Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007

Peripheral Corneal Thinning

Background Peripheral ulcerative keratitis (PUK) is often idiopathic (Mooren’s ulcer) or may be associated with rheumatoid arthritis (RA) and type III autoimmune diseases (polyarteritis nodosa, relapsing polychondritis, Wegener’s granulomatosis).

Examination Scleritis is absent in Mooren’s ulcer, variably present in RA, and severe, usually necrotizing, in autoimmune diseases. PUK is destructive, beginning peripherally and progressing centrally, circumferentially, and posteriorly, leaving thinned neovascularized cornea.

Differential diagnosis See table 5.1.

Investigations PUK may be the presenting feature of potentially fatal systemic, vasculitic disease. Check cANCA, pANCA, RhF, ANA, ENA, ESR, CRP, sACE, CXR, and urine for protein and casts.

Treatment Involve senior clinicians. Unilateral Mooren’s ulcer may resolve with surgery (conjunctival resection/tissue glue), bandage contact lenses, topical treatment (steroids, acetylcysteine, antibiotic), and oral doxycyline. Severe or bilateral Mooren’s ulcer and PUK associated with type III autoimmune disease requires systemic immunosuppression.

Follow-up Aim for 1 year of remission (and ANCA normalization in Wegener’s granulomatosis) then taper immunosuppressants. Monitor for side effects of systemic treatment (p. 343). ‘Burnt-out’ Mooren’s ulcer may reactivate with cataract or corneal graft surgery, so immunosuppress beforehand.

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Peripheral corneal thinning

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Chapter5CORNEA

Interstitial Keratitis

Background A corneal stromal inflammation without epithelial loss, usually caused by an immune reaction to trapped antigens. Interstitial keratitis (IK) is a sign rather than a diagnosis. It may be necrotising or non-necrotising. Causes are listed in Table 5.2.

Symptoms Red eye, irritation, tearing, photophobia, and reduced VA if the visual axis is involved.

History Ask about previous episodes (especially herpetic eye disease), sarcoidosis, maternal syphilis (congenital syphilis may present age 5–20), previous sexually transmitted infection (syphilis, chlamydia), reduced hearing (syphilis, Cogan’s syndrome), foreign travel (parasites), rashes (measles, mumps, syphilis).

Examination

Face Look for features of congenital syphilis (saddle nose; frontal bossing; Hutchinson’s triad of IK, notched upper central incisors and sensorineural deafness), or leprosy (loss of temporal eyebrow; hypopigmented/anaesthetic skin patches). Herpes zoster ophthalmicus (HZO) may have frontal scarring.

Conjunctiva Exclude follicular conjunctivitis (chlamydia).

Cornea Bilateral or unilateral? (Mycobacteria spp, mumps, HSV, HZV, acquired syphilis, congenital syphilis may initially have unilateral onset). Focal (HSV disciform lesions), multifocal (HZO nummular keratitis) or diffuse (greyish pink ‘salmon patch’ of syphilitic IK) distribution. Check IOP. Long-standing IK results in stromal scarring with deep neovascularisation or ghost vessels.

Anterior chamber Granulomatous uveitis may occur.

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Interstitial keratitis

Pupil/iris Nodules (leprosy, sarcoidosis), miosis (syphilis, secondary to uveitis).

Fundus Salt and pepper chorioretinopathy of syphilis. Optic atrophy.

Differential diagnosis Acanthamoeba, fungi, or low virulence microbial keratitis with epithelial healing e.g. Nocardia.

Investigations Check syphilis serology; sACE (sarcoid); CXR (TB, sarcoid); tuberculin skin test; hearing (Cogan’s syndrome, congenital syphilis, leprosy). Other tests as indicated.

Treatment Prescribe topical steroids (e.g. prednisolone 0.5% q.d.s.) and cycloplegia as required. Treat the underlying cause and any elevated IOP. Treatment of syphilis does not affect the course of IK.

