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

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Drainage shunts

Shunts using episcleral explants

Types

These create a communication between the anterior chamber and sub-Tenon space. All such shunts consist of a tube attached to a posterior episcleral explant. Some contain pressure-sensitive valves for regulation of aqueous flow. Reduction of IOP is due to passive, pressure-dependent flow of aqueous across the capsular wall.

1Molteno implant consists of a silicone tube connected to one or two polypropylene plates 13 mm in diameter (Fig. 10.90).

2Baerveldt implant consists of a silicone tube connected to a large area silicone plate impregnated with barium.

3Ahmed implant consists of a silicone tube connected to a silicone sheet valve held in a polypropylene body. The valve mechanism consists of two thin silicone elastomer membranes.

Fig. 10.90 (A) Molteno implant; (B) postoperative appearance

(Courtesy of P Gili – fig. B)

Indications

•Uncontrolled glaucoma despite previous trabeculectomy with adjunctive antimetabolite therapy.

•Secondary glaucoma where routine trabeculectomy, with or without adjunctive antimetabolites, is unlikely to be successful. Examples include neovascular glaucoma and glaucoma following traumatic anterior segment disruption.

•Eyes with severe conjunctival scarring precluding accurate dissection of the conjunctiva.

•Certain congenital glaucomas where conventional procedures have failed (i.e. goniotomy, trabeculotomy and trabeculectomy).

Complications

1Excessive drainage may occur due to leakage around or down the tube if the occluding suture is loose and result in hypotony and a shallow anterior chamber.

2 Malposition that may result in endothelial or lenticular touch (Fig. 10.91A). 3 Tube erosion through the sclera and conjunctiva (Fig. 10.91B).

4Early drainage failure may occur as a result of blockage of the end of the tube by vitreous, blood or iris tissue (Fig. 10.91C).

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5Late drainage failure occurs in about 10% of cases per year and is comparable to that following trabeculectomy.

Fig. 10.91 Complications of drainage implants. (A) Malposition; (B) tube erosion; (C) blockage by iris

(Courtesy of J Salmon – fig. B; R Bates – fig. C)

Results

The results depend on the type of glaucoma. In general, an IOP in the mid-teens is achieved, though as with trabeculectomy, topical medication is typically required. The long-term success rate in neovascular glaucoma is often disappointing because of progressive retinal disease with loss of vision and late development of phthisis bulbi. Adjunctive mitomycin C may enhance the success rate of drainage shunt surgery but is associated with a higher complication rate.

Mini shunts

These are generally used in uncomplicated glaucoma.

1ExPress™ Mini Shunt is a new device without a valve that is inserted under a scleral flap during a modified trabeculectomy. The technique is relatively straightforward in comparison with other shunts.

2iStent® is another novel device consisting of a tiny titanium hooked tube inserted ab interno into Schlemm canal via the trabecular meshwork, and shows promise for moderate IOP reduction.

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Chapter 11 – Uveitis

INTRODUCTION 402 CLINICAL FEATURES 402

Acute anterior uveitis 402 Chronic anterior uveitis  404

Posterior uveitis 406

SPECIAL INVESTIGATIONS 406 Indications 406

Skin tests 407 Serology 407 Enzyme assay 408 HLA tissue typing  409

Imaging 409

Radiology 410

Biopsy 410

PRINCIPLES OF TREATMENT 410 General principles 410 Mydriatics 410

Topical steroids 411 Periocular steroid injection  411

Intraocular steroids 411 Systemic steroids 412 Antimetabolites 412 Calcineurin inhibitors 413 Biological blockers 413

INTERMEDIATE UVEITIS 413

UVEITIS IN SPONDYLOARTHROPATHIES 415 HLA-B27 and spondyloarthropathies

 415

Ankylosing spondylitis 416 Reiter syndrome 416 Psoriatic arthritis 416

UVEITIS IN JUVENILE ARTHRITIS 416 Juvenile idiopathic arthritis 416

Familial juvenile systemic granulomatosis syndrome  420

UVEITIS IN BOWEL DISEASE 420 Ulcerative colitis

 420

Crohn disease 420 Whipple disease  422

UVEITIS IN RENAL DISEASE 422 Tubulointerstitial nephritis and uveitis (TINU)  422

