Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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Glaucoma in phacomatoses

Sturge–Weber syndrome

Sturge–Weber syndrome (encephalotrigeminal angiomatosis) is a congenital, sporadic phacomatosis (see Ch. 1).

Pathogenesis of glaucoma

Glaucoma develops in about 30% of patients ipsilateral to the facial haemangioma, especially if the lesion affects the upper eyelid. Elevation of IOP occurs within the first 2 years of life in 60% of glaucoma patients and may result in buphthalmos (Fig. 10.76A). In the remainder, glaucoma may develop at any time from infancy to adulthood. The pathogenesis is controversial and often obscure.

•Isolated trabeculodysgenesis may be instrumental in infants.

•Raised episcleral venous pressure (associated with an arteriovenous communication in an episcleral haemangioma (Fig. 10.76B) may be responsible in older patients.

Fig. 10.76 Glaucoma in Sturge–Weber syndrome. (A) Bilateral naevus flammeus and bilateral buphthalmos; (B) episcleral haemangioma

(Courtesy of R Bates – fig. A)

Treatment

1 Medical treatment with topical prostaglandin analogues may be successful.

2Goniotomy may be successful in eyes with angle anomalies.

3Combined trabeculotomy-trabeculectomy gives good results in early-onset cases. The rationale is that trabeculotomy addresses the barrier to aqueous outflow posed by a congenital angle anomaly, while trabeculectomy bypasses the episcleral veins. Surgery carries a high risk of choroidal effusion and suprachoroidal haemorrhage.

Neurofibromatosis type 1

Neurofibromatosis is a disorder that primarily affects cell growth of neural tissues. Inheritance is AD with irregular penetrance and variable

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expressivity (see Ch. 19). Glaucoma is relatively rare and, when present, is usually unilateral and congenital. About 50% of patients with glaucoma have an ipsilateral plexiform neurofibroma of the upper eyelid or exhibit facial hemiatrophy (Fig. 10.77A). One or more of the following may be the causative mechanism:

•Obstruction of aqueous outflow by neurofibromatous tissue in the angle.

•Developmental angle anomaly which may be associated with congenital ectropion uveae (Fig. 10.77B).

•Secondary angle-closure caused by forward displacement of the peripheral iris associated with neurofibromatous thickening of the ciliary body.

•Secondary synechial angle-closure caused by contraction of a fibrovascular membrane.

Fig. 10.77 Glaucoma in NF1. (A) Extensive neurofibromatosis and left facial hemiatrophy; (B) congenital ectropion uveae

(Courtesy of R Bates – fig. B)

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Glaucoma medications

Most glaucoma medications are administered topically. As a general rule, treatment is indicated whenever glaucomatous damage is deemed likely to occur. The decision on which medication to prescribe depends not only on the type of glaucoma, but also on the patient's medical history (e.g. presence of asthma or bradycardia). This requires a detailed knowledge of the potential side-effects. To improve compliance, patients should be fully informed not only about their disease but also the medications used, how to administer the drug, and what sideeffects to expect. The efficacy of therapy should be regularly evaluated and the regimen altered to improve efficacy, if appropriate, or to reduce adverse effects.

Beta-blockers

Pharmacology

Adrenergic neurones secrete noradrenaline at sympathetic postganglionic nerve endings. Adrenergic receptors are of the following four main types:

1Alpha-1 receptors are located in the arterioles, dilator pupillae and Müller muscle. Stimulation gives rise to hypertension, mydriasis and lid retraction.

2Alpha-2 inhibitory receptors located in the ciliary epithelium. Stimulation results in increase in the facility of aqueous outflow.

3Beta-1 receptors are located in the myocardium and give rise to tachycardia and increased cardiac output when stimulated.

4Beta-2 receptors are located in the bronchi and ciliary epithelium. Stimulation causes bronchodilatation and increased aqueous production.

