Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007
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and await symptomatic improvement over 2–4 weeks. Conjunctival follicles may last for months and corneal infiltrates persist for months to years. Significant conjunctival scarring is rare.
Trachoma
Background Caused by immunotypes A–C. Rare in the developed world but endemic to North Africa, the Middle East, India, and Southeast Asia. Usually self-limiting but repeated infection leads to conjunctival cicatrization and corneal scarring.
Clinical features Acute infection begins 5 days after inoculation as a bilateral follicular, nonpurulent conjunctivitis. After 2–3 weeks follicles appear on the superior tarsal conjunctiva and superior limbus. The diagnosis of trachoma requires at least two of the following:
■≥ 5 follicles on the superior tarsal conjunctiva
■Limbal follicles or their sequelae (Herbert’s pits, Fig. 4.10)
■Tarsal conjunctival scarring
■Vascular pannus.
There may be tender preauricular lymphadenopathy.
Management Infection provides no immunity, so endemic areas require control with community health education and mass treatment. Surgery may be required for lid deformities such as entropion and aberrant lashes, or severe corneal opacity.
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Fig. 4.10: Herbert’s pits (Courtesy DH Verity). |
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Allergic conjunctivitis
Allergic Conjunctivitis
Allergic conjunctivitis includes acute allergic conjunctivitis, seasonal allergic conjunctivitis (SAC), perennial allergic conjunctivitis (PAC), vernal keratoconjunctivitis (VKC), atopic keratoconjunctivitis (AKC), drop hypersensitivity, and contact lensassociated papillary conjunctivitis (CLPC), of which giant papillary conjunctivitis (GPC) is the most severe and drop hypersensitivity.
Acute, seasonal, and perennial allergic conjunctivitis
Background Allergic conjunctivitis, often (70%) associated with atopy or a family history of atopy.
History Ask about major (hayfever, asthma, atopic dermatitis, eczema) and minor (idiopathic urticaria, nonhereditary angioedema, food allergies) atopies. Seasonal symptoms include ocular itch, tearing, often with allergic rhinitis (sneezing and nasal congestion). Acute reactions may occur, with marked conjunctival swelling as well as systemic reactions.
Examination Ocular inflammation is usually mild with lid erythema, conjunctival oedema, papillae, and increased tear film mucus. Acute allergic reactions may produce profound chemosis with pale, boggy conjunctiva ballooning over the eyelid margins.
Treatment Acute allergic swelling of the conjunctiva can be reduced with cool compresses and G. adrenaline 0.1% stat. For recurrent allergic conjunctivitis attempt to eliminate the allergens and advise cool compresses. During periods of antigen exposure, prescribe topical mast cell stabilizers (e.g. G. nedocromil b.d.), antihistamines (e.g. G. emedastine 0.05% b.d.), or a combined mast cell stabilizer and antihistamine (e.g. G. olapatidine 0.1% b.d.). Prescribe systemic antihistamines, e.g. loratidine (Clarityn) 10 mg o.d. p.o.
Follow-up Two weeks if necessary
Vernal keratoconjunctivitis (spring catarrh)
Background A rare but serious form of chronic allergic 124 conjunctivitis. Most common in males, aged 5–15 years,
Fig. 4.11: Cobblestone papullae in severe vernal keratoconjunctivitis.
particularly Arabs and Afro-Caribbeans. Management can be challenging.
History There is frequently a family or personal history of atopy. Symptoms typically occur annually in spring or summer but may persist throughout the year. Itch is the main symptom but ropey discharge, photophobia, and pain occur.
Examination A mild mechanical ptosis may be present. Evert the lids and look for large pleomorphic, irregularly distributed cobblestone papillae (Fig. 4.11), more pronounced than in the lower tarsal conjunctiva. Follicles or scarring are rare. There may be Tranta’s dots (chalk-white, raised, superficial infiltrates straddling the limbus) (Fig. 4.12). The conjunctiva may have a pinkish tinge and mild oedema. Mucous strands are thicker and more ropey than in SAC. Superficial punctate keratitis, epithelial macroerosions or ‘shield’ ulcers (Fig. 4.13), plaques or subepithelial scarring may occur.
