Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Traumatic Glaucoma

Background Trauma may lead to early or late IOP elevation, progressing to glaucomatous optic neuropathy. Hyphaemas may cause very high IOP. The trabecular meshwork may be directly damaged (alkalis, siderosis, angle recession) but this may not reduce outflow for many years. Angle-recession results in glaucoma in 5% (10% of those with 360º recession). Traumatic cataract, significant iris injury, and lens subluxation/dislocation are also important risk factors for glaucoma.

Symptoms Acutely: pain, reduced vision, or halos. May present late with glaucomatous field loss.

Signs Iris sphincter ruptures, deep anterior chamber, anterior chamber cells (hyphaema, ghost cells), flare, or phacodonesis. Gonioscopy may show peripheral anterior synechiae, angle recession (Fig. 7.18), cyclodialysis clefts, or blood. Look for 360º angle recession by comparing both eyes. Exclude vitreous haemorrhage and posterior segment sequelae of trauma.

Differential diagnosis Primary open angle glaucoma.

History and examination Record the details of the injury and subsequent treatment; VA; IOP; iris defects; AC depth and cellular activity; pupil size; gonioscopy; RAPD; and dilated disc examination. If the injury resulted from a workplace accident or alleged assault, make careful and complete notes. Carefully examine the orbit, anterior segment, posterior segment and peripheral retina for other injury.

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Traumatic glaucoma

Investigations Baseline visual field and optic disc photography/imaging.

Treatment

■Casualty : If the IOP is elevated, commence medical treatment. Request early clinic review.

■Clinic : Anterior chamber wash out (hyphaema), vitrectomy (ghost cells), or cataract extraction (lens trauma) may be necessary if the IOP is not responsive. Treatment is determined by the likely mechanism of pressure rise. Argon laser trabeculoplasty is unlikely to be effective. Routine trabeculectomy has a high failure rate due to prior inflammation and conjunctival scarring. Mitomycin C trabeculectomy or a glaucoma drainage device (e.g. Molteno Tube) are often considered as a primary procedure.

Follow–up As indicated by IOP, disc and field. Annual IOP measurement is required for eyes with angle recession. Always check IOP when reviewed, even years later.

Glaucoma Following

Vitreoretinal Surgery

Background Temporarily raised IOP after vitreoretinal surgery is common. Progression to glaucoma occurs in <5% of cases. Risk factors include preexisting glaucoma, trauma, angle recession, steroid response, high myopia, pigment dispersion syndrome, chronic inflammatory disease, proliferative retinopathies, use of silicone oil, and vitreous haemorrhage.

Mechanism

■Scleral buckling procedures : ciliary body rotation with angle closure; anteriorly placed buckle causing angle closure; high buckle with vortex vein compression; shed photoreceptor outer segments occluding outflow (Schwartz-Matsuo syndrome).

■Vitrectomy : ghost cell glaucoma; retained lens material; pigment dispersion after cryotherapy; chronic inflammation; neovascular glaucoma.

■Vitrectomy with intravitreal tamponade : pupil block with overfill of tamponade and direct angle closure or intratrabecular obstruction and damage from emulsified silicone oil.

Signs Look for raised IOP, corneal oedema, cells or emulsified silicone oil in the anterior chamber, and iris bombé. Gonioscopy may show an open or closed angle, peripheral anterior synechiae, or new vessels. Check the patency of any inferior iridectomy in aphakic silicone-filled eyes.

Natural history IOP often settles when postoperative inflammation resolves. Steroid response within 2 weeks of surgery is unlikely. Removal of emulsified silicone oil does not affect IOP.

Medical management

■Open angle : first-line treatment is topical beta blocker and alpha-adrenergic agonists b.d. Consider prostaglandin agonists o.d. if postoperative inflammation is not severe. Oral acetazolamide may be required.

■Closed angle : difficult to control medically. Aqueous suppressants are first line, such as oral acetacolamide 250 mg q.d.s. orally, topical beta blocker b.d. and an alpha-adrenergic agonist.

■Pupil block : mydriatics, e.g. atropine 1% b.d.

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Glaucoma following vitreoretinal surgery

is often needed in eyes with closed angles and aphakic eyes. Trans-scleral diode laser ciliary ablation is used in most cases, but more than one treatment is often needed. Consider drainage tube implants if there is potential for good navigational vision (VA >6/60 and/or visual field >10 degrees).

Prognosis No perception of light in 50% of eyes with IOPs persistently >30 mmHg or hypotony after treatment. Optic disc cupping may progress despite IOP control. Cases with closed angles have the poorest prognosis.

