Ординатура / Офтальмология / Английские материалы / Medical Contact Lens Practice_Millis_2005

stroma surrounded by clear cornea, whereas Pseudomonas causes irregular ulcers with a ragged edge and a thick exudate, and may form a large ulcer resulting in perforation in hours. Escherichia coli and Serratia marcescens form gray ulcers that may be surrounded by stromal rings caused by endotoxins.

Fungal infections

Fungal infections are most often due to Candida (a yeast), Aspergillus or Fusarium spp, and may be found on contact lenses lacking proper care. The mycelia extend into the lens matrix from where they may involve the cornea. They produce a gray–white, fernlike nonstaining lesion that extends into the stroma.

Figure 9.7 Herpes simplex infection resulting in corneal thinning.

Acanthamoeba

Acanthamoeba infections are discussed in Chapter 6.

Viral keratitis

Herpes simplex

Transmission of the cold sore virus may be due to close contact with someone with lesions on the lips or from hand–eye transmission from genital infection. The initial infection usually occurs in babies and young children. The virus travels up the sensory nerve to the trigeminal ganglion, where it is inactive until illness or trauma reactivates it. It then travels along the nerve to the lips or eye to produce a clinical infection.

In primary ocular herpes simplex vesicles occur on the eyelids and round the eye. They eventually rupture and form crusts, and finally heal. Punctate epithelial lesions occur on the cornea (Fig. 9.7), and may be followed by linear, branching dendritic ulcers that stain with fluorescein or Rose Bengal (Fig. 9.8). Subepithelial infiltrates appear after 2–3 weeks, and may persist for several weeks. In some cases a disciform keratitis may develop with central epithelial and stromal edema, folds in Descemet’s membrane and a mild uveitis.

In the UK treatment is with topical antiviral drops or ointment such as acyclovir 3%. Elsewhere trifluorothymidine (1% drops) may be used, but

Figure 9.8 Dendritic ulcer staining with Rose Bengal.

are more toxic to the epithelium than acyclovir. I there is a dendritic ulcer the antiviral should b prescribed five times a day until healed, and then three times a day for 5 days. If there is stroma involvement the drug should be used five time a day for 3 weeks, then three times a day fo 2 weeks.

Corticosteroids are only used if there is no response to the antiviral, if the patient is atopic, o the attack lasts longer than 3 weeks. Cortico steroids should be withdrawn very slowly ove 6–9 months, with a very gradual reduction in th strength of the drops. It may be necessary to main tain treatment for a year or more.

Severe herpes simplex keratitis may requir systemic antiviral treatment.

Herpes zoster infection

Herpes zoster is caused by the same virus that causes chickenpox. Skin lesions form in the distribution of the first division of the trigeminal nerve (cranial nerve V), and these rupture and form crusts.

Herpes zoster infection causes conjunctivitis, episcleritis, scleritis, keratitis, uveitis and glaucoma. In the cornea there are punctate lesions, which stain with fluorescein, and these are followed by dendritiform lesions, which are wider and situated more peripherally than those of herpes simplex.

Fine granular deposits form beneath Bowman’s layer (nummular keratitis), and this may progress to a disciform keratitis. Herpes zoster may cause an anesthetic cornea and care should be taken to assess corneal sensation before instilling topical anesthetic drops or refitting a lens.

Systemic antiviral drugs are useful only in the early stages of the skin rash. If given then they can help to reduce postherpetic neuralgia. Topical acyclovir is helpful if the conjunctiva is injected, there are pseudodendritic ulcers, or nummular or disciform keratitis. Topical corticosteroids may be needed to prevent scarring and complications. If used they need to be withdrawn slowly over several months.

Postherpetic pain (neuralgia) can be very severe and may persist for years. It can be reduced by early acyclovir and topical agents (e.g. capsicum cream). Patients should receive analgesics and if necessary be referred to a pain clinic. Pain may be so severe that some patients may need antidepressants.

eventually affect the central cornea and reduce vision. The cornea thins and may perforate.