Treatment Initial treatment includes cool compresses, lid hygiene for blepharitis, antigen avoidance, and artificial tears or saline for antigen dilution. For mild to moderate VKC consider: mast cell stabilizers (e.g. G. nedocromil sodium b.d. or lodoxamide b.d.); H1 antihistamines, e.g. emedastine 0.05% b.d.; combined antihistamine/mast cell stabilizers, e.g. olopatadine 0.1% b.d. For more severe flare-ups use short-term G. fluoromethalone 0.1% t.d.s., or dexamethasone 0.1%/prednisolone 1% titrated against the disease severity, with regular IOP assessment. Trials show that topical ciclosporin (various formulations) is very effective without
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Allergic conjunctivitis
Fig. 4.12: Trantas dots (Courtesy of DH Verity).
Fig. 4.13: Vernal shield ulcer (Courtesy of DH Verity).
the side effects of steroids, but tolerance is a problem with preparations dissolved in oils. Ciclosporin (and mast cell stabilizers) are poorly tolerated during disease exacerbations and can be introduced as soon as the disease has been partially controlled with steroids. Rarely, systemic therapy with steroids and sometimes ciclosporin is needed; aspirin may be helpful in older children. Shield ulcers (vernal plaques) may heal spontaneously
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epithelial defect persists, peel off the vernal plaque with a crescent blade and the control the disease to promote healing.
Follow-up Review every 1–2 weeks until inflammation is controlled, then 3 monthly. Corneal scars (from plaques), steroidinduced glaucoma, and cataracts are the causes of visual loss in VKC, which resolves after puberty in 90% of cases.
Atopic keratoconjunctivitis
Background Severe atopic conjunctivitis associated with keratitis.
History Ask about ocular itch, burning, foreign body sensation, tearing, and mucoid discharge.
Examination Look for eyelid dermatitis, chronic blepharitis, conjunctival oedema, papillae, and increased mucus in the tear film and inferior fornix. Cicatrizing conjunctivitis may develop with chronic inflammation, as may corneal scarring, vascularization, and visual loss.
Treatment Treat as for VKC. Care of periocular skin is also very important. Moisturize with E45 cream or aloe vera b.d. Use topical steroids (e.g. 1% hydrocortisone skin ointment o.d. b.d.), with care due to the risks of systemic absorption, depigmentation, and superinfection. Tacrolimus 0.03% ointment may be effective for severe atopic eyelid disease.
Follow-up Every 2 weeks until inflammation is controlled then 3 monthly, often long-term.
Contact lens-associated papillary conjunctivitis (including giant papillary conjunctivitis)
Background Most commonly seen in contact lens and prosthesis users where the papillae are often small. CLPC shares the conjunctival features of VKC and AKC but without corneal involvement. Giant papillary conjunctivitis (GPC) is the most severe form but is rarely seen since the widespread use of disposable and frequently replaced contact lenses (Fig. 4.14). GPC is more common in prosthesis users and as a result of broken or protruding sutures.
History Contact lens wearers may report decreasing lens tolerance and mucous discharge. Ocular itch may occur. Ask about contact lens wear and cleaning regimen (p. 207).
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Allergic conjunctivitis
Fig. 4.14: Giant papillary conjunctivitis (Courtesy of DH Verity).
Examination Evert the eyelid and look for hyperaemia, infiltrate, and papillary response (best seen using 2% fluorescein drops). Giant papillae are those >1 mm. There may be epithelial erosion of the apices of the papillae and mucus trapped between the papillae. Examine contact lenses for damage.
Treatment Replace damaged lenses. If the patient must wear contact lenses, reduce the wearing time and optimize the lens cleaning regimen, including frequent (2–4 times weekly) protein removal. Daily disposable lenses, different lens material or edge design, and mast cell stabilizers may help. Remove broken sutures. Ocular prostheses can be repolished and coated. Treat any associated atopic conjunctivitis.