IgA glomerulonephritis 422

SARCOIDOSIS 422

BEHÇET SYNDROME 426

TOXOPLASMOSIS 429

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Introduction 429 Toxoplasma retinitis  430

TOXOCARIASIS 433

MISCELLANEOUS PARASITIC UVEITIS 436 Onchocerciasis 436

Cysticercosis 438

Diffuse unilateral subacute neuroretinitis  439

Choroidal pneumocystosis 440

UVEITIS IN ACQUIRED IMMUNODEFICIENCY SYNDROME 441 Introduction 441

HIV microangiopathy 442 Cytomegalovirus retinitis 442 Progressive retinal necrosis  444

MISCELLANEOUS VIRAL UVEITIS 445 Acute retinal necrosis 445

Herpes simplex anterior uveitis 445 Varicella zoster anterior uveitis 445 Congenital rubella 446

Subacute sclerosing panencephalitis  447

FUNGAL UVEITIS 447

Presumed ocular histoplasmosis syndrome  447

Cryptococcosis 449

Endogenous fungal endophthalmitis 449 Coccidioidomycosis 450

BACTERIAL UVEITIS 450

Tuberculosis 450

Syphilis 451 Lyme disease 452 Brucellosis 454

Endogenous bacterial endophthalmitis  454

Cat-scratch disease 456 Leprosy 456

WHITE DOT SYNDROMES 457

Multiple evanescent white dot syndrome 457

Acute idiopathic blind spot enlargement syndrome 458 Acute posterior multifocal placoid pigment epitheliopathy  458

Multifocal choroiditis and panuveitis 459 Punctate inner choroidopathy 460 Serpiginous choroidopathy 461

Progressive subretinal fibrosis and uveitis syndrome 461 Acute macular neuroretinopathy 462

Acute zonal occult outer retinopathy  463

PRIMARY STROMAL CHOROIDITIS 464 Vogt–Koyanagi–Harada syndrome  464

Sympathetic ophthalmitis 465 Birdshot retinochoroidopathy 467

MISCELLANEOUS ANTERIOR UVEITIS 469 Fuchs uveitis syndrome

 469

Lens-induced uveitis 469

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MISCELLANEOUS POSTERIOR UVEITIS 471 Acute retinal pigment epitheliitis 471 Acute idiopathic maculopathy 472

Acute multifocal retinitis 473 Solitary idiopathic choroiditis 473 Frosted branch angiitis 473

Idiopathic retinal vasculitis, aneurysms and neuroretinitis syndrome  473

Introduction

Anatomical classification

The uvea is the vascular layer of the eye and comprises the iris, ciliary body and choroid (Fig. 11.1).

1Uveitis, by strict definition implies an inflammation of the uveal tract. However, the term is commonly used to describe many forms of intraocular inflammation involving not only the uvea but also the retina and its vessels.

2Anterior uveitis may be subdivided into:

•Iritis in which the inflammation primarily involves the iris.

•Iridocyclitis in which both the iris and the pars plicata of the ciliary body are involved.

3 Intermediate uveitis is defined as inflammation predominantly involving the pars plana, the peripheral retina and the vitreous.

4Posterior uveitis involves the fundus posterior to the vitreous base.

•Retinitis with the primary focus in the retina.

•Choroiditis with the primary focus in the choroid.

•Vasculitis which may involve veins, arteries or both.

5Panuveitis implies involvement of the entire uveal tract without a predominant site of inflammation.

6 Endophthalmitis implies inflammation, often purulent, involving all intraocular tissues except the sclera.

7Panophthalmitis involves the entire globe, often with orbital extension.

Fig. 11.1 Anatomical classification of uveitis

Anterior uveitis is the most common, followed by posterior, intermediate and panuveitis.

Definitions

1Onset may be sudden or insidious.

