Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

treated with glasses or contact lenses. Unilateral cataract is managed the same way but with a contact lens, rather than glasses, postoperatively. Intraocular lens implants can be used from 4 months of age, but are associated with an increased complication rate, and posterior capsular thickening will require YAG or surgical capsulotomy. Lens implantation before age 4 months is possible, but controversial. The lens power depends on the age of the child, with infants and younger children left hyperopic to allow for later ‘myopic shift’ as the eye grows.

Consent Warn the parents that paediatric cataract surgery is not the same as adult surgery and that the visual result is less predictable. Considerable parental input is required after surgery. The major complications are glaucoma, amblyopia, and strabismus. Aphakic glaucoma is a significant complication, particularly for children undergoing early surgery when the risk can be up to 50%. It would appear to reduce when surgery is performed later, even by waiting until over 4 weeks of age. Strabismus and amblyopia occur in virtually all cases of unilateral cataract, whether treated or not. Amblyopia is also common with bilateral cataracts. In children undergoing lens implantation, primary posterior capsulorrhexis or later capsulotomy will be required. After unilateral surgery, failure to patch the nonaffected eye is the leading cause of poor vision. Also, discuss the more general risks of cataract surgery.

Follow–up Even if no surgery is undertaken, clinic review is required to ensure that the good eye develops normally, and to review the cataractous eye. Long-term, regular follow-up after surgery is mandatory to monitor for complications. Children should be seen at 1 day, then 1, 2, and 4 weeks after surgery, and regularly thereafter. Refract at the second postoperative visit and prescribe contact lenses or glasses initially for near vision (give the retinoscopy with no subtraction for working distance). Refraction should be regularly updated, and glasses or contact lenses altered accordingly, with bifocal or varifocal correction from about 2 years of age. Check IOP at every visit. Increased corneal thickness may give falsely elevated IOP readings and examination under anaesthesia may be required. Patching will be required for amblyopia. Postoperative therapy includes topical antibiotic, steroid and mydriatic.

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Coats’ disease

Coats’ Disease

The main features are unilateral, idiopathic retinal telangiectasia with intraand subretinal exudation and retinal detachment (Fig. 12.2). Apparently bilateral Coats’ disease is usually familial exudative vitreoretinopathy (p. 546) or another disorder. Coats’ disease typically present in boys at a median age of 5 years, but there is a large range from neonate to adult, with severity inversely related to the age of presentation. There is no racial predisposition, and it is nonheritable in >95% of cases. Telangiectasia is temporal or inferior in the majority of cases, and anterior to the equator in half. B-scan ultrasound aids diagnosis. Fluorescein angiography may help identify the telangiectasia. Treatment is cryotherapy to telangiectatic vessels (or laser photocoagulation if less exudation). Vitrectomy has been considered in severe cases where laser and cryotherapy have failed. When there is macular involvement or extensive exudation, the visual prognosis is poor even after treatment.

Persistent Hyperplastic

Primary Vitreous

Persistent hyaloid artery represents a remnant of the hyaloid vascular system. This occasionally runs from the disc to the lens; more commonly an anterior remnant gives a Mittendorf dot on the posterior lens surface or a posterior remnant gives a Bergmeister’s papilla over the disc.

Persistent hyperplastic primary vitreous (PHPV) occurs when the primary vitreous fails to regress. It may be anterior or posterior. The commonest type is anterior with a microphthalmic eye and a vascularized retrolental mass. Cataract develops early. In the posterior form the lens is usually clear and there is a retinal fold or detachment. It is unilateral in >95% cases with no racial/ sex predisposition and is nonheritable in >95%. Observe for angle closure glaucoma secondary to progressive anterior chamber shallowing or direct fibrovascular angle invasion. Exclude other causes of leucocoria (p. 561). Secondary tractional retinal detachment (usually tentlike or sickle-shaped) occurs in a minority of cases. Surgery is rarely required and would normally only be undertaken if the anterior chamber shallowing was causing glaucoma. The final vision is related to the extent of posterior involvement, development of glaucoma, or phthisis.

Toxocariasis

Ocular toxocariasis is caused by infection with the nematode Toxocara cani which is commonly found in dogs and is excreted in their faeces. If faecally contaminated matter is ingested, the ova develop into larvae in the gut and then travel to other organs. Ocular infection is always unilateral and presents in the age range 2–10 years as a severe endophthalmitis, or in a slightly older child with posterior or peripheral granuloma formation. Vitreous activity is very variable, and macular dragging or retinal detachment may occur. The eosinophil count may be raised on full blood count or aqueous examination. Immunodiagnostic tests are only about 50% sensitive. Treatment is with local or systemic corticosteroids and albendazole (10 mg/kg of body weight/day in two divided doses).

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Retinopathy of prematurity

Retinopathy of Prematurity

Background Retinopathy of prematurity (ROP) is a proliferative retinopathy developing in immature retinal vessels. It is still an important cause of visual loss in premature babies (the major cause is cerebral visual impairment) especially in those of 23–26 weeks gestation. Despite a reducing incidence, >50% of babies <1000 g birth weight develop some ROP. Most ROP will regress, and in the UK only about 2% of screened babies require treatment.

