Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

countries such as the UK, where quinolone resistance is rare. Some streptococcal species are less sensitive to fluoroquinolones. Treat day and night for 2 days then day only. Admit if rapid onset, only eye, risk of perforation, or poor compliance. Otherwise, review with microbiology results in 2 days. If responding, continue treatment unaltered and review in a corneal clinic in 5 days. If improving at that visit, reduce antibiotics to q.d.s. and consider adding G. prednisolone 0.5% q.d.s. to reduce inflammation. Address any precipitating factors. If not responding, consider early review, admission, re-scraping, and altering antibiotics based on sensitivities.

CORNEA 5 Chapter

Fungal keratitis

Fungal Keratitis

History Ask about ocular or systemic disease: candida keratitis is commonest in debilitated patients or those with preexisting corneal disease. Ocular trauma is associated with filamentous fungi, e.g. Aspergillus or Fusarium spp.

Symptoms Unilateral red eye, tearing, and blurred vision. Pain and photophobia are initially mild, but become severe relative to the clinical signs.

Signs The corneal surface typically appears grey with a dry rough texture. Filamentous fungi classically grow in a feathery branching pattern, but may be very rapidly progressive and indistinguishable from bacterial keratitis (Fig. 5.13). Candida produces a small ulcer with expanding infiltrate in a collar-stud configuration, often superimposed on a debilitating corneal condition. There may be an endothelial plaque under the lesion and satellite lesions at the edges. Suppurative keratitis, fibrinoid uveitis, hypopyon, and elevated IOP may occur.

Differential diagnosis Herpes simplex virus, acanthamoeba, and atypical bacterial keratitis, e.g. Nocardia,

Mycobacterium, Propionibacterium.

Investigations Take a corneal scrape for smear and culture (p. 172). The diagnosis can often be made with the smear. Liaise with the microbiologist. If culture negative after 7 days and the patient is not responding, perform a partial-thickness corneal biopsy. This must be large (3 mm) and deep enough to include the affected areas. Send half to microbiology, half in formalin to histology. If available, in vivo confocal microscopy may be diagnostic.

Treatment

■Discontinue any steroid treatment immediately.

■Candida keratitis: G. amphotericin 0.15% (from i.v. preparation) hourly for 5 days then reducing to 4–6 times daily until the disease resolves. Use systemic treatment for peripheral or deep corneal ulceration (e.g. fluconazole

400 mg p.o. stat then 200 mg daily p.o. or i.v.). The frequency of topical therapy is as for candida keratitis above.

■Filamentary fungal keratitis: G. amphotericin (as above) or G. econazole 1%, and itraconazole 100 mg b.d. for deep or peripheral lesions.

■Shield without pad if the cornea is thinned.

■Treat raised IOP.

■Provide cycloplegia and analgesia as required.

Follow-up Initially 1–2 times weekly until there are signs of improvement or deterioration halts. This may take days or weeks. A minimum of 12 weeks’ therapy is required for deep infection. Topical steroids are contraindicated in filamentary fungal infection as they promote fungal growth. Consider keratoplasty if the disease progresses after 2 weeks of optimal therapy; persisting with conservative treatment in this situation will lead to intraocular invasion (without perforation). A therapeutic penetrating keratoplasty is required in ≈25%, enucleation in 3%. Steroids should not be introduced after keratoplasty for 1–3 months because of the risk of recurrance in the host corneal ring. Continue antifungals 4 times daily for several weeks after therapeutic keratoplasty.

CORNEA 5 Chapter

Acanthamoeba keratitis

Acanthamoeba Keratitis

Background Most (85%) cases occur in contact lens wearers. Protozoa may be isolated from contact lenses, water (fresh, salt, tap, swimming pools, hot tubs), dust, soil, or sewage.

History Ask about contact lens cleaning regimen, swimming and showering in lenses, and the use of tapwater to clean lenses. Initially, pain and photophobia are mild; later they are often, but not always, severe relative to the clinical signs.

Examination Signs are usually unilateral and highly variable. The cornea may show superficial punctate keratitis, reduced sensation, and dendritiform lesions. Perineural infiltrates may be peripheral or central. Stromal infiltrates are initially minimal, patchy, and widespread. Focal lesions are uncommon. Paracentral infiltrates may coalesce to form characteristic ring infiltrates (Fig. 5.14). Other features include disciform oedema, scleritis, and mild uveitis. Hypopyon suggests bacterial superinfection.

Differential diagnosis Herpes simplex, fungal, or bacterial keratitis (e.g. Nocardia ).

Investigations A corneal scrape must be taken (p. 172). Culture contact lenses, cases, and solutions. Explain that these will be destroyed in the process. A corneal trephine biopsy may be necessary in culture-negative cases that progress. Confocal microscopy, if available, can be diagnostic.

Treatment Acanthamoeba cysts are highly resistant and in vitro susceptibility correlates poorly with in vivo activity.

■First line: G. PHMB 0.02% or G. chlorhexidine 0.02% hourly, as signs of resolution appear reduce to q.d.s.

■Second line: add G. propamidine 0.1%, G. hexamidine 0.1% or G. metronidazole 0.5% (from i.v. preparation) hourly.

■First and second line drugs are often combined (G. PHMB 0.02% with G. hexamidine 0.1%).

Provide NSAID analgesia. Consider oral steroids and ciclosporin for painful scleritis resistant to treatment with NSAIDs.