Beta-blockers are drugs that antagonize the effects of catecholamines at beta receptors. Non-selective beta-blockers are equipotent at beta- 1 and beta-2 receptors, while cardioselective are more potent at beta-1 receptors. The advantage of the latter, at least in theory, is that the bronchoconstrictive effect of beta-2 blockade is minimized. Betaxolol is the only cardioselective agent currently available for the treatment of glaucoma.

Mode of action

Beta-blockers reduce IOP by decreasing aqueous secretion and are therefore useful in all types of glaucoma, irrespective of the state of the angle. The exact pharmacological basis for this is unclear. However, in approximately 10% of cases the pressure response decreases with time: tachyphylaxis. This may occur within a few days of starting treatment (‘short-term escape’) or within a few months (‘long-term drift’). As a general rule, little additional effect is obtained if a topical beta-blocker is used in a patient who is already on a systemic beta-blocker. During sleep, aqueous flow is normally less than half the daytime flow and beta-blockers have limited effect. When a beta-blocker is used in combination with brimonidine or a topical carbonic anhydrase inhibitor, an additional 15% reduction in IOP may be achieved. When combined with a prostaglandin analogue, the reduction is even greater (20%).

Side-effects

1Ocular side-effects include occasional allergy, corneal punctate epithelial erosions and reduced aqueous tear secretion.

2Systemic side-effects tend to occur during the first week of administration. Although uncommon they may be serious.

•Bradycardia and hypotension can result from beta-1 blockade. The patient's pulse must be palpated before prescribing a beta-blocker.

•Bronchospasm may be induced by beta-2 blockade and may be fatal in pre-existing asthma or severe chronic pulmonary obstruction.

•Miscellaneous side-effects include sleep disorders, hallucinations, confusion, depression, fatigue, headache, nausea, dizziness, decreased libido and possible reduction of plasma high-density lipoprotein level.

3Reduction of systemic absorption may be achieved by:

•Lacrimal occlusion following instillation, by closing the eyes and applying digital pressure over the lacrimal sac area for about 3 minutes. Apart from obstructing lacrimal drainage and reducing systemic absorption this also prolongs eye–drug contact and increases therapeutic efficacy.

•Merely closing the eyes for 3 minutes will reduce systemic absorption by about 50%.

4Contraindications to beta-blockers include asthma and obstructive airways disease, bradycardia, congestive cardiac failure, and second or third degree heart block. Beta-blockers should not be instilled at bedtime because they may cause a profound drop in blood pressure while the individual is asleep, thus reducing optic disc perfusion and potentially causing visual field deterioration; as noted above their Iop effect is also lower.

Preparations

1Timolol is available in three forms:

•0.25% and 0.5% used b.d.

•Timoptol LA 0.25% and 0.5% used once daily.

•Nyogel (timolol 0.1% gel) used once daily.

2Betaxolol (Betoptic) 0.5% b.d. has less hypotensive effect than timolol, but the effect on preservation of the visual field may be

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superior. Betaxolol may increase optic disc blood flow, probably because of a calcium-channel blocking effect on the microcirculation of the disc.

3Levobunolol (Betagan) 0.5% daily or b.d. is similar to timolol.

4Carteolol (Teoptic) 1%, 2% b.d. is similar to timolol and also exhibits intrinsic sympathomimetic activity. It has a more selective action on the eye than on the cardiopulmonary system and may therefore induce less bradycardia than timolol.

5Metipranolol 0.1%, 0.3% b.d. is similar to timolol but it may occasionally cause a granulomatous anterior uveitis. It is available only in preservative-free units.

Alpha-2 agonists

Alpha-2 agonists decrease IOP by both decreasing aqueous secretion and enhancing uveoscleral outflow. Because the drugs cross the blood-brain barrier they should not be used in children.