2Duration of an attack may be either limited, if 3 months or less in duration, or persistent, if longer.

3Acute uveitis describes the course of a specific uveitis syndrome characterized by sudden onset and limited duration.

4Chronic uveitis describes persistent inflammation characterized by prompt relapse (in less than 3 months) after discontinuation of therapy.

5Recurrent uveitis is characterized by repeated episodes of uveitis separated by periods of inactivity without treatment lasting at least 3 months.

6Remission refers to inactive disease for at least 3 months after discontinuation of treatment.

7Resistant

•To steroids if there is no clinical improvement despite 2 weeks of treatment with maximal dose.

•To immunosuppressives if there is no clinical improvement despite 3 months of treatment.

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Clinical features

Acute anterior uveitis

Anterior uveitis is the most common form of uveitis. Acute anterior uveitis (AAU) is the most common form of anterior uveitis, accounting for three-quarters of cases. It is characterized by sudden onset and duration of 3 months or less. It is easily recognized due to the severity of symptoms which will force the patient to seek medical attention.

1Presentation is typically with sudden onset of unilateral pain, photophobia and redness, which may be associated with lacrimation. Occasionally patients may notice mild ocular discomfort a few days before the acute attack when clinical signs are absent.

2Visual acuity is usually good at presentation except in eyes with severe hypopyon.

3External examination shows ciliary (circumcorneal) injection which has a violaceous hue (Fig. 11.2A).

4Miosis due to sphincter spasm (Fig. 11.2B) may predispose to the formation of posterior synechiae unless the pupil is pharmacologically dilated.

5Endothelial dusting by a myriad of cells is present early and gives rise to a ‘dirty’ appearance (Fig. 11.2C). True keratic precipitates (KP) usually appear only after a few days and are usually non-granulomatous (see below).

6Aqueous cells indicate disease activity and their number reflects disease severity (Fig. 11.2D). Grading of cells is performed with a 2 mm long and 1 mm wide slit beam with maximal light intensity and magnification. This must be performed before mydriasis because in normal eyes cells and pigment clumps may develop after pupillary dilatation. Table 11.1 shows the grading system.

•Improvement of inflammation is defined as either a two-step decrease in the level of activity or a decrease to ‘inactive’.

•Worsening is defined as either a two-step increase in the level of activity or an increase to the maximum grade.

7Anterior vitreous cells indicate iridocyclitis.

8Aqueous flare reflects the presence of protein due to a breakdown of the blood–aqueous barrier (see Fig. 11.2D). Flare may be graded by laser interferometry using a flare meter or clinically by observing the degree of interference in the visualization of iris using the same settings as for cells (Table 11.2).

9 Aqueous fibrinous exudate typically occurs in HLA-B27-associated AAU (Fig. 11.2E).

10Hypopyon is a feature of intense inflammation in which cells settle in the inferior part of the anterior chamber (AC) and form a horizontal level (Fig. 11.2F).

•In AAU associated with HLA-B27 the hypopyon has a high fibrin content which makes it dense, immobile and slow to absorb.

•In patients with Behçet syndrome the hypopyon has minimal fibrin and therefore shifts according to the patient's head position and may disappear quickly.

•Hypopyon associated with blood may occur in herpetic infection and in eyes with associated rubeosis iridis.

11Posterior synechiae may develop quickly (Fig. 11.3A) and must be broken down before they become permanent (Fig. 11.3B).

12Low intraocular pressure (IOP) may occur as a result of reduced secretion of aqueous by the ciliary epithelium. Occasionally the intraocular pressure may be elevated (hypertensive uveitis) as in herpetic uveitis and Posner–Schlossman syndrome.

13Fundus examination is usually normal, but should always be performed to exclude ‘spillover’ anterior uveitis associated with a posterior focus, notably toxoplasmosis and acute retinal necrosis.

14Duration. With appropriate therapy the inflammation tends to completely resolve within 5–6 weeks.