Treatment is with eyelid hygiene, topical corticosteroids and systemic tetracycline.

Episcleritis

The episcleral vessels lie beneath the conjunctiva, in Tenon’s capsule and radiate from the limbus. They can be moved with a sterile cotton bud over the sclera.

Episcleritis is a relatively common mild inflammation, which usually resolves spontaneously, but causes concern because of the obvious redness. It may be asymptomatic or there may be discomfort, tenderness, watering, and mild photophobia. Hyperemia may be localized or generalized, with swelling of the episclera, or less commonly, a nodule may form (Fig. 9.9). In a minority of cases the condition is associated with rheumatoid arthritis and can cause dellen due to drying of the adjacent cornea.

Most cases resolve spontaneously, but a topical nonsteroidal anti-inflammatory is useful, or topical corticosteroids may be given, but these are often unnecessary, and may lead to rebound redness on withdrawal.

Scleritis

Inflammation of the sclera is much less common, but can permanently damage sight. It is due to an immune-mediated inflammation of the blood

vessels, which destroys the sclera. It is associated with pain, which is often severe and may be worse at night, and tenderness of the globe. Dilated vessels are integral to the sclera, cannot be moved with a sterile cotton bud, and tend to be deep red or purplish in color. The nodular form may be confused with nodular episcleritis, but does not move on the underlying sclera. Necrotizing scleritis may cause scleral melting and perforation.

Anterior uveitis

Uveitis (Fig. 9.10) is idiopathic in most cases, but may result from injury to the uvea, or be secondary to systemic disease (e.g. ankylosing spondylitis, sarcoidosis or infection by microorganisms).

The patient complains of pain, photophobia and decreased vision. On examination there is circumcorneal injection, often with a small pupil,

which may be adherent to the anterior lens cap sule if the inflammation is severe or has persisted for some time. When such a pupil is dilated it wil appear festooned by posterior synchechiae, which are adhesions that form between the iris and the anterior lens surface. There are cells in th anterior chamber, which can be seen moving within the convection currents in the aqueous; they should be graded 0–4 to assist in monitoring th condition.

Collections of inflammatory cells (keratitic pre cipitates) may form on the endothelium, which gradually becomes pigmented and crenated. In severe cases a sterile hypopyon, consisting o inflammatory cells, forms in the anterior chamber.

The pupil should be kept dilated with a mydri atic and the inflammation reduced with topica corticosteroids such as dexamethasone eye drops In severe cases corticosteroids may need to b administered hourly. A careful check should b kept on the intraocular pressure.

(A)

(B)

Figure 9.10 A: Endothelial dusting in acute anterior uveitis. B: Medium-sized keratitic precipitates.

Primary angle-closure glaucoma

Primary angle-closure glaucoma (PACG) is char acterized by a shallow anterior chamber and narrow drainage angle. It is related to lens size which increases throughout life, leading to a shal low anterior chamber. Hyperopic eyes with short axial length and small corneal diameters and an anteriorly placed lens are at greatest risk o PACG.

An acute attack arises when there is a sudden total angle closure with a very raised pressure The eye is red and painful with reduced vision The patient may feel very unwell and may suffe nausea and vomiting and complain of haloe round lights at night. There is ciliary conjunctiva injection with a very raised intraocular pressure corneal edema and a very shallow anterior cham ber. Flare and cells may be visible in the anterio chamber, but there are no keratitic precipitates The pupil is fixed, mid-dilated, and vertically ova and does not react to light or accommodation.

The patient requires immediate referral fo intensive miotic therapy to lower the pressure, fol lowed by bilateral peripheral iridectomies. Failur to refer as an emergency may result in permanen loss of vision.

1.Coroneo MT, Di Girolamo N, Wakefield D. The pathogenesis of pterygia. Curr Opin Ophthalmol 1999;10:282–288.

