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

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Chapter 10 – Glaucoma

INTRODUCTION 312 Aqueous secretion 312 Aqueous outflow 312 Intraocular pressure 313 Overview of glaucoma  313

TONOMETRY 313 Goldmann tonometry 313 Other types of tonometry  315

GONIOSCOPY 316 Introduction 316 Indirect gonioscopy 316 Direct gonioscopy 318

Identification of angle structures  319

Grading of angle width 320 Pathological findings 323

EVALUATION OF THE OPTIC NERVE HEAD 323 Normal optic nerve head

 323

Changes in glaucoma 324

IMAGING IN GLAUCOMA 327 Stereo disc photography 327

Confocal scanning laser tomography  327

Scanning laser polarimetry 330 Optical coherence tomography 331 Anterior chamber depth measurement  331

PERIMETRY 331 Definitions 331

Types of perimetry 333 Sources of error 333 Humphrey Field Analyzer 334 Short-wave automated perimetry  338

Frequency-doubling contrast test  338

OCULAR HYPERTENSION 338 PRIMARY OPEN-ANGLE GLAUCOMA 340

Introduction 340

Screening 341

Diagnosis 341 Visual field defects  342 Management 343

NORMAL-PRESSURE GLAUCOMA 346 PRIMARY ANGLE-CLOSURE GLAUCOMA 348

Introduction  348 Diagnosis 350

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Treatment 351

CLASSIFICATION OF SECONDARY GLAUCOMA 353 Open-angle 353

Angle-closure  354

PSEUDOEXFOLIATION 355 Pseudoexfoliation syndrome  355

Pseudoexfoliation glaucoma  355

PIGMENT DISPERSION 357 Pigment dispersion syndrome  357

Pigmentary glaucoma 359

NEOVASCULAR GLAUCOMA 359 Introduction 359

Rubeosis iridis 360

Secondary open-angle glaucoma 361 Secondary angle-closure glaucoma  361

INFLAMMATORY GLAUCOMA 361 Introduction 361

Angle-closure glaucoma with pupillary block 362 Angle-closure glaucoma without pupillary block  362

Open-angle glaucoma 362 Treatment 363 Posner–Schlossman syndrome 364

LENS-RELATED GLAUCOMA 364 Phacolytic glaucoma 364 Phacomorphic glaucoma 366

Lens dislocation into the anterior chamber  367

Incarcerated lens in the pupil 367

TRAUMATIC GLAUCOMA 367 Hyphaema 367

Angle recession glaucoma  368

IRIDOCORNEAL ENDOTHELIAL SYNDROME 368 GLAUCOMA IN INTRAOCULAR TUMOURS 369 GLAUCOMA IN EPITHELIAL INGROWTH 371 GLAUCOMA IN IRIDOSCHISIS 371

PRIMARY CONGENITAL GLAUCOMA 372 Introduction 372

Diagnosis 374

Management 374 Differential diagnosis  376

IRIDOCORNEAL DYSGENESIS 376 Posterior embryotoxon 376 Axenfeld–Rieger syndrome

 377

Peters anomaly 378 Aniridia 378

GLAUCOMA IN PHACOMATOSES 382 Sturge–Weber syndrome

 382

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Neurofibromatosis type 1  382

GLAUCOMA MEDICATIONS 383 Beta-blockers 383

Alpha-2 agonists 384 Prostaglandin analogues 384 Topical carbonic anhydrase inhibitors  385

Miotics 385

Combined preparations 386 Systemic carbonic acid inhibitors 386 Osmotic agents 386

LASER THERAPY 387

Argon laser trabeculoplasty 387 Selective laser trabeculoplasty  388

Nd:YAG laser iridotomy 388 Diode laser cycloablation 390 Laser iridoplasty 390

TRABECULECTOMY 391

Technique 391

Shallow anterior chamber 391 Failure of filtration 394

Late bleb leakage 394

Bleb-associated bacterial infection and endophthalmitis  395

NON-PENETRATING SURGERY 396

ANTIMETABOLITES IN FILTRATION SURGERY 397

DRAINAGE SHUNTS 399

Introduction

Aqueous secretion

Aqueous humour is produced in two steps:

•Formation of a plasma filtrate within the stroma of the ciliary body.

•Formation of aqueous from this filtrate across the blood-aqueous barrier.

Two mechanisms are involved:

1Active secretion by the non-pigmented ciliary epithelium accounts for the vast majority, and involves a metabolic process that depends on several enzyme systems, especially the Na+/K+ ATPase pump which secretes sodium ions into the posterior chamber.

