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

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Fig. 10.37 Severe damage. (A) Marked cupping; (B) dense arcuate scotoma/nasal step connecting with the blind spot

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Fig. 10.38 Very severe damage; (A) Gross cupping; (B) ring scotoma

Global indices should always be taken into account (Fig. 10.39); on average annual deterioration in mean total deviation of just over 1.0 dB can be expected in treated patients.

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Fig. 10.39 Progression of visual field defects and deterioration of global indices over a period of 30 months

Management

The primary aim of treatment is to prevent functional impairment of vision within the patient's lifetime by slowing the rate of ganglion cell loss closer to that of the normal population (approximately 5000/year). Currently the only proven method of achieving this is the lowering of IOP.

Patient instruction

An explanation should be offered concerning the nature of the disease, and an explanatory booklet provided. The timing of medication use should be specified, and the patient educated in the technique of eye drop instillation. At follow-up visits the patient's proficiency at instilling drops should be checked. In order to maximize drug contact time with the anterior segment and to minimize systemic absorption the patient should be instructed either to perform lacrimal sac occlusion (by applying fingertip pressure at the medial canthus) or to close the eyes for about 3 minutes after instillation. Common or severe potential adverse effects should be explained at the commencement of treatment and their occurrence enquired about at follow-up visits.

Treatment goals

1Target pressure. It is assumed that the pre-treatment level of IOP has damaged the optic nerve and will continue to do so. An IOP level is identified below which further damage is considered unlikely (‘target pressure’). This is identified taking into account the severity of existing damage, the level of IOP, CCT, the rapidity with which damage occurred if known, as well as the age and general health of the patient. Therapy should maintain the IOP at or below the target level. If not achievable by conservative modalities, a decision is made regarding whether to proceed with surgery or to continue monitoring with an above-target IOP.

2Proportional reduction. An alternative strategy is to aim for a reduction in IOP by a certain percentage – often 30% – and then monitor, aiming for a further reduction if progression occurs. There may be a smaller margin for error with this approach if advanced damage is present.

3Monitoring of the optic nerve and visual fields is performed. In the event of further damage the target IOP is reset at a lower level. Although there is no ‘safe’ level, progression is uncommon if the IOP is <16 mmHg. It appears that each 1 mmHg reduction in IOP leads to a 10% reduction in the rate of nerve fibre loss. As the disease progresses the degree of redundancy or ‘reserve capacity’ within the visual system diminishes and the loss of each remaining ganglion cell has a greater proportional impact on visual function. Lower target pressures therefore tend to be set in patients with advanced disease.

Medical therapy

1Commencing medical therapy

•Any chosen drug should be used in its lowest concentration, instilled as infrequently as possible consistent with the desired therapeutic effect.

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•Ideally the drug with the fewest potential side-effects should be used.

•Initial treatment is usually with one drug, usually a prostaglandin analogue or beta-blocker; a range of considerations is taken into account when deciding which to select.

2Review

•The interval to review after starting medication is set according to the individual patient, but is usually 4–8 weeks.

•Response to the drug is assessed against the target IOP.

•If the response is satisfactory subsequent assessment is generally set for a further 3–6 months.

•If there has been little or no response the initial drug is withdrawn and another substituted.

•If there has been an apparently incomplete response another drug may be added or a fixed combination substituted.

•When two separate drugs are used the patient should be instructed to wait five minutes before instilling the second drug to prevent washout of the first.

•Sometimes it may be worthwhile allowing a further month or two of treatment before altering a regimen, as response may improve over time.

•Poor compliance or inadequate drop instillation technique should be considered as a cause of unsatisfactory response.

•When drops are administered in the morning, it is good practice always to enquire about whether today's dose has been used prior to the examination.

3Perimetry. If IOP control is good and glaucomatous damage mild or moderate with no substantial threat to central vision, annual perimetry is generally sufficient.

4Gonioscopy should be performed annually in most patients because the anterior chamber angle tends to narrow with age.

