Ординатура / Офтальмология / Английские материалы / Moorfields Manual of Ophthalmology_Jackson_2007
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Recurrent Corneal Erosion
Background Traumatic, dystrophic, or degenerative damage interferes with corneal epithelium–basement membrane adhesion, resulting in recurrent epithelial breakdown (recurrent erosion syndrome). Determining the causative mechanism is important in selecting appropriate therapy. See also persistent corneal epithelial defects (p. 155).
Symptoms Recurrent attacks of pain, tearing, and redness, typically during sleep or at awakening.
History Ask about prior corneal abrasions, especially those from organic material such as a tree branch or finger nail. Ask if there is a family history of recurrent erosions or corneal disease.
Examination Epithelial defects vary from focal superficial punctate keratopathy (SPKs) or immature epithelium (Fig. 5.4), to full-thickness defects. The anterior chamber may have scanty cells. Examine the other eye with fluorescein and retroillumination for signs of a corneal dystrophy.
Differential diagnosis Epithelial basement membrane dystrophy (syn. Cogan’s, or map-dot-fingerprint dystrophy) is the most common cause and often presents with recurrent erosion. Recurrent erosion is also frequent in Thiel-Behnke, Reis-Bücklers, lattice, granular, and Meesman’s dystrophies.
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Fig. 5.4: Recurrent corneal erosion with subsequent |
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subepithelial cysts in the affected area in a patient with |
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map-dot-finger print dystrophy. |
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Recurrent corneal erosion
Management Most cases respond to conservative management with stat G. homatropine 1%, Oc. chloramphenicol and pressure pad, with review in 24 hours if not settled. Repeat if the epithelium has not healed. If not healed in 3 days insert a bandage contact lens (BCL), e.g. ‘Night and Day’, to relieve discomfort and promote healing. Inflamed eyes may better tolerate a BCL if treated with topical NSAID (G. diclofenac 0.1% b.d.) and cylcoplegic (G. homatropine 1% b.d.) for 2 days. Use the BCL for 2–3 months. Cases not responding to padding and BCL may benefit from focal debridement of loose epithelium using a cellulose sponge under topical anaesthesia. Remove any residual strands with plain forceps. Avoid sharp instruments. Focal abnormalities occurring off the visual axis may respond to anterior stromal puncture using the needle on an insulin syringe (bend the tip at 90° to the shaft with tying forceps, leaving a point shorter than the corneal thickness to avoid a corneal perforation): make multiple fine punctures through Bowman layer in the affected area. Use surgical superficial keratectomy or phototherapeutic keratectomy (PTK) for recalcitrant cases, particularly if there is excessive aberrant epithelial basement membrane and subepithelial collageneous pannus (commonest in map-dot- fingerprint dystrophy).
Once healed, prescribe a lubricant ointment at night until asymptomatic for at least 3 months.
Follow-up Review daily until the epithelial defect has closed (see comments above). Those with ocular surface disease, BCLs or on topical steroids are at increased risk of microbial superinfection and require close follow-up.
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Persistent Epithelial Defect
Background Persistent corneal epithelial defects (PCEDs) occur in association with a large and heterogeneous group of ocular and systemic diseases. Detection and treatment of any underlying autoimmune diseases may facilitate corneal healing and avoid potentially lethal vasculitis.
History and examination Look for facial, eyelid, and tear film abnormalities. Test corneal sensation and note the location and size of epithelial defects (usually oval with slightly heaped edges, in the palpebral aperture), the percentage of stromal thinning, and presence of any infiltrate. Exclude the following potential causes:
■Local : eyelid or eyelid margin disease; neurotrophic keratitis; neuroparalytic keratitis (e.g. Bell’s palsy); following corneal infections, burns, and surgery (including keratorefractive procedures); diabetes; skin disease (e.g. acne rosacea; psoriasis); atopic or vernal keratoconjunctivitis; Mooren’s ulcer; staphylococcal marginal ulcer; herpetic keratitis; allograft rejection.