2Passive secretion by ultrafiltration and diffusion, which are dependent on the capillary hydrostatic pressure, oncotic pressure (colloid osmotic pressure exerted by proteins in blood plasma) and the level of IOP, is thought to play a minor role in the genesis of aqueous humour under normal conditions.

Aqueous outflow

Anatomy

1The trabecular meshwork (trabeculum) is a sieve-like structure at the angle of the anterior chamber, through which 90% of the aqueous humour leaves the eye (Fig. 10.1). It is made up of the following three portions (Fig. 10.2):

aThe uveal meshwork is the innermost portion and consists of cord-like endothelial cell-covered strands arising from the iris and ciliary body stroma, and extending from the root of the iris to Schwalbe line. The intertrabecular spaces are relatively large and offer little resistance to the passage of aqueous.

bThe corneoscleral meshwork forms the larger middle portion which extends from the scleral spur to Schwalbe line. The layers are sheet-like and composed of connective tissue strands also with overlying endothelial-type cells. The intertrabecular spaces are smaller than those of the uveal meshwork, conferring greater resistance to flow.

cThe juxtacanalicular (cribriform) meshwork is the outer part of the trabeculum, and links the corneoscleral meshwork with the endothelium of the inner wall of the Schlemm canal. This offers the major proportion of normal resistance to aqueous outflow, consisting of cells embedded in a dense extracellular matrix with narrow intercellular spaces.

2Schlemm canal is a circumferential channel in the perilimbal sclera, bridged by septa. The inner wall is lined by irregular spindleshaped endothelial cells containing infoldings (giant vacuoles) which are thought to convey aqueous via the formation of transcellular pores. The outer wall is lined by smooth flat cells and contains the openings of the collector channels which leave the canal at oblique angles and connect directly or indirectly with episcleral veins.

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Fig. 10.1 Scanning electron micrograph of the trabecular meshwork

Fig. 10.2 Anatomy of outflow channels. (A) Uveal meshwork; (B) corneoscleral meshwork; (C) Schwalbe line; (D) Schlemmcanal; (E) connector channels; (F) longitudinal muscle of the ciliary body; (G) scleral spur

Physiology

Aqueous flows from the posterior chamber via the pupil into the anterior chamber, from where it exits the eye by two different routes (Fig. 10.3):

1Trabecular (conventional) route accounts for approximately 90% of aqueous outflow. The aqueous flows through the trabeculum into the Schlemm canal and is then drained by the episcleral veins. This is a bulk flow pressure-sensitive route so that increasing the pressure head will increase outflow. Trabecular outflow can be increased by drugs (miotics, sympathomimetics), laser trabeculoplasty and filtration surgery.

2Uveoscleral (unconventional) route accounts for the remaining 10% in which aqueous passes across the face of the ciliary body into the suprachoroidal space and is drained by the venous circulation in the ciliary body, choroid and sclera. Uveoscleral outflow is decreased by miotics and increased by atropine, sympathomimetics and prostaglandin analogues. Some aqueous also drains via the iris.

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Fig. 10.3 Routes of aqueous outflow. (A) Trabecular; (B) uveoscleral; (C) iris

Intraocular pressure

The IOP is determined by the balance between the rate of aqueous secretion and aqueous outflow. The latter is in turn related to the resistance encountered in the outflow channels and to the level of episcleral venous pressure. The rate of aqueous outflow is proportional to the difference between the intraocular and episcleral venous pressure.

Concept of normal intraocular pressure

The distribution of IOP within the general population has a range of 11–21 mmHg. Although there is no absolute pathological point, 21 mmHg is considered the upper limit of normal and levels above this are viewed with suspicion. However, in some patients glaucomatous damage occurs with IOPs less than 21 mmHg (normal-tension or normal-pressure glaucoma) whilst others remain unscathed with IOPs up to

30 mmHg (ocular hypertension). Although the actual level of IOP is important in the development of glaucomatous damage, other factors are also significant.

Fluctuation

Normal IOP varies with the time of day, heartbeat, blood pressure level and respiration. The diurnal pattern varies, with a tendency to be higher in the morning and lower in the afternoon and evening. Normal eyes manifest a mean diurnal pressure variation of 5 mmHg; ocular hypertensive or glaucomatous eyes, however, exhibit a wider fluctuation. A single normal reading, particularly if taken during late afternoon, may therefore be misleading and it may be necessary to take several readings at different times of day (‘phasing’). In clinical practice phasing during the morning hours may be sufficient because 80% of patients peak between 8.00 a.m. and noon.