Classification Categorized by the international classification of ROP (ICROP) on location, severity or stage, extent, and plus disease. Normal vascularization proceeds centrifugally from the optic disc to the ora serrata, reaching the nasal edge at about 36 weeks’ gestation and the temporal edge at term; thus, any baby born prematurely will have immature retinal vascularization, increasing with decreasing gestation.

■Location : described as 3 concentric zones centred on the disc (Fig. 12.3). Zone I extends 30 degrees from the optic disc, a radius of twice the distance from the disc to the fovea. To define the temporal edge of zone I clinically, view the posterior pole with a 28 D lens and align one edge of the lens with the nasal side of the disc: the temporal lens edge then aligns with the temporal zone edge. Zone II surrounds zone I, up to the nasal ora serrata. Zone III is the residual retina anterior to zone II.

■Stage : Stage 1 is a thin white demarcation line at the junction of anterior avascular and posterior vascularized retina (Fig. 12.4). Stage 2 has a ridge at the avascular/vascular junction. Also included in this stage is ‘popcorn’ or small retinal tufts of new vessels posterior to the ridge. Stage 3 has neovascularization extending from the ridge into the vitreous. Stage 4, with partial retinal detachment, is subdivided into 4A which is extrafoveal and 4B which involves the fovea. Total retinal detachment is present in stage 5 disease. The most posterior disease present in an eye determines its staging.

■Extent : recorded by the number of clock hours of retina involved.

■Plus disease : is a marker of severity in active ROP and includes engorgement and tortuosity of the posterior pole vessels, iris vessel engorgement, poor pupil dilatation, and

vitreous haze. The presence of plus disease is shown by the addition of a plus sign (+) to the staging. Plus disease involves

12 o’clock

Zone III

Zone II

Zone I

Fovea

Optic nerve

6

Right eye

Fig. 12.3: Retinopathy of prematurity, zones I to III.

6 or more clock hours of vessel change. Pre-plus disease involves <6 clock hours and is an intermediate level between normal posterior pole vessels and frank plus disease (Fig. 12.5).

Extremely low birth weight babies may have a different morphology to typical ROP.

Aggressive posterior ROP (AP-ROP) is a deceptively featureless form of ROP which progress rapidly to stage 5 and does not progress through stages 1–3. It usually occurs in zone 1 but can occur in posterior zone 2. There is plus disease with flat brushlike neovascularization at a poorly defined vascular/avascular border.

Screening guidelines In the UK all babies ≤31 weeks gestation (including 31 weeks and 6 days ) or ≤1500 g birth weight should be screened. For those <27 weeks gestational age (including 26 weeks and 6 days), start screening at 30–31 weeks post-menstrual age. For those born at or after 27 weeks, start at 4–5 weeks post-natal age. Note the different ways of expressing age. For example, a child born at 23 weeks would be screened 7–8 weeks after birth, and a child born at 28 weeks would be screened at 32–33 weeks gestational age. Examine every 1–2 weeks until vascularization progresses into zone 3. Severe ROP (stage 3 and above) develops between 33 and 43 weeks’ gestation.

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Treatment for stages 4 and 5 ROP is currently not recommended in the UK.

Follow–up Long-term review is advised for all infants with stage 3 ROP or worse. Issues include subnormal vision, myopia, strabismus, and field loss.

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Conjunctivitis of the newborn (ophthalmia neonatorum)

Conjunctivitis of the Newborn

(Ophthalmia Neonatorum)

Background Defined as conjunctivitis in neonates aged <4 weeks. The infection may be acquired during delivery (if the mother has vaginal infection or if born in an unhygienic environment) or from postnatal caregivers. Causes include

Chlamydia trachomatis, Staphylococcus aureus, Streptococcus viridans, enterococci, Neisseria gonorrhoeae, and herpes simplex virus (HSV). Gram-positive cocci are the commonest pathogens.

Signs Look for injected conjunctiva, lid swelling, and discharge. Skin vesicles and keratitis occur with HSV. N. gonorrhoeae can cause corneal ulceration and perforation. The causative organism cannot be accurately diagnosed from the clinical presentation but gonococcal conjunctivitis tends to be more severe with earlier onset, usually 2–5 days after birth, whilst chlamydial infection has a creamy white discharge, a velvety conjunctival appearance, and presents at 5–12 days after delivery. Staphylococcal infection often produces a yellow discharge.

Differential diagnosis Conjunctivitis secondary to nasolacrimal duct obstruction. Test for mucopurulent reflux on lacrimal sac massage.

Investigations Arrange an urgent Gram stain to identify any Gram-negative diplococci (N. gonorrhoea ) and take swabs for bacteria and Chlamydia. A special Chlamydia swab is required, with the specimen obtained from the everted lid – this must include conjunctival cells and not just exudate. Parents should be warned that the conjunctiva is friable and may bleed after taking the chlamydial swab. If the infant has chlamydial or gonococcal infection, both the mother and her partner require treatment and contact tracing.

Treatment If there is mild to moderate conjunctivitis without a history of maternal vaginal infection, treat empirically with lid hygiene and broad-spectrum topical antibiotic (e.g. ofloxacin 0.3% q.d.s. for 1 week.) until the microbiology results are available.

■N. gonorrhoea : admit and treat with ceftriaxone 25–50 mg/kg i.m. or i.v. o.d. (max 125 mg) if only conjunctivitis. Some advocate a single i.v. injection, others advise 3 days of i.m.