15The prognosis is usually very good. Complications and poor visual prognosis are related to delayed or inadequate management. Steroid-induced hypertension may occur but glaucomatous damage is uncommon.

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Fig. 11.2 Signs of acute anterior uveitis. (A) Ciliary injection; (B) miosis; (C) endothelial dusting by cells; (D) aqueous flare and cells; (E) fibrinous exudate; (F) hypopyon

(Courtesy of JS Schuman, V Christopoulos, DK Dhaliwal, MY Kahook and RJ Noecker, from Lens and Glaucoma in Rapid Diagnosis in Ophthalmology, Mosby 2008 – fig. D).

Table 11.1 -- Grading anterior chamber cells

Table 11.2 -- Grading of aqueous flare

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Fig. 11.3 Posterior synechiae. (A) Early synechiae formation in active acute anterior uveitis; (B) extensive synechiae and pigment on the lens following a severe attack of acute anterior uveitis

Chronic anterior uveitis

Chronic anterior uveitis (CAU) is less common than the acute type and is characterized by persistent inflammation that promptly relapses, in less than 3 months, after discontinuation of treatment. The inflammation may be granulomatous or non-granulomatous. Bilateral involvement is more common than in AAU.

1Presentation is often insidious and many patients are asymptomatic until the development of complications such as cataract or band keratopathy. Because of the lack of symptoms patients at risk of developing CAU should be routinely screened; this applies particularly in patients with juvenile idiopathic arthritis.

2External examination usually shows a white eye. Occasionally the eye may be pink during periods of severe exacerbation of inflammatory activity.

3Aqueous cells vary in number according to disease activity but even patients with numerous cells may have no symptoms.

4Aqueous flare may be more marked than cells in eyes with prolonged activity and its severity may act as an indicator of disease activity (contrary to previous teaching).

5KP are clusters of cellular deposits on the corneal endothelium composed of epithelioid cells, lymphocytes and polymorphs (Fig. 11.4A). Their characteristics and distribution may indicate the probable type of uveitis.

•Large KP in granulomatous disease have a greasy (‘mutton-fat’) appearance. They are often more numerous inferiorly and may form in a triangular pattern with the apex pointing up (Arlt triangle – Fig. 11.4B). This is the result of gravity and normal convection flow of aqueous.

•Resolved mutton-fat KP leave behind a ground-glass appearance (ghost KP), which is evidence of previous granulomatous inflammation (Fig. 11.4C).

•Long-standing non-granulomatous KP may become pigmented and less dense centrally (Fig. 11.4D).

6 Dilated iris vessels (pseudorubeosis) are occasionally seen in long-standing cases and resolve with treatment.

7Iris nodules typically occur in granulomatous disease.

•Koeppe nodules are small and situated at the pupillary border (Fig. 11.5A).

•Busacca nodules involve the iris stroma (Fig. 11.5B).

•Large pink nodules are characteristic of sarcoid uveitis (Fig. 11.5C).

8Iris atrophy that is sectoral occurs characteristically in herpes simplex and herpes zoster (see Fig. 11.44). Diffuse iris atrophy occurs in Fuchs uveitis syndrome (see Fig. 11.75D).

9The duration is prolonged and in some cases the inflammation may last for many months or even years. Remissions and exacerbations of inflammatory activity are common and it is difficult to determine when the natural course of the disease has come to an end.

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10 The prognosis is guarded because of complications such as cataract, glaucoma and hypotony.

Fig. 11.4 Keratic precipitates. (A) Aggregate of inflammatory cells on the corneal endothelium; (B) large ‘mutton-fat’ keratic precipitates; (C) ‘ghost’ keratic precipitates; (D) old pigmented keratic precipitates

(Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – fig. A)

Fig. 11.5 Iris nodules in granulomatous anterior uveitis. (A) Koeppe nodules; (B) Busacca nodules; (C) very large nodule in sarcoid uveitis

(Courtesy of J Harry and G Misson, from Clinical Ophthalmic Pathology, Butterworth-Heinemann 2001 – fig. A; C. Pavésio – figs B, C)

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