Overview of glaucoma

Definition

It is difficult to define glaucoma precisely, as it encompasses a diverse group of disorders. All forms of the disease have in common a potentially progressive and characteristic optic neuropathy which is associated with visual field loss as damage progresses, and in which intraocular pressure is usually a key modifying factor. On a molecular level, glaucoma of diverse aetiology is linked by the presence of endothelial leucocyte adhesion molecule-1 (ELAM-1), which indicates activation of a stress response in trabecular meshwork cells.

Epidemiology

Glaucoma affects up to 2% of those over the age of 40 years globally, and up to 10% over the age of 80; 50% may be undiagnosed. In a population of European or African ethnic origin, primary open-angle glaucoma (POAG) is the most common form. On a worldwide basis, primary angle-closure constitutes up to half of cases, with particularly high prevalence in individuals of Far Eastern descent.

Classification

Glaucoma may be congenital (developmental) or acquired. Sub-classification into open-angle and angle-closure types is based on the mechanism by which aqueous outflow is impaired with respect to the anterior chamber angle configuration. Distinction is also made between primary and secondary glaucoma; in the latter a recognizable ocular or non-ocular disorder contributes to elevation of IOP.

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Tonometry

Goldmann tonometry

Principles

Goldmann applanation tonometry (GAT) is based on the Imbert–Fick principle, which states that for an ideal, dry, thin-walled sphere, the pressure (P) inside the sphere equals the force (F) necessary to flatten its surface divided by the area (A) of flattening (i.e. P = F/A). Theoretically, average corneal rigidity and the capillary attraction of the tear meniscus cancel each other out when the flattened area has the 3.06 mm diameter contact surface of the Goldmann prism (Fig. 10.4A), which is applied to the cornea with a variable amount of measurable force from which the IOP is deduced. The Goldmann tonometer is shown in Figure 10.4B. Disposable tonometer prisms and tonometer caps have been introduced to counter fears of infection from reusable prisms.

Fig. 10.4 Goldmann tonometry. (A) Physical principles; (B) tonometer

(Courtesy of J Salmon – fig. B)

Technique

a The patient is positioned at the slit-lamp with the forehead firmly against the headrest.

bTopical anaesthetic and fluorescein are instilled into the conjunctival sac.

cWith the cobalt blue filter and the brightest beam projected obliquely at the prism, the prism is centred in front of the apex of the cornea.

dThe dial is preset between 1 and 2 (i.e. 10–20 mmHg).

e The prism is advanced until it just touches the apex of the cornea (Fig. 10.5A).

fViewing is switched to the ocular of the slit-lamp.

gA pattern of two semicircle mires will be seen, one above and one below the horizontal midline, which represent the fluoresceinstained tear film touching the upper and lower outer halves of the prism.

h The dial on the tonometer is rotated to align the inner margins of the semicircles (Fig. 10.5B, right). i The reading on the dial, multiplied by 10, gives the IOP.

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Fig. 10.5 Applanation tonometry. (A) Tonometer touching the cornea; (B) fluorescein-stained semicircles during tonometry (see text)

Sources of error

1Inappropriate fluorescein pattern. Excessive fluorescein will make the mires too thick and the radius too small (Fig. 10.5B, left), when IOP will be overestimated, whereas insufficient fluorescein will make the semicircles too thin and the radius too large (Fig. 1.5B, centre) with consequent IOP underestimation.

2Pressure on the globe from the examiner's fingers, the patient squeezing the eyelids or from restricted extraocular muscles (e.g. thyroid myopathy) may result in an artificially high reading.

3Central corneal thickness (CCT). Calculations of IOP by GAT assume that central corneal thickness is 520 µm, with minimal normal variation. If the cornea is thinner, underestimation of IOP may result, and if thicker an overestimation. Individuals with ocular hypertension tend to have corneas thicker than average, whereas those with normal-pressure glaucoma tend to have thinner corneas. Following refractive surgery procedures the cornea is both thinner and structurally altered such that IOP is likely to be underestimated. New methods of IOP measurement (see below) have been developed with the intention of reducing the effect of the various structural confounding variables.

4Corneal oedema may result in artificial lowering of IOP, presumably due to a boggy softening; notably the associated increased CCT seems to be more than offset.