■Systemic : nutritional disorders (e.g. keratomalacia); leukaemia, Sjögren’s syndrome; graft-versus-host disease; collagen vascular disorders (rheumatoid arthritis, ocular mucous membrane pemphigoid, Stevens-Johnson syndrome, relapsing polychondritis, systemic lupus erythematosus, polyarteritis nodosa, Wegener’s granulomatosis).
Treatment Treatment is directed at the underlying cause.
■Discontinue unnecessary topical medications and use ointment that may reduce the shearing forces of the eyelids on the corneal epithelium.
■A low-toxicity unpreserved antibiotic drop or ointment such as chloramphenicol is usually used as prophylaxis against bacterial infection.
■Use preservative-free drops if possible, especially if the patient requires more than six drops daily.
■Manage infiltrates as microbial keratitis (p. 171). Patients on topical steroids may have infection without an infiltrate.
■Treat dry eye with tear substitutes, serum tears, or punctal
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occlusion. Avoid continuous use of hydrogel bandage contact |
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lenses if there is aqueous tear deficiency. The risk of |
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superinfection is high. |
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Persistent epithelial defect
Box 5.2: Applying corneal glue
1.Apply topical anaesthetic, e.g. proxymetacaine 0.5%.
2.Trephine a circular patch of clear plastic from a sterile drape using a 4 mm skin punch. To one side apply a drop of KY jelly. This allows the patch to be picked up using an applicator, such as a cotton-tipped stick.
3.Lift the patch and turn it over. To the other side apply a small drop of cyanoacrylate (e.g. Histacryl) tissue glue.
4.Dry the corneal defect with a cellulose (e.g. Weccel) sponge.
5.Place the patch over the defect, glue-side down. Leave the polythene patch in place.
6.Use a cellulose sponge to confirm that the defect is sealed.
7.Apply a bandage contact lens.
Complications include early loss of glue, neovascularization, and infection. Advise patients not to rub the eye and use preservative-free drops while the contact lens remains in situ. Review within 24 hours. Tectonic corneal grafting may be required if the leak continues.
■If treatment of the underlying disorder and the use of lubricants fails, then consider lid closure with Botox injection (p. 24) or a temporary central tarsorrhaphy with a 4/0 mattress suture and bolster. Human amniotic membrane grafting is an alternative for refractory PCED or if rapid stromal thinning threatens perforation.
■Treat small perforations (<1 mm) with tissue glue (Box 5.2), a contact lens and prophylactic topical antibiotics. For larger perforations, a therapeutic lamellar or penetrating keratoplasty is necessary.
■If all these treatments fail, a conjunctival flap will sacrifice vision but reduces discomfort and ocular inflammation, and promotes healing. If no conjunctiva is available due to scarring, a free buccal mucous membrane graft will usually result in a stable epithelium.
Follow-up Weekly until healed.
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Dry Eye
(Keratoconjunctivitis Sicca)
Background Tear dysfunction occurs in 15–33% of the population with a female preponderance. It may be idiopathic or result from a variety of causes:
■Abnormal wetting (mucin deficiency) : e.g. conjunctival cicatricial disease, trachoma, chemical burns and lid margin disease.
■Aqueous tear deficiency (reduced lacrimal gland function) : postmenopause, autoimmune disease (e.g. Sjögren’s syndrome, rheumatoid arthritis, SLE, sarcoidosis), drug induced (diuretics, topical or systemic beta blockers, antimuscarinics, antihistamines, sedatives, nasal decongestants, opiate based medicines, e.g. some antitussives, analgesics and antidiarrhoeals), corneal anaesthesia, Riley Day syndrome, lacrimal gland disease, lymphoma, HIV, amyloidosis, and irradiation.
■Abnormal spreading and lagophthalmos : reduced blink frequency when concentrating on tasks such as driving, facial nerve palsy, parkinsonism, lid malposition, proptosis, pingeculae, pterygia, and contact lenses.
Symptoms Complex symptomatology may include surface discomfort, photophobia, redness, itch, ropey discharge, eyelid fatigue, and blurred or fluctuating vision. Paradoxically, tear deficiency can cause excessive compensatory lacrimation. Symptom severity may correlate poorly with the signs.