2.Frucht-Pery J, Solomon A, Siganos CS, et al. Treatment of inflamed pterygium and pinguecula with topical indomethacin 0.1% solution. Cornea 1997;16:42–47.

CHAPTER CONTENTS

Histopathology 103 Pathogenesis and etiology 104 History 104

Personality 104 Clinical findings 104

Management of keratoconus 106 Complications of lens wear in

keratoconus 108 References 108 Further reading 109

Keratoconus is a noninflammatory degeneratio of the central or paracentral cornea of unknow etiology. It is characterized by the formation of localized protrusion (ectasia) and thinning of th stroma, which is greatest at the apex of the cone and results in increasing, irregular astigmatism The disease is usually bilateral, although it ma commence earlier in one eye than the other, an one eye may be more severely affected than th other.

There is a family history in 6–8% of cases, but i most there is no definite pattern of inheritance Nevertheless topography may reveal subclinica evidence of the disease in other members of th family.

Keratoconus commences in the teens and earl twenties, and progresses slowly, but may cease t progress at any time, and many cease to progres after 40 years of age. There is a low recurrence rat after keratoplasty.

HISTOPATHOLOGY

All layers of the cornea are affected. There ar breaks and irregularity in Bowman’s membrane which are greater in oval sagging cones than i small central cones. There is stromal thinning an deposition of iron in the basal layer of the epithe lium at the base of the cone. In more severe cases folds and breaks occur in Descemet’s membrane which is duplicated at the site of the break. Acut hydrops may occur and scars form.

PATHOGENESIS AND ETIOLOGY

The etiology of keratoconus is unknown, but recent work has suggested that endogenous toxic substances or metabolic breakdown products accumulate in the cornea.1,2 These may damage corneal cells so that apoptosis occurs. Apoptosis is a controlled form of cell death used by an organism to rid itself of unwanted cells without the release of degradative enzymes and other cellular elements that would damage surrounding tissue and cells.3 Apoptosis is found in keratoconus, especially in the anterior stroma, near the breaks in Bowman’s membrane. Those cells that are not permanently damaged undergo repair, and may result in scar formation.

Atopy, including a family history of atopy has been associated with the disease.4

HISTORY

A history of atopy and allergic eye disease can mean that lens tolerance is reduced and earlier surgery is required. Conditions associated with keratoconus include vernal conjunctivitis, atopic dermatitis, tapetoretinal degeneration (including retinitis pigmentosa), systemic collagen disorders and genetic conditions such as Down’s syndrome.

conclusive evidence has been found. Nevertheless some of these patients appear very anxious. This is understandable if one considers that they have poor vision from a young age, often associated with other distressing diseases, and they have careers to consider. They are also concerned that they may be unable to drive and take part in activities that are normal for their age.

Rigid lenses are often necessary to obtain the best visual acuity and many of these patients find them difficult to tolerate. It helps to show the patient their topography map, when the problems faced by the clinician can be demonstrated, and an explanation for the choice of lens can be given.

CLINICAL FINDINGS

Visual acuity

Increasing irregular astigmatism results in a progressive, painless loss of vision that cannot be corrected by spectacles. Contrast sensitivity is affected before visual acuity measured by a Snellen chart, and patients may therefore complain of poor vision while apparently seeing well by normal means of testing. Retinoscopy is characterized by a distorted, “scissors” reflex.

PERSONALITY

Several papers5–7 have explored the possibility of a particular personality trait in keratoconus, but no

Cone

The cone may be a small, round, “nipple” cone (Fig. 10.1) or a larger oval, sagging, cone (Fig. 10.2). It

commences in the inferotemporal quadrant of the cornea and extends through the inferonasal, superotemporal to the superonasal quadrant, which is affected last. As the ectasia extends below there is a compensatory superior flattening.

The keratometry and Placido’s disc mires are distorted. Steepening of the cornea is reflected in disc rings that are closer together. Keratometry readings (K-readings) become increasingly steep as the disease progresses, and the mires become progressively distorted, until they are no longer within the range of the instrument.