1Brimonidine (Alphagan) 0.2% b.d. is a highly selective alpha-2 agonist which also has a neuroprotective effect. Its efficacy in isolation is less than timolol but generally better than betaxolol. It exhibits an additive effect with beta-blockers. The major ocular side-effect is allergic conjunctivitis that may be delayed for up to 18 months after commencement of therapy (Fig. 10.78A). Acute granulomatous anterior uveitis has been reported. Systemic side-effects include xerostomia, drowsiness and fatigue.

2Apraclonidine (Iopidine) 1% is mainly used after laser surgery on the anterior segment to offset an acute rise in IOP. The 0.5% concentration may be used short-term, typically whilst a patient is awaiting glaucoma surgery. It is not suitable for long term use because of tachyphylaxis (loss of therapeutic effect over time) and a high incidence of local side-effects.

Fig. 10.78 Side-effects of topical medication. (A) Allergic conjunctivitis due to brimonidine; (B) lengthening and hyperpigmentation of lashes due to prostaglandin analogues; (C) darkening of irides due to prostaglandin analogues; (D) blepharoconjunctivitis due to topical carbonic anhydrase inhibitors

(Courtesy of J Salmon – fig. A; P Watson – fig. C)

Prostaglandin analogues

This group of agents have a sustained IOP-lowering effect which probably extends for several days in most patients.

Pharmacology

Prostanoid receptors are located on many ocular tissues, with involvement in functions such as regulation of intraocular pressure and blood flow.

1Latanoprost and travoprost are F2-alpha analogues that act as selective agonists of the FP prostanoid receptor; both of these agents enhance aqueous humour outflow through the uveoscleral route.

2Bimatoprost is a synthetic prostamide analogue structurally similar to prostaglandins that selectively mimics naturally occurring prostamide. It lowers IOP by promoting outflow through both uveoscleral and trabecular routes.

3Tafluprost is a synthetic analogue of the prostaglandin F2α, also acting through the FP receptor.

Preparations

1Latanoprost (Xalatan®) 0.005% used once daily at bedtime is superior to timolol although a proportion of patients show no response. Latanoprost produces an additive reduction of IOP of 14–28% when combined with timolol but not with pilocarpine.

2Travoprost (Travatan®) 0.004% once daily is similar to latanoprost except in black patients in whom it may be more effective. Conjunctival hyperaemia occurs in up to 50% of patients but tends to subside with time.

3Bimatoprost (Lumigan®) 0.03% once daily at bedtime is similar to latanoprost but may cause more conjunctival hyperaemia but fewer headaches and perhaps also less iris hyperpigmentation. A newer 0.01% preparation seems to leave a comparable IOPlowering effect but with less hyperaemia.

4Tafluprost (Saflutan™, Taflotan®) 0.0015% once daily at bedtime is a newer prostaglandin derivative, and the first available in preservative-free form.

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Side-effects

1Ocular

•Conjunctival hyperaemia and a foreign body sensation are common.

•Eyelash lengthening, thickening, hyperpigmentation and occasionally increase in number (Fig. 10.78B).

•Iris hyperpigmentation, which is irreversible, occurs in 11–23% of patients after 6 months (Fig. 10.78C). The highest incidence is in green-brown irides, less in yellow-brown irides and least in blue-grey/brown irides. Hyperpigmentation is caused by an increase in the number of pigmented granules within the superficial stroma rather than an increase in the number of melanocytes. Iris naevi and freckles are, however, not affected.

•Hyperpigmentation of periorbital skin is common but reversable.

•It is possible that these drugs increase the frequency of cystoid macular oedema after cataract surgery.

•Anterior uveitis is very rare and usually responsive to steroid therapy. The drug should therefore be used with caution in uveitic glaucoma.

•Increase in severity and recurrence of herpetic keratitis is also rare.

•Conjunctival hyperpigmentation has also been reported.

2Systemic side-effects include occasional headache, precipitation of migraine in susceptible individuals, skin rash and mild upper respiratory tract symptoms. These preparations should be avoided in pregnancy as animal studies have shown potential teratogenic effects.