Follow-up 1–2 weekly until signs of resolution occur, then monthly as treatment is tapered off. Delay topical steroid use for at least 2 weeks as this may interfere with macrophage activity required to clear cysts. Do not use steroids if the inflammation is subsiding spontaneously.

Herpes simplex keratitis

Herpes Simplex Keratitis

Background Herpes simplex virus keratitis (HSVK) may occur as a primary infection in adults and children, but is more commonly due to reactivation of latent viral infection. Nonocular primary infection may be asymptomatic.

History Ask about potential triggers for recurrence such as UV light, trauma, cold, menstruation, psychological stress, systemic illness, and immunosuppression. Ask about previous labial, genital, or ocular HSV.

Examination Test corneal sensation: hypoaesthesia occurs early. Examine the eye fully, as multiple sites may be involved.

■Primary HSV

Common signs include eyelid rash (clear vesicles on

erythematous eyelids and later crusting), conjunctival follicles (± pseudomembrane), punctate keratitis, subepithelial corneal infiltration or ulceration, dendritic ulcers, and disciform lesions.

■Recurrent HSV keratitis

1.Epithelial HSV: Blotchy, stellate, or a filamentary keratitis usually progresses in 1–2 days to a classic dendritic pattern (branching lesions with feathery edges, and bulbs at the end) (Fig. 5.15). Fluorescein stains the ulcer and rose bengal stains the swollen epithelial cells at the ulcer’s

edge. There may be underlying, slightly larger subepithelial ghost infiltrates. With prolonged infection or steroid use, a geographic or amoeboid ulcer may occur. There may be a mild anterior chamber cellular reaction.

2.Stromal HSV: Three main patterns of disease exist:

a.Disciform ± endotheliitis: A circular area of oedema with minimal infiltrate or vascularization (except in recurrent disease) (Fig. 5.16). Fluorescein staining shows an intact epithelium, pushed forward by the underlying oedema. Oedema also produces folds in Descemet’s membrane. Granulomatous KPs occur under the disciform or elsewhere. There may be anterior chamber cells and the IOP is often raised.

b.Necrotizing interstitial keratitis: typically shows intact epithelium, greyish-white stromal patches, corneal thinning, and neovascularization.

c.Necrotising interstitial keratitis with loss of the epithelium: beware rapid corneal melting. A hypopyon may occur with stromal necrosis or secondary to bacterial superinfection.

CORNEA 5 Chapter

Herpes simplex keratitis

Differential diagnosis

■Epithelial disease: varicella-zoster keratitis, recurrent corneal erosion, healing abrasion, and contact lens pseudodendrite.

■Stromal disease: other causes of interstitial keratitis, acanthamoeba, and bacterial keratitis.

Investigations Viral cultures have an approximate 70% recovery rate if taken within 2–3 days and prior to antiviral therapy (only 4% after treatment).

Treatment

■Lid involvement

In the immunocompetent host, HSV is usually self-limiting. Lid lesions can be treated with warm compresses and Oc. aciclovir 3% t.d.s., or aciclovir 400 mg t.d.s. p.o.

■Epithelial HSV

1.Debride loose epithelium using topical anaesthetic and a cotton wool swab. Instil G. homatropine 1%, Oc. chloramphenicol and pad overnight. Avoid if there is stromal involvement.

2.Oc. aciclovir 3% five times daily for 14 days or for 7–10 days after healing. Treatment may initially aggravate subepithelial ghosting. This usually fades within a year and does not require steroid therapy.

3.Treat mild uveitis with G. homatropine 1% b.d.

4.While ulceration persists use G. chloramphenicol q.d.s. as prophylaxis against bacterial superinfection.

5.Do not use topical steroids.

■Stromal HSV

1.Steroids may be unnecessary for disciform HSVK as some episodes resolve spontaneously. Epithelial breakdown during steroid use can lead to rapidly progressive corneal thinning.

2.If steroids are necessary (e.g. failure of antiviral therapy, moderate to severe involvement, raised IOP) use G. prednisolone 1.0% q.d.s. or G. dexamethasone 0.1% q.d.s.

3.Prescribe Oc. aciclovir 5 times daily or aciclovir 400 mg t.d.s.p.o.

4.Prescribe G. chloramphenicol q.d.s. if there is an epithelial

Herpes zoster ophthalmicus (Ophthalmic shingles)

Herpes Zoster Ophthalmicus

(Ophthalmic Shingles)

Background Years to decades after primary varicella infection (chickenpox), latent virus in the trigeminal ganglion may reactivate. This produces eye disease and frontal/eyelid/nasal rash (ophthalmic division, V1).

Symptoms Headache, fever, malaise, chills, and neuralgia. Ask about precipitating factors such as physical trauma, surgery, immunosuppression, and systemic illness.

Signs Multiple sites may be involved.

■Skin/lids: crops of clear vesicles on inflamed hyperaesthetic

skin with V1 distribution, typically occurring 2 days after neuralgia. Vesicular fluid becomes turbid and remains contagious until scabbed (Fig. 5.17). Occasionally dermatitis does not develop.

■Conjunctiva: a follicular or papillary conjunctivitis is extremely common.

■Episclera/sclera: focal inflammation.

■Cornea: keratitis develops in ≈65% of patients, often with a marked decrease in corneal sensation and a varied appearance. Fine or coarse punctate epithelial keratitis occurs. ‘Dendrites’ differ from those of herpes simplex virus (p. 178) in that they are fine, greyish, nonulcerated, elevated, linear