Follow-up Depends upon underlying cause e.g. IK of congenital syphilis lasts 3–4 weeks. Residual scarring may necessitate corneal grafting. Beware recurrence in the graft.

Phlyctenulosis

A type IV hypersensitivity reaction historically associated with tuberculosis, but now with staphylococcus, herpes simplex virus (HSV), and varicella-zoster virus (Fig. 5.10). Granulomatous lesions form at the limbus and ulcers develop within a few days. Treatment with topical steroids causes involution in 2–4 days e.g. prednisalone 1% b.d., then taper. Treat associated staphylococcal lid disease with topical antibiotic and lid hygiene, and add oral aciclovir for HSV.

Fig. 5.10: Phlycten.

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Marginal keratitis

Marginal Keratitis

Patients with staphyloccal disease of the eyelids or conjunctiva may present with small superficial round infiltrates as an immunological response to the organism or its toxins (Fig. 5.11). Initially, the epithelium is intact, but may later break down. No culture is required. The infiltrates resolve with topical steroids (e.g. G. prednisolone 0.5% q.d.s.) and lid hygiene, followed by topical antibiotic ointment to the lid margin (e.g. Oc. fucithalmic b.d.). Taper treatment according to response.

Fig. 5.11: Marginal keratitis.

Bacterial Keratitis

Symptoms Unilateral red eye, discharge, tearing, and blurred vision.

History Ask about onset, progression, treatment, level of discomfort, trauma, contact lens wear, and ocular or systemic disease.

Examination Examine adnexae, eyelids, conjunctiva, and cornea of both eyes for predisposing factors, e.g. dry eyes. Draw the size, location, depth, shape and colour of corneal infiltrate. Test corneal sensation. Perform Seidel’s test (p. 147) if perforation is suspected. Document anterior chamber cellular activity, including the size of any hypopyon. These are usually sterile unless Descemet’s membrane has been breached (Fig. 5.12).

A

B

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Bacterial keratitis

Differential diagnosis Consider herpes simplex, acanthamoeba keratitis, or fungal keratitis, sterile peripheral infiltrates from contact lenses, and phlyctenular keratitis. Rarer causes of progressive infection include anaerobic bacteria (propionobacterium, capnocytophaga), Nocardia, mycobacterium (particularly post-LASIK), and microsporidia.

Management Perform a corneal scrape (Box 5.3) to guide therapy, remove debris, and improve antibiotic penetration. Prescribe regular cycloplegia (e.g. G. homatropine 0.5% b.d.). If the cornea is thinned, apply a shield, without padding. Start empiric therapy with G. cefuroxime 5% and gentamicin 1% hourly, 30 mins apart, or alternatively G. ofloxacin 0.3% hourly in

Box 5.3: Taking a corneal scrape

1.Liaise with microbiology staff. Request an urgent Gram stain.

2.Warm refrigerated media to room temperature.

3.Instil G. proxymetacaine 0.5% then G. amethocaine 1%.

4.Explain the procedure.

5.At the slit lamp, use a Kimura spatula, No. 15 Bard Parker blade, or 20-gauge needle to remove superficial debris from the ulcer, and then scrape the edges and base.

6.Streak material onto two glass slides for Gram and Giemsa staining (or other preferred stain). Air dry and label with pencil.

7.Take additional scrapes, one for each culture medium. Streak material onto agar plates without breaking the surface. Flame the blade and cool for 20 seconds between scrapes, or select a fresh needle.

8.Plate onto blood agar, chocolate agar, and Sabouraud’s agar.

9.If acanthamoeba is suspected, streak onto the centre of a nonnutrient agar plate.

10.Tape covers onto the plates to prevent evaporation.

11.Inoculate brain–heart infusion and cooked meat broth by agitating the blade or needle in the media, (or by dropping a sterile cotton swab into the media).

12.Culture contact lenses, cases, and solutions. Document that the patient understands these will be destroyed in the process.

13.Label all material, and transport immediately to the laboratory.

14.Cultures may be positive in 24 hours, but can take up to 3