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Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

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Bleb-Related Infection

Background Bleb related infection is a potentially blinding, late complication of glaucoma filtering surgery. It refers to a spectrum of disease ranging from blebitis (isolated bleb infection) to blebrelated endophthalmitis (BRE). The organisms usually responsible for BRE (Streptococcus and Haemophilus spp.) are different to, and more virulent than, those of early postoperative endophthalmitis. Thin-walled, cystic, leaking blebs are at risk.

Early and aggressive antimicrobial therapy often permits retention of functional VA and a filtering bleb.

Symptoms Redness, photophobia, pain, reduced VA, and discharge.

Signs Bleb opalescence or mucopurulent infiltrate with surrounding conjunctival injection (‘white on red’), ±bleb leak, and intraocular inflammation and purulent discharge (Fig. 7.21).

History and examination Ask about the duration and severity of symptoms (prodrome of a few days suggests blebitis; sudden onset with rapid progression suggests BRE), ocular trauma (accidental or iatrogenic, e.g. bleb needling), contact lens use, and risk factors such as blepharitis, trichiasis, and dry eyes. Record VA and test for the presence of a bleb leak using 2% fluorescein (Seidel’s test).

Differential diagnosis Bleb leak alone may produce mild ocular discomfort and AC activity. Recent corticosteroid withdrawal or rapid tapering may result in rebound inflammation. In both these cases the bleb is clear, the AC reaction mild, and VA unchanged.

Investigations Blebitis associated with 1+ AC cells is considered as BRE, even in the absence of vitritis. BRE requires anterior chamber tap plus vitreous biopsy. A conjunctival swab is not indicated as cultures often correlate poorly with intraocular cultures. A B-scan is indicated if vitritis cannot be excluded or the fundal view is inadequate.

Treatment See Box 7.6.

Follow–up Following an episode of bleb-related infection, surgery is advisable but its risks and benefits must be evaluated for each patient. Surgical revision of the bleb usually involves bleb excision with conjunctival advancement. If present, scleral thinning or a defect must also be repaired with a scleral or Tenon’s graft to avoid the recurrence of cystic blebs. Treat chronic blepharitis, ocular surface, and lid disorders. Prophylactic topical antibiotics are not advised.

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Bleb-related infection

Box 7.6: Treatment of bleb-related infection

Instil povidon-iodine 5% into the conjunctival sac.

G. ofloxacin hourly and G. cefuroxime hourly (day and night) for at least 24 hours, reducing frequency as clinically indicated.

Ciprofloxacin 750 mg b.d. p.o. and co-amoxiclav 625 mg t.d.s. p.o.

(azithromycin 500 mgs b.d. p.o. if penicillin allergy) for

7 days.

Review patients with blebitis or bleb-related infection within 6 hours to exclude progression to bleb-related endophthalmitis (BRE).

Intravitreal vancomycin 2 mg and either amikacin 0.4 mg or ceftazidime 2 mg in cases of BRE.

G. prednisolone 1% q.d.s. (once the course of infection is clear in blebitis).

Prednisolone 1 mg/kg p.o. commenced 12 hours after admission.

Consider intravitreal dexamethasone 0.4 mg to minimize inflammation-related retinal toxicity in cases of BRE.

Fig. 7.21: Bleb-related endophthalmitis.

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Primary Angle Closure

Background Angle closure is contact between the iris and trabecular meshwork accompanied by a significant impairment of aqueous outflow. It may be primary (PAC) or secondary, with 75% of primary cases due to pupil block. Frequently associated with glaucomatous optic neuropathy. The symptomatic form (‘acute’ angle closure) is a common ophthalmic emergency.

Classification The traditional classification of acute, intermittent, chronic, and latent phases fails to identify the disease stage and mechanism of closure. Classify as follows:

Stage.

1. Narrow angles (angle closure suspect).

2. Primary angle closure: a narrow angle with either high IOP or peripheral anterior synechiae (PAS).

3. Angle closure with glaucomatous optic neuropathy (PACG).

Mechanism of angle closure.

1. Pupil block.

2. Anterior, non-pupil-block (includes plateau iris).

3.Lens induced.

4.Causes behind the lens.

Nuclear sclerosis is almost invariably present. This is part of the primary disease and distinct from phakolytic/phakomorphic glaucoma (p. 311).

Symptoms Blurring of vision sometimes accompanied by halos around lights, redness and periocular or hemicranial pain. There may be nausea and vomiting. However, angle closure is often asymptomatic, especially in Asian people.

Signs Signs mirror symptoms in acute disease; VA is reduced, there is circum-limbal injection with corneal oedema, raised IOP, and an immobile pupil. Refraction is often (but not always) hypermetropic.

History and examination A positive family history is common. Dynamic gonioscopy is essential to make the diagnosis. Record the estimated geometric angle width, angle structures visible, iris profile (steep, regular, or plateau), iris pigment on the trabecular meshwork, and extent of PAS. Asymmetry between the two eyes suggests a secondary cause.

