30% will have an increase of 6–15 mmHg if given topical steroids for up to 6 weeks. POAG patients are often particularly sensitive to this steroid effect.

Possible mechanisms include prostaglandin inhibition (e.g., PGF2A) and structural changes in the extracellular matrix (glycosaminoglycans) and trabecular meshwork (cross-linking of actins).

A history of steroid administration should be specifically asked for, since patients may not volunteer use of steroid-containing anabolics, skin creams, or episodic courses of steroids (e.g., for exacerbations of asthma or COPD). While steroids by any route may cause increased IOP, pressure elevation is more common with increased frequency and potency of steroid exposure (e.g., more common after intravitreal triamcinolone).

Treatment

Ideally, decrease frequency and potency or stop steroid and/or use other immunomodulators. If it is not possible to reduce steroids, then treat as POAG (p. 269).

Red cell glaucoma

Hyphema (usually traumatic) leads to blockage of the trabecular meshwork by red blood cells. In 10% cases a rebleed may occur, usually at around day 5.

Patients with sickle cell disease/trait do worse and are harder to treat, as sickled cells more easily obstruct the TM, and sickled cells within the optic nerve vasculature lead to earlier optic nerve damage. Sickling may be worsened by the acidosis induced by carbonic anhydrase inhibitors.

Treatment

•Hyphema: strict bed rest, topical steroid (e.g., dexamethasone 0.1% 4x/ day), mydriatic (e.g., atropine 1% 2x/day) (p. 100), avoid anticoagulants (aspirin, NSAIDS), use eye shield.

•Increased IOP: topical (e.g., B-blocker, A2-agonist, carbonic anhydrase inhibitor) or systemic (e.g., acetazolamide) agents as required; surgical: AC paracentesis ± AC washout.

Ghost cell glaucoma

Vitreous hemorrhage leads to blockage of the trabecular meshwork by degenerated red blood cells, usually 2–4 weeks after the hemorrhage. These cells, which may be seen in the AC and the angle, are tan-colored, having lost hemoglobin.

Treatment

Medical treatment (as for POAG, p. 269) is usually sufficient. If this fails, consider AC washout + vitrectomy to remove persistent vitreous hemorrhage.

OTHER SECONDARY OPEN-ANGLE GLAUCOMAS 287

Angle recession glaucoma

Blunt trauma may cause angle recession and associated trabecular damage. Traumatic angle recession carries a 10% risk of glaucoma at 10 years, the risk increasing with extent of recession. Look for asymmetry of AC depth, pupil, and angle.

•Screening: periodic IOP check (e.g., 3 months, 6 months, yearly) if known angle recession.

•Treatment: as for POAG (p. 269).

Raised episcleral venous pressure

Aqueous drainage is reduced as episcleral venous pressure increases (p. 262). This may occur as a result of vascular abnormalities in the orbit (Sturge–Weber syndrome, orbital varices), cavernous sinus (arteriovenous fistulae), or superior vena cava (SVC obstruction).

Episcleral venous pressure manifests as unilateral or bilateral engorged episcleral veins, chemosis, and proptosis, with blood in Schlemm’s canal on gonioscopy.

Treatment

Treatment is primarily directed at the underlying pathology, although medical and occasionally surgical lowering of IOP may be necessary.

Tumors

Tumors may cause increased IOP via open-angle mechanisms (clogging or infiltration of trabecular meshwork with tumor cells) or rubeosis (secondary to ischemia or radiation), or larger posterior segment tumors may cause it via secondary angle closure (anterior displacement of lens–iris diaphragm).

Suspect tumor in atypical unilateral glaucoma; if there is a poor view of posterior segment (usually due to cataract), a B-scan ultrasound is essential. Approximately 20% of malignant melanomas are associated with increased IOP.

Treatment

Treatment is directed by the underlying tumor, although increased IOP itself suggests a poor prognosis.

288 CHAPTER 10 Glaucoma

Other secondary closed-angle glaucomas

Iridoschisis

Bilateral splitting and atrophy of anterior iris leaf is associated with increased IOP usually secondary to angle closure (due to pupillary block), but sometimes due to debris blocking the trabecular meshwork (open angle). It is uncommon and usually occurs in the elderly.

Treatment

Closed-angle closure type is with Nd-YAG PI; open-angle type is the same as for POAG (p. 269).

Iridocorneal endothelial syndrome (ICE)

ICE is a unilateral condition in which abnormal corneal endothelium migrates across the angle, the trabecular meshwork, and the anterior iris, causing significant anterior segment distortion. ICE syndrome is rare, usually occurs in 20to 40-year-old females, and carries a 50% risk of glaucoma. HSV has been implicated.

Three overlapping syndromes are described: Chandler’s syndrome (predominantly corneal), essential iris atrophy (predominantly iris changes, most highly associated with glaucoma), and iris nevus (Cogan–Reese) syndrome (appearance of a diffuse nevus or pigmented nodules that probably represent protrusions of iris stroma).

Clinical features

•Unilateral pain, blurred vision.

•Unilateral fine corneal guttata (“beaten-metal”), corneal edema (increased IOP), iris atrophy corectopia (displaced pupil), pseudopolycoria (accessory pupil).