Topical carbonic anhydrase inhibitors

The carbonic anhydrase inhibitors (CAIs) are chemically related to the sulphonamides. They lower IOP by inhibiting aqueous secretion.

1Dorzolamide (Trusopt) 2% is used t.i.d. as monotherapy or b.d. as adjunctive treatment, and is similar in efficacy to betaxolol but inferior to timolol. The main side-effects are allergic blepharoconjunctivitis (Fig. 10.78D) and a transient bitter taste. The drug should be used with caution in patients with corneal endothelial dysfunction as it may precipitate decompensation.

2Brinzolamide (Azopt) 1% b.d. or t.i.d. is similar to dorzolamide, but with a lower incidence of stinging and local allergy.

Miotics

Pharmacology

Miotics are parasympathomimetic drugs that act by stimulating muscarinic receptors in the sphincter pupillae and ciliary body.

1In POAG miotics reduce IOP by contraction of the ciliary muscle, which increases the facility of aqueous outflow through the trabecular meshwork.

2In PACG contraction of the sphincter pupillae and the resultant miosis pulls the peripheral iris away from the trabeculum, thus opening the angle. It is often necessary to reduce IOP with systemic medication before miotics can take effect.

Ocular side-effects include miosis, brow ache, myopic shift and exacerbation of symptoms of cataract. Visual field defects appear denser and larger.

Preparations

1Pilocarpine is equal in efficacy to beta-blockers and is available in the following forms:

•Pilocarpine drops 0.5%, 1%, 2%, or 4% is used q.i.d. as monotherapy. When used in combination with a beta-blocker, b.d. administration is adequate.

•Pilocarpine gel (Pilogel®) 4% consists of pilocarpine adsorbed on to a plastic gel, instilled once daily at bedtime so that the induced myopia and miosis last only during sleep. The main disadvantage is the development of a diffuse superficial corneal haze in 20% of users, although this rarely affects visual acuity.

2Carbachol 3% t.i.d. is an effective alternative to pilocarpine in resistant or intolerant cases.

Combined preparations

Combined preparations with similar ocular hypotensive effects to the sum of the individual components improve convenience and patient compliance. They are also more cost effective. Examples include:

1 Cosopt (timolol + dorzolamide) b.d.

2 Xalacom (timolol + latanoprost) once daily.

3 TimPilo (timolol + pilocarpine) b.d.

4 Combigan (timolol + brimonidine) b.d.

5 DuoTrav (timolol + travoprost) once daily.

6 Ganfort) (timolol + bimatoprost) once daily.

7 Azarga (timolol + brinzolamide) b.d.

Systemic carbonic acid inhibitors

Preparations

1Acetazolamide is available in the following forms:

•Tablets 250 mg. The dose is 250–1000 mg daily in divided doses with onset of action within 1 hour, a peak at 4 hours and duration up to 12 hours.

•Sustained-release capsules 250 mg used 250–500 mg daily with duration of up to 24 hours.

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hours. This is the only CAI preparation available for injection and is useful in acute angle-closure glaucoma.

2Dichlorphenamide tablets 50 mg. The dose is 50–100 mg b.d. or t.i.d. with onset of action within 1 hour, peak at 3 hours and duration up to 12 hours.

3Methazolamide tablets 50 mg. The dose is 50–100 mg b.d. or t.i.d. with onset of action within 3 hours, peak at 6 hours and duration of 10–18 hours. This is a useful alternative to acetazolamide with a longer duration of action but is currently not available in the UK.

Systemic side-effects

Systemically administered CAIs may be useful as short-term treatment, particularly in patients with acute glaucoma. Because of their systemic side-effects long-term use is reserved for patients at high risk of visual loss. The patient should always be warned of potential sideeffects as this decreases anxiety and improves compliance.

1Paraesthesia characterized by tingling of the fingers, toes, hands or feet, and occasionally at the mucocutaneous junctions, is a universal finding and usually innocuous. Compliance is suspect if the patient denies this symptom.