5Optic disc examination should be performed at appropriate intervals. Serial imaging may also provide useful additional information.

6Causes of treatment failure

•Inappropriate target pressure. If the IOP is maintained in the upper part of the statistically normal range, progressive field loss is relatively common.

•Poor compliance with therapy occurs in at least 25% of patients.

•Wide fluctuations in IOP frequently occur in patients treated medically, and may be associated with progression.

•Patients may deteriorate despite apparently good IOP control. Causes include occult compliance failure, undetected diurnal variation, and possibly impaired optic nerve perfusion. The possibility of an alternative pathology, particularly a compressive lesion, should always be considered.

Laser trabeculoplasty

In argon laser trabeculoplasty (ALT) or selective laser trabeculoplasty (SLT) argon or Nd:YAG laser is applied to the trabeculum to enhance aqueous outflow and lower IOP. The therapeutic effect is highly variable, and when effective tends to be transient, although typically lasting for months to years. The following are the main indications:

1Intolerance of topical medication including allergy.

2Failure of medical therapy, as a less aggressive treatment measure than surgery.

3Avoidance of polypharmacy, usually with more than two preparations. In this situation laser therapy may be considered as a substitute for an additional drug.

4Avoidance of surgery, for example in:

•Patients in whom laser may defer the need for surgery beyond life expectancy.

•Patients in whom filtration surgery carries a poorer prognosis.

5Primary therapy in accordance with patient preference, or in patients who are unable or unwilling to comply with medical therapy. Since IOP reduction with laser is seldom greater than 30%, an IOP higher than 28 mmHg is unlikely to be adequately controlled by laser alone.

Surgery

Trabeculectomy is the surgical procedure most commonly performed for glaucoma, although non-penetrating surgery is gaining in popularity. If significant lens opacity is present, phacoemulsification alone may be associated with a fall in IOP; alternatively it can be combined with a filtration procedure (phacotrabeculectomy). Progressive damage is thought to be less likely after surgery than with medical therapy, probably because the resultant IOP is often significantly lower and less likely to fluctuate, and because compliance is no longer a factor. The following are the main indications:

1 Failed medical therapy when laser trabeculoplasty is likely to be inadequate or inappropriate.

2Intolerance of or allergy to medical therapy when trabeculoplasty is inappropriate.

3 Avoidance of polypharmacy, though the option of using three or more medications should be discussed with the patient.

4Progressive deterioration despite seemingly adequate IOP control.

5Primary therapy. Advanced disease requiring a very low target pressure may achieve a superior long-term outcome from early surgery, though the risks must be carefully assessed on an individual basis.

6Patient preference. Occasionally patients express a strong desire to be free of the commitment to chronic medical treatment.

Prognosis

The great majority of patients diagnosed with POAG will not become blind in their lifetime, but the rate of glaucoma progression varies considerably.

•Untreated, the mean time for progression to blindness has been estimated at 20 years.

•The average period from diagnosis to death is around 15 years.

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•Older 20 year follow-up data for functional blindness in one eye showed that this occurred in 25% of patients, with blindness in both eyes in 10%, but recent figures are considerably lower, with about 15% of patients' worse eyes becoming blind; ongoing advances in management are likely to lead this to fall further.

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Normal-pressure glaucoma

Definition

Normal-pressure glaucoma (NPG), also referred to as normalor low-tension glaucoma, is a variant of POAG. It is characterized by:

•IOP consistently equal to or less than 21 mmHg.

•Signs of optic nerve damage in a characteristic glaucomatous pattern.

•An open anterior chamber angle.

•Visual field loss as damage progresses, consistent in pattern with the nerve appearance.

•No features of secondary glaucoma or a non-glaucomatous cause for the neuropathy.

The distinction between NPG and POAG is based on an epidemiologically-derived range of normal IOP. It is essentially an arbitrary division and may not have significant clinical value, though there is the possibility that a spectrum exists in which, towards the NPG end, IOPindependent factors are of increasing relative importance.

