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

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Fig. 10.58 Intumescent cataract, shallow anterior chamber, dilated pupil and corneal oedema in phacomorphic glaucoma

Treatment

Treatment is initially similar to acute PACG, but miotics are omitted as they tend to increase iris-lens apposition and shift the lens anteriorly. Systemic hyperosmotic agents may be required more commonly than in PACG. Laser iridotomy may be worthwhile but is often not possible (due to corneal oedema or lens-cornea proximity) or ineffective. Definitive treatment consists of early cataract extraction, ideally when the IOP is normal and the eye quiet.

Lens dislocation into the anterior chamber

Causes

1Blunt ocular trauma, even if relatively trivial, may result in lens dislocation in eyes with a weak zonule as in pseudoexfoliation and homocystinuria (Fig. 10.59A).

2Small lenses (microspherophakia) as in Weill–Marchesani syndrome.

Fig. 10.59 Lens-induced pupillary block glaucoma. (A) Lens dislocation into the anterior chamber; (B) lens incarceration in the pupil

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Diagnosis

The dislocated lens causes acute pupillary block and a sudden and severe elevation of IOP with associated visual impairment. This constitutes an acute emergency because lenticulocorneal contact may cause permanent endothelial damage.

Treatment

The IOP is initially reduced with osmotic agents. Subsequent management is dependent on the absence or presence of some remaining zonular attachments and the hardness of the lens as follows:

1Intact zonule. The patient is placed into a supine posture and the pupil dilated in an attempt to reposition the lens into the posterior chamber.

2Soft lens without zonular attachments. A lensectomy is performed through a limbal incision. Lenses in patients over the age of 35 years are usually too hard to be removed by this technique.

3Hard lens without zonular attachments. A pars plana vitrectomy and lensectomy is performed.

Incarcerated lens in the pupil

1Pathogenesis. The rise in IOP is caused by pupillary block by a microspherical lens in which only part of the zonule has been disrupted so that the intact zonule acts as a hinge (Fig. 10.59B).

2Treatment involves relieving pupillary block with mydriatics or Nd:YAG laser iridotomy. Miotics are contraindicated because they will worsen pupillary block. The fellow eye should undergo prophylactic laser iridotomy.

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Traumatic glaucoma

Hyphaema

Pathogenesis

A traumatic hyphaema may be associated with IOP elevation due to trabecular blockage by red blood cells. Pupillary occlusion by a blood clot may be superimposed on an angle-closure component. Secondary haemorrhage, often more severe than the primary bleed, may develop within 3–5 days of the initial injury. Patients with sickle-cell haemoglobinopathies are at increased risk of developing complications associated with traumatic hyphaema.

Risk of glaucoma

Although most traumatic hyphaemas are relatively innocuous and transient, severe and prolonged elevation of IOP may damage the optic nerve and cause blood staining of the cornea; the latter can progress very rapidly. The size of a hyphaema is a useful indicator of visual prognosis and risk of complications:

•Hyphaema involving less than half the anterior chamber (Fig. 10.60) is associated with a 4% incidence of raised IOP, a 22% incidence of complications and a final visual acuity of >6/18 in 78% of eyes.

•Hyphaema involving over half the anterior chamber is associated with an 85% incidence of raised IOP, 78% incidence of complications and a final visual acuity of >6/18 in only 28% of eyes.

Fig. 10.60 Small hyphaema with a low risk of glaucoma

Treatment

1General

•A coagulation abnormality, particularly a haemoglobinopathy, should be excluded.

•Any current anticoagulant medication should be discontinued after liaison with a general physician to assess the risk; NSAIDs should not be used for analgesia.

•Hospital admission may be required for large hyphaemas.

•Strict bed rest is probably unnecessary, but substantially limiting activity is prudent, and the patient should remain in a sitting or semi-upright posture, including during sleep.

2Medical

•A beta-blocker and/or a topical or systemic CAI is administered (not in sickle haemoglobinopathies if possible) depending on the IOP. Miotics should be avoided as they may increase pupillary block and disrupt the blood-aqueous barrier, and prostaglandins as they may promote inflammation. Alpha-agonists may be useful, but are avoided in small children and sickling disorders.

•Occasionally a hyperosmotic agent is needed.

•Topical steroids should be used since they reduce inflammation and possibly the risk of secondary haemorrhage.

•Mydriatics are controversial. Atropine is recommended by some authorities to achieve constant mydriasis rather than a mobile pupil, in order to minimize the chances of secondary haemorrhage.