2Malaise complex is characterized by a combination of malaise, fatigue, depression, weight loss and decreased libido. A supplemental 2-week course of sodium acetate may be helpful.

3Gastrointestinal complex is characterized by gastric irritation, abdominal cramps, diarrhoea and nausea. This can occur independently of the malaise syndrome and is unrelated to any specific changes in blood chemistry.

4Renal stone formation is uncommon.

5 Stevens–Johnson syndrome may rarely occur since CAIs are sulphonamide derivatives.

6Blood dyscrasias are extremely rare and may be of two types:

•Dose-related bone marrow suppression which usually recovers when treatment is stopped.

•Idiosyncratic aplastic anaemia is not dose-related and has a mortality of 50%.

7Hypokalaemia may occur with long-term treatment and blood potassium levels should be monitored.

Osmotic agents

Physiological principles

Osmotic pressure is dependent on the number rather than on the size of solute particles in a solution. Lower molecular weight solutes therefore exert a greater osmotic effect per gram. Osmotic agents remain intravascular, thus increasing blood osmolality. They lower IOP by creating an osmotic gradient between blood and vitreous so that water is ‘drawn out’ from the vitreous. The higher the gradient, the greater the reduction in IOP. To be effective in the eye, an osmotic agent must therefore be unable to penetrate the blood-aqueous barrier. If penetration occurs, an osmotic equilibrium is set up and any further effect is lost. Osmotic agents are therefore of limited value in the treatment of inflammatory glaucomas in which the integrity of the blood-aqueous barrier is compromised.

Clinical uses

When a temporary drop in IOP is required that cannot be achieved by other means.

•In acute angle-closure glaucoma.

•Prior to intraocular surgery when the IOP is very high as may occur from dislocation of the lens into the anterior chamber.

•These preparations should be given fairly rapidly and the patient should not subsequently be given fluids to quench thirst until a useful effect has been exerted.

Side-effects

1Cardiovascular overload may occur as a result of increased extracellular volume. Osmotic agents should therefore be used with great caution in patients with cardiac or renal disease.

2Urinary retention may occur in elderly men following intravenous administration. Catheterization may be necessary in those with prostatism.

3Miscellaneous side-effects include headache, backache, nausea and confusion.

Preparations

1Mannitol is the most widely used intravenous osmotic agent. The dose is 1 g/kg body weight or 5 mL/kg body weight (20% solution in water) over 30–60 minutes. Peak of action is achieved within 30 minutes, with duration up to 6 hours.

2Glycerol is an oral agent with a sweet and sickly taste. Pure lemon (not orange) juice often needs to be added to avoid nausea. The dose is 1 g/kg body weight or 2 mL/kg body weight (50% solution). Peak action is within 1 hour, with duration up to 3 hours. Although glycerol is metabolized to glucose, it may be given to well-controlled diabetics.

3Isosorbide is an oral agent with a minty taste. Metabolically inert, it may be given to diabetics without insulin cover. The dose is the same as for glycerol.

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Laser therapy

Argon laser trabeculoplasty

Overview

Argon laser trabeculoplasty (ALT) involves the application of discrete laser burns to the trabecular meshwork. This enhances aqueous outflow and lowers IOP. ALT is performed in open-angle glaucomas, usually as an adjunct to medical therapy. It is believed that the procedure causes increased outflow facility by the following mechanisms: (a) mechanical tightening of the trabecular meshwork to open the adjacent, untreated trabecular spaces, and/or (b) inducing cell division and migration of macrophages to clear the trabecular meshwork of debris. ALT is ineffective in paediatric glaucoma and in most secondary glaucomas, with the exception of pigmentary and pseudoexfoliation.