Pathogenesis

Any aetiological factors distinct from those in POAG have not been conclusively determined although various mechanisms have been postulated including anomalies of local and systemic vascular function, structural optic nerve anomalies and autoimmune disease. With the introduction of widespread central corneal thickness (CCT) assessment, NPG in some patients has been explained by very low CCT, and overall CCT in patients with NPG is lower than in POAG. A small proportion of NPG patients have been found to have marked nocturnal IOP spikes, sometimes only detected on testing in the supine position.

Risk factors

1 Age. Patients tend to be older than those with POAG, though this may be due to delayed diagnosis.

2Gender. Some studies have found a higher prevalence in females.

3Race. NPG occurs more frequently in Japan than in Europe or North America.

4Family history. The prevalence of POAG is greater in families of patients with NPG than in the normal population. Mutations in the OPTN gene coding for optineurin have been identified in some patients with NPG as well as patients with POAG.

5CCT is lower in patients with NPG than POAG.

6Abnormal vasoregulation, particularly migraine and Raynaud phenomenon, have been found more commonly in NPG than POAG by some investigators; others have found abnormalities just as commonly in POAG.

7 Systemic hypotension including nocturnal blood pressure dips of >20%, particularly in those on oral hypotensive medication.

8Obstructive sleep apnoea syndrome may be associated, perhaps via an effect on ocular perfusion.

9Autoantibody levels have been found to be higher in NPG patients than the general population by some investigators.

Differential diagnosis

1POAG presenting with apparently normal IOP because of wide diurnal fluctuation. Plotting a diurnal IOP curve over an 8-hour period (phasing) during office hours may detect daytime elevation, but detection of nocturnal IOP spikes requires substantial resource commitment.

2Spontaneously resolved pigmentary glaucoma. The typical examination features of pigmentary glaucoma tend to become less evident with increasing age.

3Previous episodes of raised IOP may have occurred as a result of ocular trauma, uveitis or local or systemic steroid therapy.

4Masking by systemic treatment such as an oral beta-blocker, commenced after glaucomatous damage has already been sustained.

5 Progressive retinal nerve fibre defects not due to glaucoma such as may occur in myopic degeneration and optic disc drusen.

6Congenital disc anomalies simulating glaucomatous cupping such as disc pits and colobomas.

7Neurological lesions causing optic nerve or chiasmal compression can produce visual field defects which may be misinterpreted as glaucomatous, and neuroimaging should be performed if there is any suspicion; some practitioners routinely perform a cranial MRI in all cases of NPG.

8Previous anterior ischaemic optic neuropathy (AION) may give rise to a disc appearance and visual field defect consistent with glaucoma. Non-arteritic AION often occurs in a ‘crowded’ disc, and the fellow eye should be examined for this.

9Previous acute optic nerve insult, such as hypovolaemic or septicaemic shock, or head injury.

Diagnosis

History and examination are essentially the same as for POAG but specific points warrant attention:

1History

•Migraine and Raynaud phenomenon.

•Episodes of shock.

•Head injury.

•Headache and other neurological symptoms (intracranial lesion).

•Medication such as systemic steroids and hypotensives including beta-

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blockers.

2IOP is usually in the high teens, but may rarely be in the low teens. In asymmetrical disease the more damaged disc typically corresponds to the eye with the higher IOP.

3Optic nerve head

•Although the optic nerve head may be larger in NPG than in POAG glaucomatous cupping is similar and acquired optic disc pits are possibly more common.

•Peripapillary atrophic changes may be more prevalent.

•Splinter haemorrhages (see Fig. 10.20F) may be more frequent than in POAG.

4Visual field defects are essentially the same as in POAG although it has been suggested that they tend to be closer to fixation, deeper, steeper and more localized. In probably more than half of patients, field changes are non-progressive over a period of 5 years or more without treatment. However, possibly because of delayed diagnosis, patients tend to present with more advanced damage than those with POAG.

5Other investigations are as for POAG although in selected patients the following can be considered.

•Assessment of systemic vascular risk factors.