•Systemic antifibrinolysis (aminocaproic acid or tranexamic acid) is rarely given now; topical aminocaproic acid shows

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promise but remains investigational at present.

3Surgical evacuation of the blood is indicated if it is judged there is a risk of permanent corneal staining (rare) or persistently intolerable IOP. If a total hyphaema persists for more than 5 days consider evacuation to prevent the occult development of peripheral anterior synechiae and chronic secondary glaucoma; a low threshold is required in haemoglobinopathy patients (even moderate pressure elevation can lead to optic atrophy) and in young children with a risk of amblyopia. A glaucoma filtration procedure may be necessary in some cases.

4On discharge the patient should be advised to avoid any activity with a risk of even minor eye trauma for several weeks; symptoms of a rebleed should prompt immediate review.

Angle recession glaucoma

Pathogenesis

Angle recession involves rupture of the face of the ciliary body, the portion that lies between the iris root and the scleral spur, due to blunt trauma. Although a large percentage of eyes with traumatic hyphaema exhibit some degree of angle recession, only 6–9% develop glaucoma after 10 years. The rise in IOP is secondary to associated trabecular damage rather than from angle recession itself; however, the risk of glaucoma is directly related to the extent of angle recession. Since glaucoma may not develop until months or even years after the initial injury, angle recession mandates periodic review.

Diagnosis

1Presentation is with unilateral chronic glaucoma.

2Slit-lamp biomicroscopy may show signs of previous blunt trauma, which may be mild, such as a small sphincter rupture.

3Gonioscopy may initially show irregular widening of the ciliary body (Fig. 10.61A). In long-standing cases, the cleft may become obscured by fibrosis and the angle may show hyperpigmentation (Fig. 10.61B).

Fig. 10.61 (A) Angle recession; (B) old angle recession with hyperpigmentation

(Courtesy of R Curtis – fig. A)

Treatment

1Medical treatment is as for other types of secondary open-angle glaucoma but is frequently unsatisfactory and laser trabeculoplasty is ineffective.

2Trabeculectomy with adjunctive antimetabolites is generally an effective procedure.

3 An artificial filtering shunt or cyclodiode should be considered if trabeculectomy fails.

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Iridocorneal endothelial syndrome

Classification

The iridocorneal endothelial (ICE) syndrome typically affects one eye of a middle-aged woman. It consists of the following three very rare and frequently overlapping disorders: (a) progressive iris atrophy, (b) iris naevus (Cogan–Reese) syndrome and (c) Chandler syndrome.

Pathogenesis

The common link between the three variants of ICE syndrome is an abnormal corneal endothelial cell layer which has the capacity to proliferate and migrate across the angle and onto the surface of the iris. The term ‘proliferative endotheliopathy’ has therefore been suggested to describe this disorder. The ICE syndrome may progress to glaucoma, corneal decompensation or both. Glaucoma is due to synechial angle closure secondary to contraction of this abnormal tissue. Polymerase chain reaction shows the presence of herpes simplex virus DNA in a substantial percentage of ICE syndrome corneal specimens, suggesting that the condition may be of viral origin.

General features

1Slit-lamp biomicroscopy

•Corectopia (malposition of the pupil – Fig. 10.62A).

•Pseudopolycoria (supernumerary false pupils) in a previously normal iris (Fig. 10.62B).

•Iris atrophy of varying severity (Fig. 10.62C and D).

2 Gonioscopy shows broad-based PAS that often extend anterior to Schwalbe line (Fig. 10.62E).

3Glaucoma is present in about 50% of cases.

Fig. 10.62 Iridocorneal endothelial syndrome. (A) Corectopia; (B) pseudopolycoria; (C) iris atrophy; (D) very severe iris atrophy; (E) broad peripheral anterior synechiae; (F) iris nodule in Cogan–Reese syndrome

(Courtesy of L MacKeen – fig. E; R Martincova – fig. F)

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Specific features

In their purest form, the three conditions are easily distinguished from each other. However, there is frequently considerable overlap and clear differentiation may be difficult. Occasionally, during follow-up one condition can be observed changing into another. The differentiation depends primarily on the iris changes.

1Progressive iris atrophy is characterized by severe iris changes.