Technique

a A drop of apraclonidine 1% is instilled to avert an early post-laser IOP rise.

bTwo drops of a topical anaesthetic are instilled.

cA goniolens is inserted with the mirror at the 12 o'clock position to visualize the inferior angle (usually the easiest part to see).

dThe scleral spur, Schwalbe line (which may be pigmented) and the three-dimensional ground-glass appearance of the trabecular meshwork are identified.

eThe aiming beam is focused at the junction of the pigmented and non-pigmented trabecular meshwork ensuring that the spot is round and has a clear edge (Fig. 10.79A). An oval spot with an indistinct outline (Fig. 10.79B) means that the aiming beam is not perpendicular to the trabecular surface.

fInitial laser settings are commonly: 50 µm spot size, 0.1 sec and duration and 700 mW power.

gThe laser is fired; the ideal reaction is a transient blanching (Fig. 10.80A) or appearance of a minute gas bubble (Fig. 10.80B) at the point of incidence. A large gas bubble (Fig. 10.80C) is excessive.

hIf the reaction is inadequate, the power is increased by 200 mW. In a heavily pigmented meshwork, a power setting of 400 mW may suffice, whereas a non-pigmented meshwork may require up to 1200 mW (the average is about 900 mw).

iTwenty-five burns are applied at regularly spaced intervals from one end of the mirror to the other.

jThe goniolens is rotated clockwise by 90° and a further 25 burns applied making a total of 50 over 180° of the angle. It is important to be familiar with the rotational pattern of the mirror so that adjacent quadrants are treated systematically. With practice it is possible to perform ALT by continuously rotating the goniolens and applying each burn through the centre of the mirror. Some ophthalmologists initially treat 180° and later treat the other 180° if the response is unsatisfactory. Others, however, treat the entire circumference with 100 burns at the initial sitting.

kApraclonidine 1% is instilled.

lTopical fluorometholone or prednisolone 0.5% q.i.d. daily for a week is prescribed; glaucoma medical therapy is continued.

Fig. 10.79 Laser trabeculoplasty. (A) Correct focus of aiming beam; (B) incorrect focus

Fig. 10.80 Laser trabeculoplasty. (A) Blanching of trabecular meshwork – appropriate; (B) small bubble – also appropriate; (C) large bubble – excessive; (D) peripheral anterior synechiae due to poor technique

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Follow-up

Four to 6 weeks should be allowed for the treatment to take effect. If the IOP is reduced significantly by 6 weeks, gradual withdrawal of medication may be attempted, although total withdrawal is seldom possible. The main aim of ALT is to obtain a safe IOP; the reduction of medication is usually a secondary consideration. If IOP remains high and only 180° has been treated, the remaining 180° is treated. Following 360° ALT, re-treatment is less likely to be beneficial and filtration surgery merits consideration.

Complications

1Peripheral anterior synechiae (Fig. 10.80D) may develop if the burns are applied too posteriorly or if the energy level is high. In the majority of cases this does not compromise aqueous outflow.

2Small haemorrhages may develop if the blood vessels on the peripheral iris or ciliary body are inadvertently treated. Such bleeding is easily stopped by applying pressure on the globe with the goniolens.

3Acute elevation of IOP may occur, especially if prophylactic apraclonidine or brimonidine is not used. The IOP should be monitored carefully in the subsequent weeks in patients with severe glaucomatous damage.

4Anterior uveitis is fairly common but usually mild, transient and innocuous.

5Adverse effect on subsequent filtration surgery. The incidence of encapsulated blebs following filtration surgery may be higher in eyes previously treated by ALT.

Results

1In POAG the initial success rate is 75–85%. The average reduction in IOP is about 30% – eyes with initially high IOPs therefore manifest a greater reduction. Up to 50% of eyes are still controlled after 5 years and about 33% after 10 years. Failure occurs most frequently in the first year; therefore if the IOP is still controlled at 1 year, the probability of control after 5 years is 65% and after 10 years, 40%. If ALT is used as primary treatment, 50% of cases require additional medical therapy within 2 years. Following initially successful ALT, re-treatment carries a low success rate (30% after 1 year and only 15% after 2 years). In general, the results are worse in patients under the age of 50 years. Black patients respond as well as whites initially, but tend to have a more rapid loss of effect.