Aqueous Misdirection

(‘Malignant Glaucoma’)

Background Characterized by axial shallowing of the anterior chamber and raised IOP. Occurs in 2% of patients undergoing trabeculectomy for angle closure. May occur after any type of intraocular surgery. Crowding of the ciliolenticular space (possibly from anterior rotation of ciliary body) is believed to block aqueous flow. Posterior aqueous diversion into the vitreous increases retrolenticular pressure and shallowing of the anterior chamber. Risks are high in nanophthalmic eyes.

Symptoms Unilateral pain, reduced vision, lacrimation, and photophobia.

Signs Shallow or flat anterior chamber, IOP >21 mmHg. Choroidal detachment, haemorrhage, or signs of pupil block are absent.

History Ask about the duration/severity of symptoms, previous history of angle closure, and recent ocular surgery.

Examination Record VA and IOP. Shallowing of the anterior chamber is axial, unlike iris bombé in pupil block. Exclude hypotony/overdrainage or choroidal effusions. Confirm patency of any iridotomy.

Differential diagnosis

■Symptomatic angle closure.

■Choroidal detachment : IOP is typically low with choroidal elevation visible on fundoscopy.

■Choroidal/vitreous haemorrhage : sudden onset of elevated IOP associated with severe pain. Blood may be visible.

Investigations Arrange preoperative biometry ± ultrasound to identify nanophthalmic eyes prior to glaucoma surgery (axial length <21 mm, scleral thickness ≥ 2 mm). B-mode ultrasound is useful in excluding choroidal detachment or haemorrhage.

Treatment Identify high-risk eyes preoperatively: suture the scleral flap watertight using releasable sutures, and give postoperative cycloplegia.

Established cases:

■Cycloplegia: G. atropine 1% t.d.s. and phenylephrine 10% b.d.

■Reduction of aqueous production:

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Aqueous misdirection (‘malignant glaucoma’)

1. Topical beta blockers (e.g. timolol 0.25% b.d.) and topical alpha agonist (e.g. apraclonidine 0.5% t.d.s).

2. Oral carbonic anhydrase inhibitors (e.g. acetazolamide

250 mg q.d.s.).

■Reduction of vitreous volume : if unresponsive consider hyperosmotic agents (e.g. oral glycerol 50% 1 mL/kg, or intravenous mannitol 2 g/kg).

In 50% of cases, IOP is lowered and the anterior chamber deepens with atropine and ocular hypotensive drugs. If unsuccessful, or when lens–cornea touch is present, laser and/or surgical intervention is required.

Laser/surgical management YAG laser disruption of the posterior capsule/anterior hyaloid is performed in pseudophakic eyes. It is important to extend the capsulotomy to the periphery. If this fails, pars plana vitrectomy is effective in two-thirds of cases. In phakic eyes, direct argon laser through an existing peripheral iridectomy may shrink the ciliary processes: trans-scleral diode can also be used. Vitrectomy alone has a poor success rate. Combined cataract extraction with primary posterior capsulotomy and anterior vitrectomy is recommended in any patient with even mild lens opacity. With no opacity, clear lens extraction is an option. The treatment algorithm in Figure 7.19 outlines the management of malignant glaucoma.

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Malignant glaucoma

Fig. 7.19: Management of aqueous misdirection from Rubin, Tsai, and Hitchings (Br J Ophthalmol 1997) with permission.

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Congenital glaucoma

Congenital Glaucoma

Background Congenital glaucoma is a rare disease with an incidence of 1 : 20 000 in the Caucasian population. Cases are usually sporadic, but can be autosomal recessive.

Classification

■Primary congenital glaucoma (isolated trabeculodysgenesis): the most common form of neonatal glaucoma.

■Secondary to ocular disease : anterior segment dysgenesis (Axenfeld-Rieger’s syndrome, Peters anomaly), aniridia, aphakic glaucoma, and uveitic glaucoma.

■Secondary to systemic disease : metabolic, chromosomal, and connective tissue disorders.

Clinical features Classic triad of epiphora, photophobia, and blepharospasm. May also present with enlarged cornea (buphthalmos), corneal clouding, or after screening in families with early-onset glaucoma. Late presentation may lead to reduced vision and nystagmus, strabismus and rapidly progressing myopia.

History and examination Record any complications during pregnancy and labour, age at onset of symptoms (earlier onset indicates worse prognosis), developmental milestones, family history, and consanguinity. Full examination usually requires anaesthesia.

Congenital glaucoma

inflammation and phthisis, particularly if used on multiple occasions. Occlusion therapy and correction of refractive error are essential.

Follow–up Intensive surveillance is required, particularly postoperatively. This is usually carried out in specialists units. Education, social support, and counselling are important in managing the family as a whole.