History Enquire about the exact nature of symptoms, relieving and exacerbating factors including the effect of blinking. Take a full medical and drug history, noting the potential causes listed above.
Examination
1.Lids: blink, contour, and lid margin disease.
2.Tears.
■Quantity : The inferior marginal tear strip is usually 0.5– 1 mm high, if <0.5 mm suspect dry eye. Perform the Schirmer I test (p. 147).
■Quality : Look for excessive foam, oils or mucous debris
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(best seen by gently pushing up the lower lid so they can |
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Dry eye (Keratoconjunctivitis sicca)
be viewed against the pupil). Measure the tear film break up time (TBUT).
a.Prior to lid manipulation or any eyedrops, instil a small volume of fluorescien on an applicator strip with unpreserved saline.
b.Ask the patient to blink a few times then stare straight ahead.
c.Use a slit lamp with a broad, tangential, blue beam.
d.The time between a complete blink and the appearance of a corneal tear film defect (dark blue spot) is the TBUT.
e.A normal TBUT is >10 seconds, a TBUT more than the blink interval lacks significance, <1–2 seconds is usually abnormal, suggesting mucin deficiency.
3.Conjunctiva: note any injection, scarring, keratinisation, and symblephara. Fluorescein or rose bengal staining suggest mucin deficiency. Eyes with disturbed tear function quickly become red during examination.
4.Cornea: note the pattern and extent of rose bengal and fluorescein staining, focal abnormal wetting, thinning (dellen), infection, keratinization, scarring, and filaments (strands of mucous and degenerated corneal epithelial cells).
Treatment There is no panacea for dry eye.
■Eliminate underlying causes : Treat meibomian gland dysfunction with warm compresses, lid hygiene, and doxycycline (p. 114). Treat ocular surface inflammation with a weak preservative-free steroid (e.g. prednisolone 0.1–0.5% 2–4 times daily) for 2 weeks. Treat excess mucus with G. N acetyl cysteine 5% q.d.s. Discontinue unnecessary eyedrops, especially those with preservative. If available, use vitamin A for conjuctival keratinization, e.g. G. retinoic acid 0.01–0.1% q.d.s.
■Tear substitutes : Many products are available. Inappropriate, excessive, or long-term treatment may cause intolerance, especially with drops containing preservative, e.g. benzalkonium or cetrimide, that is not diluted by normal tear flow. Limit preservative-containing drops if possible, but if unavoidable use no more than 6 times daily in severe aqueous tear deficiency. For refractory cases autologous serum may be
beneficial but is expensive, time-consuming to manufacture, 158 and can become contaminated.
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Punctal occlusion : This prevents tear drainage and prolongs |
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the effect of tear substitutes. Treat any blepharitis beforehand |
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as occlusion may exacerbate symptoms. Options include |
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temporary collagen or silicone plugs, and permanent surgical |
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occlusion. Try plugs first to assess the therapeutic effect and |
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the risk of epiphora, but note that not all temporary plugs fully |
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occlude the canaliculi and may fail to predict epiphora. Permanent occlusion is achieved by cautery: anaesthetise, insert the tip of a hand-held cautery fully into the canaliculus, activate, then withdraw, denuding the adherent epithelial lining.
■ Contact lenses : Rigid gas permeable scleral contact lenses cover the cornea and most of the conjunctiva, preventing tear evaporation. They also protect from abnormal lids.
Treatment options also depend on disease severity:
■Mild : G. preserved tear substitutes 3–4 times daily (e.g. G. hypromellose 0.3% or G. polyvinyl alcohol).
■Moderate : Unpreserved tear substitute (e.g. G Hypromellose 0.3% unpreserved up to 2 hourly). Use spectacles to reduce evaporation from the surface (about 30% reduction); wrap around spectacles or side shields increase effectiveness.
■Severe : If there is some lacrimation (see Schirmer I Test,
p. 147), occlude the lower punctum with temporary plugs, if not, plug the upper and lower puncti. Consider permanent occlusion depending on the effect. Use hourly unpreserved tear substitute.