2 In NPG 50–70% of patients have a good response, but the absolute reduction in IOP is less than in POAG.

3In pigmentary glaucoma results are generally good, although less so in older patients.

4In pseudoexfoliation glaucoma initial results are excellent, although failure may occur earlier than in POAG and subsequent rise may be rapid.

Selective laser trabeculoplasty

Selective laser trabeculoplasty (SLT) is a relatively new procedure which uses a 532 nm frequency-doubled, Q-switched Nd:YAG laser, which selectively targets melanin pigment in the trabecular meshwork cells, leaving non-pigmented structures unscathed. Targeting is easier than with ALT, which may lead to more consistent results being achieved. It may be safer than ALT as there is no thermal tissue damage and it is thought that treatment can therefore be repeated. Initial results show that it is probably as effective as ALT.

Nd:YAG laser iridotomy

Indications

•PACS, PAC and PACG.

•Secondary angle-closure with pupillary block.

Technique

aA drop of apraclonidine 1% or brimonidine 0.2% is instilled 30–60 minutes prior to the procedure.

b The pupil should be miosed with topical pilocarpine, although this may not be possible in acute glaucoma.

cA topical anaesthetic is instilled.

dA special contact lens such as the Abraham iridotomy lens (Fig. 10.81A) is inserted.

eA site is selected, preferably in the superior iris, so that it is covered by the eyelid thus minimizing the risk of monocular diplopia or glare (highest risk if an iridotomy is half-covered by the lid margin). Radially, the iridotomy should be located within the outer third in order to minimize the risk of damage to the crystalline lens. Targeting an iris crypt is beneficial but not essential.

fLaser settings and effective power vary between machines. Most iridotomies are made with settings of 4–5 millijoules (mJ). For a thin blue iris the required energy level is 1–4 mJ per shot. Thick, velvety smooth, brown irides may necessitate higher energy levels.

gThe beam is focused precisely and the laser fired. Successful penetration is characterized by a gush of pigment debris. Approximately 10 shots are generally required to produce an adequate iridotomy (Fig. 10.81B) although with an iris crypt this can be reduced to two or three.

h A second drop of apraclonidine 1% is instilled; oral acetazolamide may also be given if necessary.

iA strong topical steroid (e.g. dexamethasone) is prescribed every 10 minutes for 30 minutes and thereafter four times daily for 1 week.

jThe IOP should be checked 1–2 hours after the procedure to exclude an early spike. Routine review is usually at 1 or 2 weeks, with subsequent monitoring according to individual circumstances. Patients with marked glaucomatous damage may require extended ocular hypotensive cover and earlier review.

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Fig. 10.81 Nd:YAGiridotomy. (A) Abrahamlens; (B) appropriate size opening; (C) too small; (D) not covered by the eyelid and perhaps not sufficiently peripheral

Technical problems

1Initial failure

•Increasing the energy level may be sufficient.

•Re-treat the same site after allowing a few minutes for pigment and debris to clear, or move to a different site.

•Over-treatment should be avoided due to the risk of substantial postoperative inflammation and pressure spikes; further treatment can be applied after a few days.

•In thick brown irides, relatively gentle pre-treatment with argon laser can be beneficial: 10 shots of 0.1 s duration, 200 µm spot size and 200 mW are approximately effective settings.

2Opening too small (Fig. 10.81C). The optimal iridotomy diameter is 150–200 µm. It is sometimes easier to create an additional opening at a different site rather than to try to enlarge the opening.

Complications

1Bleeding occurs in about 50% of cases. It is usually slight and stops after several seconds. Persistent bleeding can be terminated by pressing the contact lens against the cornea.

2IOP elevation within one hour of treatment is common. It is mild and usually transient (see above).