2The iris naevus (Cogan–Reese) syndrome is characterized by either a diffuse naevus which covers the anterior iris or iris nodules (Fig. 10.62F). Iris atrophy is absent in 50% of cases and in the remainder it is usually mild to moderate although corectopia may be severe. It is important not to misdiagnose a diffuse iris melanoma as the iris naevus syndrome

3Chandler syndrome is characterized by ‘hammered-silver’ corneal endothelial abnormalities (Fig. 10.63A) and frequently presents with blurred vision and haloes due to corneal oedema (Fig. 10.63B). Stromal atrophy is absent in about 60% of cases and in the remainder is variable in its severity; corectopia is mild to moderate. Glaucoma is usually less severe than in the other two syndromes, and at presentation the IOP may be normal.

Fig. 10.63 Chandler syndrome. (A) Hammered-silver endothelial changes; (B) corneal oedema due to endothelial decompensation

(Courtesy of J McAllister – fig. B)

Treatment of glaucoma

1Medical treatment may be tried but is often ineffective.

2Trabeculectomy, even when combined with adjunctive antimetabolites, is frequently unsuccessful because of late-onset bleb failure.

3Artificial filtering shunt or cyclodiode is eventually required in many cases.

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Glaucoma in intraocular tumours

Approximately 5% of eyes with intraocular tumours develop a secondary elevation of IOP. Depending on the location of the tumour one or more of the following mechanisms may be responsible:

Trabecular block

Trabecular block may be the result of one of the following:

1Angle invasion by a solid iris melanoma (Fig. 10.64A).

2Trabecular infiltration by neoplastic cells originating from an iris melanoma (Fig. 10.64B). Rarely, tumour seeding from a retinoblastoma may also invade the trabeculum.

3Melanomalytic glaucoma may occur in some eyes with iris melanoma; it is due to trabecular blockage by macrophages which have ingested pigment and tumour cells (Fig. 10.64C), similar to phacolytic glaucoma.

Fig. 10.64 Glaucoma in intraocular tumours. (A) Angle invasion by a solid iris melanoma; (B) melanoma cells infiltrating the trabeculum; (C) melanomalytic glaucoma;

(D) angle-closure by a large ciliary body melanoma

(Courtesy of R Curtis – figs A and C; J Harry – figs B and D)

Secondary angle closure

Secondary angle closure may be the result of one of the following:

1Neovascular glaucoma is the most common mechanism in eyes with choroidal melanoma or retinoblastoma.

2Anterior displacement of iris-lens diaphragm may occur in an eye with a ciliary body melanoma (Fig. 10.64D) or a large tumour of the posterior segment.

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Glaucoma in epithelial ingrowth

Pathogenesis

Epithelial ingrowth is a rare and potentially blinding complication of anterior segment surgery or trauma. Conjunctival or corneal epithelial cells migrate through the wound and proliferate in the anterior segment, in a cystic or diffuse manner. The latter is characterized by the proliferation of sheets of epithelial cells over the posterior cornea, trabeculum, iris and ciliary body (Fig. 10.65A) and is more commonly associated with secondary glaucoma than the cystic variety. Elevation of IOP is caused by a combination of often pre-existing PAS, obstruction of the trabeculum by the epithelial membrane, and desquamated epithelial and inflammatory cells.

Fig. 10.65 Diffuse epithelial ingrowth. (A) Stratified squamous epitheliumlining the anterior iris surface and filtration angle; (B) translucent membrane with a scalloped border involving the posterior corneal surface

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

Diagnosis

•Persistent postoperative anterior uveitis.

•Diffuse epithelialization is characterized by a translucent membrane with scalloped border involving the posterior corneal surface (Fig. 10.65B) in the sector of the incision.

•Pupillary distortion.

Treatment

The aim of treatment is to eradicate the invading epithelium to avoid recurrence or the conversion of epithelial cysts into diffuse epithelialization with consequent intractable glaucoma.

1Block excision involves simultaneous excision of adjacent iris, pars plicata of the ciliary body, together with all layers of the sclera and cornea in contact with the lesion. The resultant defect is covered with a tectonic corneoscleral graft. The area of iris involvement may be delineated by applying argon laser burns which will cause whitening of the affected area.

2Cryotherapy may be applied trans-sclerally to devitalize the epithelium remaining on the posterior surface of the cornea, in the

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angle and on the ciliary body. Intraocular air is used to insulate other tissues from the effects of the cryotherapy.

3Artificial filtering shunts are of value for medically uncontrolled glaucoma associated with extensive epithelial ingrowth unsuitable for surgical excision.

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