5Astigmatism, if significant, may give distorted mires. If over three dioptres, the average reading of two can be taken with the prism rotated 90° for the second, or preferably, the prism is rotated so that the red line on the tonometer housing is aligned with the prescription of the minus axis.

6Incorrect calibration of the tonometer can result in a false reading. It is therefore important to check this before each clinical session using the calibration arm supplied.

7Wide pulse pressure. It is normal for there to be a small oscillation in IOP in time with the rhythm of ocular perfusion. If this ‘pulse pressure’ is substantial, the mid-point is taken as the reading.

8Repeated readings over a short period will often be associated with a slight fall in IOP due to the massaging effect on the eye.

9Other factors that may be associated with over-estimation of IOP include a tight collar and breath-holding, both of which obstruct venous return.

Other types of tonometry

1Pneumotonometers are also based on the principle of applanation but, instead of using a prism, the central part of the cornea is flattened by a jet of air. The time required to sufficiently flatten the cornea relates directly to the level of IOP. Contact is not made with the subject's eye and topical anaesthesia is not required, so it is particularly useful for screening in the community. Its main disadvantage is that it is accurate only within the low-to-middle range. The jet of air can startle the patient both with its apparent force and noise. A pneumotonometer may be non-portable (Fig. 10.6) or portable (Fig. 10.7A).

2Reichert ocular response analyzer is a recently-developed form of pneumotonometer which measures IOP whilst attempting to compensate for corneal biomechanical properties by using two sequential measurements to assess corneal hysteresis, a function of viscous damping.

3Dynamic contour tonometry (‘Pascal’) uses a solid state sensor and a corneal contour-matching surface to measure IOP. The instrument has been designed with the aim of measuring IOP relatively independently of corneal mechanical factors such as central corneal thickness. It is used on the slit lamp in a similar fashion to the Goldmann tonometer.

4Perkins applanation tonometer uses a Goldmann prism adapted to a small light source. It is hand-held (Fig. 10.7B), and can therefore be used in bed-bound or anaesthetized patients.

5Tono-Pen® is a hand-held, self-contained, battery powered, portable, miniaturized electronic contact tonometer (Fig. 10.7C). The probe tip contains a transducer that measures applied force. The instrument correlates well with the Goldmann. Its main advantage is the facility to measure IOP in eyes with distorted or oedematous corneas, through a bandage contact lens and in supine patients.

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6iCare® tonometer is a recently developed small hand-held device based on a new measuring principle, rebound or dynamic tonometry, in which a very light probe makes momentary contact with the cornea. Because only a very small force is applied to the cornea a topical anaesthetic is not required. The instrument can be used for self-monitoring (Fig. 10.7D) and screening in the community.

7Schiotz tonometer uses the principle of indentation tonometry, in which the extent of corneal indentation by a plunger of known weight is measured; it is now seldom used in clinical practice.

Fig. 10.6 Non-portable pneumotonometer

Fig. 10.7 Portable tonometers. (A) Keeler pneumotonometer; (B) Perkins; (C) TonoPen®; (D) iCare®

(Fig. D, Courtesy of Mainline Instruments Ltd)

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Gonioscopy

Introduction

Overview

1Gonioscopy is a method of evaluating the anterior chamber angle to provide information regarding the type of glaucoma. It can also be utilized therapeutically for procedures such as laser trabeculoplasty and goniotomy.

2Other means of anterior chamber angle assessment such as high-frequency ultrasound biomicroscopy (UBM), and anterior segment optical coherence tomography (OCT), offer advantages in some aspects of angle analysis and may be used to supplement visual gonioscopic findings.

Optical principles

The angle of the anterior chamber cannot be visualized directly through the intact cornea because light from angle structures undergoes ‘total internal reflection’ at the anterior surface of the precorneal tear film (Fig. 10.8). Because the refractive index of a goniolens is similar to that of the cornea, it eliminates total internal reflection by replacing the tear film-air interface with a new tear film-goniolens interface. Light rays can then be viewed as they exit the contact lens. The two main types of goniolenses are indirect and direct (see below).

Fig. 10.8 Optical principles of gonioscopy; n = refractive index; i = angle of incidence

Indirect gonioscopy

Indirect goniolenses use a mirror to reflect rays from the angle such that they exit the lens at much less than the critical angle. They provide a mirror image of the opposite angle and can be used only in conjunction with a slit lamp.

Non-indentation gonioscopy

1Goniolenses

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