3Iritis is common and usually mild. Severe iritis, which may result in the formation of posterior synechiae, is invariably caused by over-treatment and inadequate post-laser steroid therapy. It is more likely in darker irides, including that due to prostaglandin derivatives.

4Corneal burns may occur if a contact lens is not used or if the anterior chamber is shallow; they usually heal very rapidly without problems.

5Lens opacities which are localized and non-progressive occasionally develop at the treatment site; cataract formation may be accelerated by iridotomy.

6Glare and diplopia may rarely occur if the iridotomy is not sited under the upper eyelid (Fig. 10.81D), particularly if at the eyelid margin.

Diode laser cycloablation

Diode laser ablation (cyclodiode) lowers IOP by destroying part of the secretory ciliary epithelium, thereby reducing aqueous secretion. In the past it was used mainly in uncontrolled end-stage secondary glaucoma with minimal visual potential, mainly to control pain. However, it is now apparent that it can safely be used in eyes with good vision which may be retained provided control of IOP is adequate. More than one treatment session is commonly required for adequate pressure control.

1Technique

aA sub-Tenon or peribulbar anaesthetic is administered.

b Laser settings are 1.5–2 s and 1500–2000 mW; the spot size is not adjustable.

cThe power is adjusted over sequential shots until a ‘popping’ sound is heard and then reduced to just below that level.

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dApproximately 12–24 burns are placed posteriorly to the limbus over 360°, avoiding the neurovascular bundles at 3 and 9 o'clock (Fig. 10.82).

eA lower-intensity regimen can be used for eyes with good vision, in order to reduce the risk of over-treatment; more treatment sessions are likely to be required using this approach.

fA strong topical steroid is prescribed hourly on the day of treatment and then 2-hourly for 2 days and q.i.d. for at least 2 weeks. A topical antibiotic and a cycloplegic (cyclopentolate 1% b.d.) are used for 3 days.

gPre-laser glaucoma treatment may be continued, or reduced slightly.

hOral non-steroidal anti-inflammatory agents may be prescribed for 2 days.

iReview is generally after 3 or 4 days, because of the risk of significant reactive inflammation.

2Complications. Mild pain and anterior segment inflammation are common. A temporary IOP rise is not uncommon during the first few weeks. Serious complications are rare and include chronic hypotony, phthisis bulbi, suprachoroidal haemorrhage, corneal decompensation and retinal detachment.

3Results depend on the type of glaucoma; frequently the procedure has to be repeated. Pain relief is generally good, but does not appear to be solely related to pressure control.

Fig. 10.82 (A) Diode laser cycloablation; (B) close up of the probe

(Courtesy of J Salmon – fig. A; Krachmer, Mannis and Holland, from Cornea, Mosby 2005 – fig. B)

Laser iridoplasty

Laser iridoplasty is performed to widen the anterior chamber angle by causing contraction of the peripheral iris away from the angle recess. It can be used to attempt to break an episode of acute angle-closure, but is more commonly applied on an elective basis (see ‘Primary angle-closure).

aA topical anaesthetic is instilled.

bOne drop each of 1% pilocarpine and 1% apraclonidine is instilled.

cVia an iridotomy lens, 1–2 burns per clock hour are applied to the periphery, 500 µm size, 100–200 mW, 0.5 s duration, aiming for slight visible iris contraction; overtreatment should be avoided as prolonged IOP spikes can occur.

d Post-procedure 1% apraclonidine is given (consider oral acetazolamide if significant glaucomatous optic neuropathy is present).

eTopical prednisolone 1% or dexamethasone 0.1% hourly for the first day then four times daily.

fReview 1–2 hours post-laser, then after 1 week and subsequently depending on progress and glaucomatous damage – patients with significant glaucomatous neuropathy may need regular review for the first few weeks to detect and treat an IOP spike.

gAltered accommodation is fairly common but almost always transient.

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