Videokeratography can identify subclinical disease, will demonstrate the site, size and shape of the cone, and may provide assistance with contact lens design. If the design needs to be discussed with the laboratory it may help to send them a numeric topography map. In keratoconus, axial and instantaneous maps differ significantly in apical position and curvature. Instantaneous maps are better at representing shape, and axial maps are more useful to predict the base curve when fitting RGP lenses.8

Fleischer’s ring

Fleischer’s ring is a yellow–brown deposit of iron in the basal layer of the epithelium that encircles the base of the cone, but is often incomplete above. It arises where the tear film is stagnant and its iron is taken up by the epithelium. It is best viewed with

the cobalt light on the slit lamp. An incomplete ring may be easier to see using retroillumination.

Vogt’s striae

In all, but the earliest cases fine vertical stress line or striae (Vogt’s striae, Fig. 10.3) may be found in the deep stroma. They disappear if finger pressur is applied through the eyelid.

A recent report associates the presence of Vogt’ striae, Fleischer’s ring or corneal scarring and increased corneal steepening.9

Tears in Descemet’s membrane

Tears in Descemet’s membrane may result in edema and, more rarely, acute hydrops when

Figure 10.3 Scarring and Vogt’s striae.

aqueous enters the stroma posteriorly. It resolves spontaneously, but leaves a scar at the base of the affected area. However the visual acuity may be less affected than one might suppose due to flattening of the cone. In some patients, particularly those with allergic or inflammatory eye disease, topical corticosteroids are needed to prevent corneal vascularization.

Munson’s sign

Munson’s sign is the V-shaped deformation of the lower eyelid caused by the cone, and is seen on downward gaze in moderate to severe cases.

Rizzuti’s sign

Lateral illumination of the cornea results in a sharply focused beam at the medial limbus.

MANAGEMENT OF KERATOCONUS

Spectacles are worn as long as the visual acuity is adequate. Patients with only one affected eye, or in whom one eye is much less affected than the other, may be happy to continue with spectacles, but should be kept under regular supervision. If the vision in the affected eye is fairly good with spectacles there is often insufficient motivation for the patient to build up the wearing time with a rigid lens.

For those in whom visual acuity deteriorates, contact lenses are prescribed. Although these patients are difficult to fit, a wide variety of lenses and fitting techniques is now available, and many patients with keratoconus can maintain good vision and do not require surgery. If contact lens correction is not sufficient then penetrating or lamellar keratoplasty should be considered.

Contact lens correction

Keratoconus is usually managed with RGP lenses although a few patients with early disease who cannot tolerate rigid lenses may prefer to have slightly reduced acuity and wear a soft toric lens. This can be satisfactory if the demands of work are met and consideration is given to the need to drive.

There is no evidence that fitting a lens alters the progression of the disease. The aim is to achieve good vision. Small cones are best fitted with small lenses, and large cones with large lenses. Spherical lenses are useful in the early stages, but moderate disease may achieve a stable fit and good vision with a bielliptical or aspheric lens. Severe keratoconus requires specially designed lenses. It is preferable to select a lens material that is resistant to flexure.

Spherical lenses

Spherical lenses may be fitted as follows:

●Flat with apical touch.

●With touch at apex and midperiphery – threepoint touch – it is important to avoid a ring of midperipheral touch that causes stagnation of tear film beneath the lens and edema. It is better to fit with apical touch and two areas of kidney-shaped touch in the midperiphery. Fit on or near flat K; aim for 2 mm light apical touch, take care to avoid too flat a fit that may result in a corneal abrasion. If the lens is too large for the cone, heavy peripheral touch will result. If the lens is too small the area of touch will be greater than 2 mm.

●Steep with vaulting of the apex. The fit should aim for minimal clearance and sufficient flattening of the peripheral curves to fit the flatter superior cornea.

Fitting with eyelid attachment can minimize lens loss, particularly with a large diameter lens. Large lenses may have three, four or five well blended curves.