•24-hour ambulatory BP monitoring to exclude nocturnal systemic hypotension.

•Blood tests for other causes of non-glaucomatous optic neuropathy such as vitamin B12, red cell folate, full blood count, erythrocyte sedimentation rate/C-reactive protein, treponemal serology including Lyme disease, and serum ACE level, plasma protein electrophoresis and autoantibody screen.

•Cranial MR.

•Nail-fold capillaroscopy with cold provocation to detect blood flow abnormality. If present, calcium channel blockers may be more likely to be beneficial.

Treatment

Further lowering of IOP is effective in reducing progression in some patients. However, as many untreated patients will not deteriorate, in most cases progression should be demonstrated before commencing treatment. Exceptions to this general principle include advanced damage, particularly if threatening central vision, and young age. Regular assessment including perimetry should be performed at 4–6 monthly intervals. With treatment that reduces IOP by 30% from baseline, 80% of patients are stable and 20% show progression.

1Medical treatment in progressive cases may include betaxolol because of its beneficial effects on optic nerve blood flow in addition to its IOP-lowering properties. Prostaglandin derivatives tend to have a greater ocular hypotensive effect, which may be an over-riding consideration. It should be noted that topical beta-blockers can have a dramatic effect on BP in a minority of patients, and may contribute to nocturnal dips.

2Laser trabeculoplasty can be effective.

3Surgery should be considered if progression occurs despite IOP in the low teens.

4Control of systemic vascular disease such as diabetes, hypertension and hyperlipidaemia may be important, in order theoretically to optimize optic nerve perfusion.

5Systemic calcium-channel blockers have been advocated by some authorities to address vasospasm.

6Antihypotensive measures. If significant nocturnal dips in BP are detected, it may be necessary to reduce antihypertensive medication (especially if taken at bedtime).

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Primary angle-closure glaucoma

Introduction

Overview

The term ‘angle-closure’ refers to occlusion of the trabecular meshwork (TM) by the peripheral iris (iridotrabecular contact – ITC), obstructing aqueous outflow. Angle-closure can be primary, when it occurs in an anatomically predisposed eye, or secondary to another ocular condition. Primary angle-closure glaucoma may be responsible for up to half of all cases of glaucoma globally, with a particularly high prevalence in individuals of Far Eastern descent. It is typically associated with greater speed of progression and visual morbidity than POAG.

Classification

Recently classification has moved away from a symptom-based approach (acute, subacute and chronic), to reflect the stages in the natural history of the disease. This takes into account that the majority of patients are asymptomatic.

1Primary angle-closure suspect (PACS)

•Gonioscopy shows posterior meshwork ITC in three or more quadrants but no PAS.

•Many patients with less ITC have evidence of intermittent angle-closure, and a lower threshold for diagnosis such as two quadrants of ITC or even a very narrow angle approach of 20° may be justified (Fig. 10.40).

•Normal IOP, optic disc and visual field.

2Primary angle-closure (PAC)

•Gonioscopy shows three or more quadrants of ITC with raised IOP (Fig. 10.41) and/or PAS, or excessive pigment smudging on the TM.

•Normal optic disc and field.

3Primary angle-closure glaucoma (PACG)

•Gonioscopy shows ITC in three or more quadrants.

•Optic neuropathy.

Fig. 10.40 Primary angle-closure suspect. (A) Very narrow angle; (B) van Herick grade 3

(Courtesy of L MacKeen – fig. A)

Mechanism

The mechanisms involved in angle-closure can be categorized according to the anatomical level (anterior to posterior) at which causative forces act. In many patients more than one level is contributory.

1Pupillary block

•Failure of aqueous flow through the pupil (relative pupillary block – Fig. 10.42A), leads to a pressure differential between the anterior and posterior chambers, with resultant anterior bowing of the iris (Fig. 10.42B) and ITC (Fig. 10.42C).

•Iridotomy equalizes anterior and posterior chamber pressure, provided the TM remains sufficiently functional.