■Very Severe : Use hourly unpreserved tear substitutes, such as:
a.Low viscosity: unpreserved hypromellose 0.3%.
b.Gel: unpreserved carbomer, hyaluronic acid.
c.Viscous: carboxymethylcellulose sodium 0.5% solution or ointments.
Consider punctal occlusion (plugs initially), lacrimal stimulation with oral pilocarpine, limbal-fit or scleral gas-permeable contact lenses, autologous serum drops, and tarsorrhaphy.
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Keratoconus
Keratoconus
Background Keratoconus (KC) is the commonest primary corneal ectasia. It is characterized by noninflammatory, central corneal thinning, typically presenting in the second and third decades.
History Ask about blurred vision, rapidly changing spectacle prescription, eye rubbing, and contact lens (CL) wear. Review past refractions if available. Family history exists in ≈8%. Sudden onset of pain, redness, loss of vision, and photophobia suggests hydrops (see below). Many conditions are associated with KC, including atopic dermatitis, vernal keratoconjunctivitis, Down’s syndrome, Ehlers Danlos syndrome, and Laurence-Moon-Bardet-Biedel syndrome, among others.
Examination Corneal changes are nearly always bilateral, but may be asymmetrical. The cornea has a variably shaped cone (Fig. 5.5), that is thinned at the apex. This produces a focal lid convexity in downgaze (Munson’s sign, Fig. 5.5B). The corneal substrate may appear normal but several signs may be present including: a rust-coloured Fleischer ring at the base of the cone (best seen using oblique cobalt blue illumination); Vogt’s striae (deep stromal vertical stress lines); fine subepithelial scarring at the cone apex; a scissor reflex on retinoscopy; an oil drop red reflex; and prominent corneal nerves. Acute rips in Descemet’s membrane occur in ≈5% (higher in Down’s syndrome or allergic eye disease), resulting in a sudden onset of profound stromal hydration (hydrops ).
A B
Fig. 5.5: (A) Keratoconus. (B) Munson’s sign (Courtesy 160 of DH Verity).
Investigation Subtle irregular astigmatism is the first finding. Corneal topography is the most sensitive investigation and may show keratoconus minus (a.k.a. forme fruste) with asymmetric localized steepening of the inferior cornea (Fig. 5.6). Keratoconus plus (anterior keratoconus) is the same plus one or more classic signs.
Treatment
■Astigmatism : Progression is variable but slows with age. When spectacles no longer correct the astigmatism, try rigid gas permeable CLs. Advanced cases with CL instability require keratoplasty or scleral CLs. Keratoconus may rarely recur in the graft. Penetrating or deep anterior lamellar keratoplasty (PK or DALK) are currently the procedures of choice. Epikeratophakia (onlay lamellar keratoplasty) is only rarely used as the quality of vision is poor.
■Scarring : Consider PK or lamellar keratoplasty if scarring limits the corrected VA. DALK avoids the risk of rejection, but the extra interface may degrade the VA. Previous hydrops usually results in a posterior split during lamellar dissection and is an indication for PK.
■Hydrops : Usually resolves in 8–10 weeks but may take 6 months. Offer G. hypertonic sodium chloride 5% q.d.s. and G. homatropine 1% b.d. Examine every 2–4 weeks until resolved. PK may be required if there are no signs of improvement at 3 months, or earlier in corneas that start vascularizing.
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Fig. 5.6: Corneal topography showing keratoconus. |
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Normal astigmatism is shown in Fig. 5.1. |
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Keratoconus
Other corneal ectasias
Pellucid marginal degeneration Onset age 20–40. A characteristic arcuate band of thinning 1–2 mm wide is seen from 4–8 o’clock, located 1–2 mm central to the limbus. There may be marked central corneal flattening along the vertical meridian before inferior thinning is detectible.
Keratoglobus Stromal thinning extends to the peripheral cornea resulting in a globular corneal profile (Fig. 5.7).
Fig. 5.7: Keratoglobus (Courtesy of DH Verity).
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