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closure

Differential diagnosis Consider: primary open angle

glaucoma; phakolytic and phakomorphic glaucoma; irido-ciliary

 

 

cysts; retinopathy of prematurity; uveitis; nanophthalmos; Weill-

angle

Marchesani syndrome; Marfan’s syndrome; persistent hyperplastic

primary vitreous and lens subluxation; posterior segment

pathology; iatrogenic causes. PAC is extremely uncommon below

the age of 30. In older people, rule out neovascularization and

Primary

hypertensive uveitides. Consider posterior segment disease and

iatrogenic causes (including vitreoretinal surgery). Numerous drugs

 

 

can precipitate angle closure (topical mydriatics; anticholinergic

 

agents including bronchodilators; antispasmodics; antidepressants;

 

proprietary cold and flu medication; anticonvulsants).

 

Investigations B-mode ultrasound is invaluable in identifying

 

posterior segment disease (e.g. ciliary effusions) when the fundal

 

view is inadequate.

 

Emergency management of symptomatic PAC In

 

acute, symptomatic cases, pressure control by medical and/or

 

laser treatment is the immediate priority. If topical medication and

 

acetazolamide are unsuccessful in lowering the IOP in

 

symptomatic cases, laser iridoplasty should be considered

 

(see below).

 

Admit the patient if symptomatic and IOP >40 mmHg in an

 

eye with useful vision.

 

Stat: G. levobunolol 0.5%, G. apraclonidine 0.5%, G.

 

prednisolone 1%, acetazolamide 500 mg i.v., lie the patient

 

supine. Analgesics/antiemetics as required.

 

Check IOP at 30 minutes.

 

1. If responding : Diamox 250 mg q.d.s. p.o.; G. prednisolone

 

1% 2 hourly; G. pilocarpine 2% q.d.s. (4% if dark irides).

 

Avoid intensive pilocarpine.

 

2. If not responding : consider laser iridoplasty (see below) or

 

glycerol 50% 1 g/kg bodyweight p.o., or mannitol 20%

 

1 g/kg i.v..

 

Unless there is a clear reason not to, perform laser iridotomy

 

in both eyes as soon as corneal clarity allows (Box 7.7).

 

Subsequent management is targeted at the specific

 

mechanism of closure. If there is a visually significant cataract,

 

removing this will open the angle. If the angle remains partially

 

closed after laser iridotomy, either laser iridoplasty (Box 7.8) or

 

topical pilocarpine may be used. However, this area of

 

management is currently controversial, and some glaucoma

 

326

specialists opt for careful observation.

 

 

The presence of >6 clock hours of PAS extending across the trabecular meshwork and glaucomatous optic neuropathy both suggest that laser and medical treatment are unlikely to control IOP satisfactorily. A trabeculectomy will frequently be needed. Because of the poor success rate, trabeculectomy should be avoided soon after an acute attack, unless absolutely necessary.

Follow–up Once IOP is controlled, review patients at one week, 1 month, then annually.

Box 7.7: YAG laser iridotomy

This is the cornerstone of management

1.Premedicate with G. apraclonidine 0.5% and pilocarpine 2% (4% for dark brown irises) 30 minutes and 5 minutes before.

2.Use a Wise or Abraham’s lens. Try to treat in the base of an iris crypt (Fig. 7.22).

3.Create an iridotomy that will be covered by the upper lid. Avoid treating in an area under the marginal tear strip; this may cause glare.

4.If bleeding occurs, a little pressure with the contact lens helps to stop this.

5.Argon pretreatment is useful in patients with thick brown irises: 10–40 shots, 0.05–0.1 s, 50 microns, 200 to 1000 mW power. Avoid charring.

6.YAG laser energy varies with the machine and patient, typically 1–3 mJ, 10–20 shots.

7.Iridotomies should be 200 microns in diameter.

8.Check IOP 2 hours post laser. Prescribe G. prednisolone 1%

GLAUCOMA 7 Chapter

hourly for 24 hours, then q.d.s. 7 days.

327

 

Primary angle closure

Fig. 7.22: Laser iridotomy in the 11 o’clock position.

Box 7.8: Laser peripheral iridoplasty

Applying large, slow-contraction burns to peripheral iris is useful in both symptomatic and asymptomatic cases. Premedication and lenses are as for iridotomy.

1.Select a 500 micron spot size, 0.5 sec for all iris colours. Power: 100 mW increasing as required.

2.End point: brisk contraction of the stroma without charring or a pop.

3.Target the peripheral iris but ensure there is a gap between the endothelium and iris. This may mean starting in the midperipheral iris and spiralling out to the far periphery as a gap opens with treatment.

4.Apply 5 evenly spaced shots per quadrant.