•Gonioscopy: broad-based PAS, which may insert anterior to Schwalbe’s line.

Treatment

•Medical (e.g., B-blocker, A2-agonist, carbonic anhydrase inhibitor, prostaglandin agonist), surgery (antimetabolite-augmented trabeculectomy or tube procedures), or cyclodestruction as required.

Posterior polymorphous dystrophy (PPMD)

PMMD is a bilateral condition in which abnormal corneal endothelium may form extensive iridocorneal adhesions with angle closure. Clinically, it may appear similar to ICE syndrome but is dominantly inherited, bilateral, and usually detectable in childhood (although it may only be symptomatic later). PPMD carries a 15% risk of glaucoma.

Treat glaucoma as for POAG (p. 269).

290 CHAPTER 10 Glaucoma

Iatrogenic glaucoma

Malignant glaucoma

This is also known as aqueous misdirection syndrome, ciliary block, and ciliolenticular block.

It is thought that that posteriorly directed aqueous is trapped in the vitreous, causing anterior displacement of vitreous and lens–iris diaphragm with secondary angle closure.

Risk factors

•Short axial length, chronic angle closure, previous acute angle closure.

•Post-procedure: surgery (trabeculectomy, tube procedures, cataract extraction, peripheral iridectomy); laser (Nd-YAG PI).

•Miotic therapy (rare).

Clinical features

•Asymptomatic unless acute or very high IOP.

•Increased IOP (may be normal initially), shallow or flat AC, no pupillary block (so no iris bombé and occurs despite a patent PI), no choroidal or suprachoroidal cause (detachment/hemorrhage).

Treatment

•Ensure that a patent PI is present (repeat Nd-YAG PI if necessary).

•Dilate (atropine 1% 3x/day + phenylephrine 2.5% 4x/day).

•Systemic IOP lowering: acetazolamide 500 mg IV stat (then 250 mg PO 4x/day) ± mannitol/glycerol.

•Topical aqueous suppressant to lower IOP: B-blocker (e.g., timolol 0.5% stat then 2x/day) + sympathomimetic (e.g., apraclonidine 1% stat then 3x/day).

•If medical treatment fails, consider laser or surgical treatment.

Laser

•Nd:YAG disruption of anterior vitreous face (if aphakia/pseudophakia, perform posterior capsulotomy/hyaloidotomy; if phakic, a hyaloidotomy can be attempted through the patent PI).

•Argon laser to the ciliary processes (through the patent PI; relieves block by causing shrinkage of processes or disruption of hyaloid face).

Surgery

•If phakic: cataract extraction (phacoemulsification or ECCE), posterior capsulotomy, and anterior vitrectomy.

•If aphakic/pseudophakic: pars plana vitrectomy and posterior capsulotomy.

Post-cataract surgery

Acute postoperative increased IOP may be due to retained viscoelastic, crystalline lens particles, inflammatory debris, TM inflammation, vitreous in the AC, or a suprachoroidal hemorrhage. Iris bombé may develop after an ACIOL if a PI is not created.

IATROGENIC GLAUCOMA 291

A single dose of acetazolamide SR 250 mg may be used prophylacticly against the risk of an early postoperative pressure spike. Delayed onset of OHT may arise due to neovascular glaucoma, suprachoroidal hemorrhage, phacoanaphylaxis (p. 284), epithelial down-growth syndrome (p. 289), aqueous misdirection (see above), or uveitis glaucoma hyphema (UGH) syndrome.

Post-vitreoretinal surgery

With intraocular gases, acute postoperative increased IOP is usually due to expansion or overfill of SF6, C3F8 or silicone oil. Determine treatment according to IOP and half-life of the gas, but usually short-term medical treatment is sufficient (e.g., acetazolamide SR 250 mg 2x/day). Otherwise, remove some of the gas.

With scleral buckles, secondary angle closure may occur from ciliary body swelling and choroidal detachment (possibly due to pressure on the vortex veins). This usually resolves spontaneously; treat medically in the interim.

With silicone oil, oil in the AC blocking the trabecular meshwork and overfill of oil causing secondary angle closure or iris bombé (and possibly other mechanisms) can present from days to months after surgery. Sometimes this resolves spontaneously; treat medically in the interim. Consider oil removal, tube-shunt placement, or cyclodestruction if OHT persists. Early removal of oil (<6 months) may decrease IOP. After this period, removal of oil makes little difference because of incorporation of oil into the TM by macrophages.

Vitrectomy may facilitate ghost cell glaucoma (p. 286) and increase the risk of rubeosis in proliferative diabetic retinopathy.

292 CHAPTER 10 Glaucoma

Pharmacology of IOP-lowering agents

Prostaglandin analogues

These analogues of PGF2A increase uveoscleral outflow (see Table 10.6).

•Ocular side effects: common: hyperemia, increased pigmentation of iris (and rarely lid skin), thickening and lengthening of lashes; rare: uveitis, CME.

•Contraindications may be associated with CME after complicated cataract surgery or if used during active uveitis.