Follow up Review contact lens wearers in clinic only if symptoms persist. Ensure patients remain under regular review by their contact lens practitioner if they are not under medical review.
Drop toxicity (contact hypersensitivity)
Background A relatively common condition, particularly with certain drops including neomycin and atropine; however, prolonged treatment with any preserved (especially benzalkonium chloride) drop may result in a type IV contact hypersensitivity.
History Ask about itch and periocular rash. List all topical 128 medications.
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Fig. 4.15: Contact hypersensitivity secondary to eyedrops.
Examination Look for erythematous, dry, scaly dermatitis, particularly in the lower lid but often extending to the cheek (Fig. 4.15). There is diffuse conjunctival injection with follicles, especially in the lower fornix. The cornea is rarely involved.
Investigation Occasionally, patch testing is required.
Treatment Advise cool compresses, withdraw offending medication where possible, or replace with preservative-free drops. Rarely, dermal steroids (e.g. 0.5% hydrocortisone ointment b.d. for 5 days) are required.
Follow-up If the offending agent is withdrawn the dermatitis settles in a few days. Review any changes in long-term ocular medications as required.
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Stevens-johnson syndrome (erythema multiforme)
Stevens-Johnson Syndrome
(Erythema Multiforme)
Background A type III immune reaction most commonly affecting children, adolescents, and young adults. Circulating immune complexes trigger a skin reaction 7–14 days after stimulation. Although self-limiting, there is significant mortality and morbidity.
History Ask about fever, malaise headache, loss of appetite, nausea, vomiting, and skin rash. Try to identify the precipitating agent:
■Drugs: sulfonamides (dorzolamide, acetozolamide), sulfonylureas (chlorpropamide), antiepileptics (barbiturates, phenytoin, carbamazepine), chlorpromazine, thiazide diuretics, allopurinol, salicylates, codeine, antibiotics (tetracycline, penicillin, chloramphenicol).
■Infection: viral (herpes simplex, mumps, vaccinia), bacterial (streptococci, tuberculosis, yersinia, orf), and fungal (histoplasmosis).
■Connective tissue disease: rare.
■Malignancy: rare.
■Idiopathic: 50% of cases.
Examination Symmetrically distributed target lesions (papules with central pallor/erythematous surround or central erythema/ pale surround) spread proximally along the limbs, with bullae on the back of hands, palms, forearms, feet and soles, or dependent parts in prostrated patients (Fig. 4.16). Nasal and oral mucosa is most commonly affected by ruptured bullae and haemorrhagic crusting (Fig. 4.17). The vagina and anus may be affected. Look for bilateral conjunctivitis ± bullae. There may be superficial punctate keratopathy, mild anterior uveitis, and occasionally panophthalmitis.
Treatment Remove known precipitating factors. Supportive treatment by physicians includes fluid management, systemic antibiotics, and skin care. Ophthalmic care includes G. atropine 1% o.d. and G. chloramphenicol q.d.s.; the value of topical steroids in the acute phase is uncertain and may promote infection. The use of oral prednisolone (80–100 mg o.d.) is controversial. Immunosuppression is contraindicated. Treat tear
130 deficiency with tear substitutes, e.g. G. hypromellose 0.3%
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Fig. 4.16: Target lesion in Stevens-Johnson syndrome (Courtesy DH Verity).
Fig. 4.17: Stevens-Johnson syndrome (Courtesy of DH |
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Stevens-johnson syndrome (erythema multiforme)
preservative free, 1–2 hourly, punctal occlusion, and moisture chambers as required.
Follow-up Review daily as an inpatient. Treat symblepharon formation (maintain the fornices by removing inflammatory debris and separating symblephara with glass rods and forceps). Exclude IOP rise and corneal ulceration. Taper any topical steroids and antibiotics after eye lesions have settled. Review weekly for 1 month, then as required. May fully resolve but possible sequelae include keratinized lid margins, dry eyes, eyelid deformities, conjunctival and corneal scarring. Late recurrences are probably infrequent but include recurrent conjunctival inflammation, late cicatrizing conjunctivitis, and late sclerokeratitis, all of which can exacerbate surface failure.
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