2Non-pupillary block relating to the iris

•Specific anatomical factors include plateau iris (anteriorly positioned ciliary processes), and a thicker or more anteriorlypositioned iris.

•An element of pupillary block is invariably present, but angle-closure is not fully relieved by iridotomy.

•The term ‘mixed mechanism’ may be used to describe glaucoma in which both significant pupillary block and non-pupillary block iris-induced mechanism coexist.

•Associated with a deeper anterior chamber than pure pupillary block.

•Plateau iris configuration is characterized by a flat central iris plane in association with normal central anterior chamber depth. The angle recess is very narrow, with a sharp iris angulation over anteriorly positioned and/or orientated ciliary processes (Fig. 10.43).

•Plateau iris syndrome describes the occurrence of angle-closure despite a patent iridotomy in a patient with morphological plateau iris.

3Lens-induced angle-closure

•Includes only those cases in which a sudden change in lens volume and/or position leads to an acute or subacute IOP rise.

•Usually rapid progression of lens intumescence (phacomorphic glaucoma) or anterior lens subluxation.

•The lens contributes to angle-closure in categories 1 and 2 and virtually all pupillary block can be said to have a

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phacomorphic element that increases with age as the lens enlarges.

4Retrolenticular causes

•Malignant glaucoma (‘ciliolenticular block’ – see below).

•Posterior segment causes of secondary angle-closure (see below).

5‘Combined mechanism’ describes the combination of angle-closure and open-angle elements, although it is generally not possible to determine whether sustained elevation of IOP following successful anatomical opening of an angle is due to TM changes secondary to prior iris apposition.

Fig. 10.42 Mechanismof angle-closure. (A) Relative pupillary block; (B) anterior iris bowing; (C) iridocorneal contact

Fig. 10.43 Ultrasound biomicroscopy in plateau iris configuration shows loss of the ciliary sulcus due to anterior position of the ciliary processes

(Courtesy of J Schuman, V Christopoulos, D Dhaliwal, M Kahook and R Noecker, from Lens and Glaucoma, in Rapid Diagnosis in

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Ophthalmology, Mosby 2008)

Risk factors

1Age

•The average age at presentation is about 60 years and the prevalence increases thereafter.

•Non-pupillary block forms of primary angle-closure tend to occur at a younger age.

2 Gender. Females are more commonly affected than males.

3Race. As discussed above.

4Family history. First degree relatives are at increased risk.

5Refraction. Eyes with ‘pure’ pupillary block are typically hypermetropic, although this is not as clear-cut with non-pupillary block.

6Axial length

•Short eyes tend to have shallow anterior chambers (Fig. 10.44).

•Eyes with nanophthalmos have a very short eye with a proportionally large lens and are at particular risk.

Fig. 10.44 Shallow anterior chamber

Diagnosis

Symptoms

•Most patients with angle-closure are asymptomatic, including a majority of those with intermittently or chronically elevated IOP.

•Some patients present acutely (congestive glaucoma) with haloes around lights due to corneal oedema, ocular pain and headache.

•Other patients may have intermittent milder symptoms of blurring (‘smoke-filled room’) unassociated with pain.

•Precipitating factors include watching television in a darkened room, reading, pharmacological mydriasis or miosis, acute emotional stress and rarely systemic medication: parasympathetic antagonists or sympathetic agonists (e.g. inhalers, motion sickness patches and cold remedies) and topiramate.

Signs

1Chronic presentation

•VA is normal unless damage is advanced.

•Anterior chamber is shallower in pupillary block than non-pupillary block.

•Optic nerve signs depend on severity of damage.

•IOP elevation may be only intermittent.

•Gonioscopic abnormalities are as described above.

•‘Creeping’ angle-closure is characterized by a gradual band-like anterior advance of the apparent insertion of the iris. It starts in the deepest part of the angle and spreads circumferentially.

•Episodic (intermittent) ITC is associated with the formation of discrete PAS, individual lesions having a pyramidal (‘sawtooth’) appearance.

2Acute (congestive) angle-closure

•VA usually 6/60-HM.

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