B-Blockers

These agents reduce aqueous production probably by acting on B-receptors on the nonpigmented ciliary epithelium and vasoconstriction of the arterioles supplying ciliary processes.

•Ocular side effects: uncommon: allergic blepharoconjunctivitis, punctate keratitis.

•Contraindications: asthma/COPD (bronchospasm may occur even with

selective B1-agents), heart block, bradycardia or cardiac failure. Try to avoid B-blocker in nursing mothers as it is secreted in breast milk.

•Drug interactions: concurrent use of cardiac-directed Ca2+ antagonists such as verapamil may compound bradycardia, heart block, and hypotension.

Carbonic anhydrase inhibitors

These agents reduce aqueous production by inhibiting carbonic anhydrase isoenzyme II (and hence bicarbonate production) in the non-pigmented ciliary epithelium.

•Ocular side effects: common: burning, tearing, allergic blepharoconjunctivitis (up to 10%).

•Contraindications: sulfonamide sensitivity; renal failure, liver failure (systemic acetazolamide).

•Drug interactions: K+-losing diuretics (e.g., thiazide) may cause profound hypokalemia if used concurrently with acetazolamide. K+ supplementation is not usually required for acetazolamide used alone.

Sympathomimetics

The highly A2-selective brimonidine is well tolerated for chronic use, and apraclonidine (A1 + A2) is useful for short-term use (e.g., after laser iridotomy). Nonselective sympathomimetics such as adrenaline (epinephrine), dipivefrin, and the adrenergic neuron blocker guanethidine are now seldom used because of their frequent side effects.

•Ocular side effects: common: allergic blepharoconjunctivitis (up to 15% for brimonidine, 30% for apraclonidine); older agents: scarring, mydriasis, adrenochrome deposits; uncommon: CME in aphakia (possibly pseudophakia).

•Contraindications: heart block, bradycardia.

•Drug interactions: monoamine oxidase inhibitors.

Urinary retention

294 CHAPTER 10 Glaucoma

Miotics (parasympathomimetics)

Muscarinic receptor agonist leads to ciliary muscle contraction, which pulls on the scleral spur to open the trabecular meshwork. Pilocarpine is sometimes used as a first-line agent in narrow-angle glaucoma; it is sometimes still used in POAG.

•Ocular side effects: fluctuating myopia, miosis (constricted visual field, worse night vision).

•Contraindications: inflammatory or malignant glaucoma.

Combination agents

In the United States, two combination agents are available and have been demonstrated to have more effective IOP lowering than either of the individual components alone (but not more effective than each of the separate components alone).

Combination agents have benefits of increased convenience for patients as well as improved patient adherence and compliance (since compliance decreases with each additional drop a patient must use).

Mechanism of action, contraindications, and side-effect profiles are the same as for each individual agent.

•Dorzolamide/timolol: first fixed combination agent now available in a generic form.

•Brimonidine/timolol: most recently approved fixed combination agent.

LASER PROCEDURES FOR GLAUCOMA 295

Laser procedures for glaucoma

Nd-YAG peripheral iridotomy (PI)

Indications

•Treatment: angle closure with pupillary block—may be acute or subacute; chronic; primary or secondary.

•Prophylaxis: occludable narrow angles (including fellow eye in angle closure).

Method

•Consent: explain what the procedure does, why you are treating both eyes, and possible complications, including failure of treatment or need for retreatment, bleeding, inflammation, corneal burns, and visual effects (e.g., photopsias, monocular diplopia).

•Instill pilocarpine 2% (unfolds the iris) + apraclonidine 1% (prevents IOP spike and may reduce bleeding) + topical anesthetic (e.g., proparicaine).

•Set laser (varies according to model): commonly, bursts of one to two pulses of 3–6 mJ (an iris that is thick, velvety, and heavily pigmented may be more easily penetrated with pretreatment by argon laser:

~40 shots/50 μm/0.05 ms/500–700 mW). The beam should be angled (i.e., not perpendicular).

•Position contact lens (usually the Abraham lens; require coupling agent).

•Identify suitable iridotomy sites: superior (hidden by the normal lid position), peripheral, and ideally in an iris crypt (less energy required).

•Focus and fire laser: success is indicated by a forward gush of pigmentloaded aqueous. This usually takes 2–6 shots.

Post-procedure

•Topical steroid (e.g., dexamethasone 0.1% stat, then 4x/day for 1 week).

•Check IOP after 30–60 minutes.

•Complications: bleeding (stops with maintained pressure on lens that increases IOP), anterior inflammation (increase topical steroids), corneal burns (caution with a flatter AC), glare (avoid interpalpebral iris).

Laser trabeculoplasty

While argon laser trabeculoplasty (ALT, ~500 nm) has the longest track record and most data, newer laser energy modalities have been developed and offer theoretical advantages.

Selective laser trabeculoplasty (SLT), a 532 nm Q-switched, frequencydoubled Nd:YAG laser, uses less energy than ALT, with microscopic analysis demonstrating less tissue disruption. SLT has also been demonstrated to be repeatable.

Titanium:saphire laser trabeculoplasty (TLT) uses a longer wavelength (790 nm) and is believed to penetrate more deeply into the trabecular meshwork.