If used for medically unresponsive cases of acute angle closure, a peripheral iridotomy must be completed at the earliest opportunity within hours of pressure normalization. Monitor pressure and give topical steroids as for iridotomy.

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Optometry and General

Practice Guidelines

General comments

Cases of suspected open angle glaucoma require routine referral for assessment by an ophthalmologist, or preferably a glaucoma specialist. Acute angle closure and bleb-related infections are emergencies that require prompt action and immediate ophthalmology review.

Optometrists

Glaucoma is a progressive optic neuropathy in which the optic nerve head has characteristic changes and there is typically a corresponding visual field loss. Intraocular pressure (IOP) and age are the major risk factors but IOP on its own is not a good predictor of glaucoma (5% of the normal population have IOPs >21 mmHg and about one-third of those with open angle glaucoma have IOPs <22 mmHg). Other risk factors are ethnicity (Afro-Caribbean) and family history (a first-degree relative with glaucoma).

Consider the cup-to-disc ratio (CDR) in relation to the disc size (a large CDR may be normal if the disc is also large; see p. 279) and look for notches and variations from the normal distribution of rim thickness (see Jonas’ ISNT rule, p. 279). An IOP consistently >24 mmHg caries a 9% risk of progressing to glaucomatous optic neuropathy. A modest (20%) reduction of the IOP reduces this risk to 4%. Refer on a routine basis, or manage in line with local protocols.

General practice

The optometry guidelines also apply. Headaches and eye pain are not generally associated with glaucoma, unless the IOP is very high. If unable to assess disc and fields effectively, recommend review by an optometrist. Topical beta blockers are contraindicated in people with asthma and chronic airways disease. Note that steroids, both systemic and topical (eye, nose, skin), have the potential to generate a steroid-induced increase in IOP. People using these agents regularly for more than 6 weeks should have their IOP monitored. In general, steroid eyedrops are for shortto medium-term use, but with some exceptions, including blind painful eyes, some chronic corneal diseases, and chronic uveitis.

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Optometry and general practice guidelines

The following guide to referral urgency is not prescriptive, as clinical situations vary.

Immediate

Suspected blebitis

p. 323

Acute angle closure

p. 325

IOP >40 mm Hg

p. 325

Soon (within 1 month)

 

Advanced glaucomatous disc damage (CDR >0.8

 

and advanced field loss)

p. 279

IOP >35 mm Hg on any occasion

p. 287

Routine

 

IOP consistently in mid 20s with normal disc and

 

fields

p. 287

Suspected glaucomatous optic disc changes

 

(any IOP)

p. 279

Repeatable, suspected glaucomatous field loss

 

(any IOP)

p. 284

Pigment dispersion syndrome

p. 305

Pseudoexfoliation

p. 303

Suspected narrow angles (asymptomatic)

p. 325

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Chapter 8

UVEITIS

History and Examination

Uveitis is an umbrella term for intraocular inflammation which has a varied clinical phenotype. The diagnosis is predominately clinical, reliant upon meticulous history taking and examination. The aetiology may be primarily inflammatory, infective, or malignant, or, in about 40% of patients, it remains undetermined (organ-specific autoimmune disease), even after appropriate clinical assessment and investigation. Anatomically, uveitis

can be classified into anterior, intermediate, posterior, or panuveitis.

History A comprehensive ocular and systemic history is paramount. Note age, sex, country of origin, and ethnicity. Ask about the duration and pattern of symptoms, which may be unilateral or bilateral, acute, recurrent, or chronic, and previous eye surgery or trauma. Document a full past and current medical problem list, BCG vaccination history, any prior, recent and/or concurrent infections, and all drugs and dosages. Personal details including foreign travel, occupation, pets, social and family circumstances, are all relevant. Additional questions such as pregnancy, pregnancy intention, breastfeeding, sexual history, and intravenous drug usage may also be appropriate. Enquire about skin, joint, respiratory, gastrointestinal, genitourinary, and neurological symptoms of associated systemic disease.

Examination

Slit lamp examination : note the following: pattern of conjunctival/episcleral/scleral injection; corneal epithelial or stromal disease; size, appearance, and distribution of keratic precipitates (KPs); cells, flare, fibrin, hypopyon; iris atrophy/ nodules; cataract; posterior and peripheral anterior synechiae; rubeosis. Measure IOP.

Dilated fundoscopy : both slit lamp and indirect ophthalmoscope examination are mandatory in all patients to assess for: vitreous cells; ‘snowballs’; ‘snowbanking’ (which is

in the retinal periphery and may be missed on slit lamp

 

examination alone); disc oedema or hyperaemia; vasculitis

 

(arterial, venous, or both); perivascular exudates; cystoid

 

macular oedema; retinitis; choroiditis or choroidal infiltrates;

331

 

History and examination

chorioretinal scars; retinal detachment (rhegmatogenous, serous, and tractional).

If VA is worse than 6/9 a cause must be sought.

332