Despite the risk of corneal scarring due to flat fitting most patients in the Collaborative Longitudinal Evaluation of Keratoconus (CLEK) study wear flat fitting lenses.10

Aspheric lenses

The shape factor is improved with aspheric design because there is a more gradual flattening from central to peripheral curves, which minimizes excessive bearing. Kok et al.11 found that these lenses had a slight negative influence on visual

acuity in mild keratoconus, but recorded good acuity in severe cases.

Bielliptical lenses

Bielliptical lenses are often useful in early disease and are fitted on flattest K. The Persecon E lens (CibaVision) is available in 9.3 and 9.8 mm diameters.

Rose K lens

The Rose K lens (Nova Contact Lenses), is designed specifically for keratoconus, has a smaller optic zone diameter to minimize midperipheral impingement, and three peripheral curves, which are progressively flatter.

The lenses are designed so that the back optic zone diameter decreases as the base curve radius steepens and the peripheral clearance can be altered. Excessive touch can be identified by distortion or broadening of keratoscopy rings after the lens is removed, and can cause discomfort and a reduction in wearing time.

There should be 2.0–3.0 mm of apical touch with light midperipheral touch.12 A recent improvement in the lens aims to function better on steeper cones by incorporating front and back aberration control and reduce the flare associated with small optic zones. It is often not possible to fit the cornea superiorly without some degree of excessive edge lift inferiorly.

Piggyback lenses

Patients may wear a soft lens on the eye ont which is placed an RGP lens. This is satisfactory i a few cases, but leaves the patient with caring fo both types of lens. It is worth considering silicone hydrogel lens for the soft lens carrier o which the RGP lens is fitted.

Soft hydrogel lenses

Patients with very early keratoconus may be fitte with medium-to-low-water content soft contac lenses. Acuity may be less good than is obtainabl with an RGP lens, but may be sufficient for th patient’s needs. Some moderate cases do surpris ingly well with a toric soft lens. There is now a sof lens available that has been specifically designe for keratoconus patients.

Surgery

Surgery is only considered for keratoconus whe all other types of correction are no longer satisfac tory. A lamellar or penetrating keratoplasty is per formed in which a circumscribed full-thicknes area of cornea is removed and replaced with a simi lar disc from a donor. Although it is not necessar to match donor and host material for the avascu lar cornea, there is still the risk of graft rejectio and sometimes a contact lens needs to be fitte over the graft (Fig. 10.4) (see Ch. 12).

Softperm lenses

Softperm lenses (CibaVision) are unique lenses consisting of an RGP center with a soft, hydrophilic skirt. They often provide good vision in severe cases. The lens should be fitted with the skirt as flat as possible, so that it is almost lifting off. Large-molecular-weight fluorescein is available, which can be used with these lenses and does not stain the hydrogel part of the lens. With previous hybrid lenses there have been problems with the soft skirt separating from the low Dk RGP center, but providing the patient understands how to insert and remove the lens there is now less risk of damage.

Figure 10.4 Badly fitting lens on an eye grafted for keratoconus. The lens has dropped and is too steep below

Surgery soon after presentation has been shown to be associated with:

●poor corrected visual acuity at presentation

●high K-readings over 6.2 mm

●age over 40 years

●duration of disease longer than 5 years.13,14

The results of surgery are generally good – 70% of patients achieve a best corrected visual acuity of 6/6 or better and 95% achieve 6/12 or better.15

COMPLICATIONS OF LENS WEAR IN KERATOCONUS

Corneal staining

Evidence of corneal epithelial erosions should be sought at each visit because it may indicate too much touch and can result in corneal scarring. Despite the potential risk for corneal scarring due to flat fitting of RGP lenses, most patients wear flat fitting lenses.

Corneal staining is common in keratoconus. Mild superficial staining may be tolerated, but requires careful, frequent supervision; greater amounts will necessitate changing the lens design, but too much steepening must be avoided or bubbles will occur beneath the lens, which may themselves cause pressure.

The lenses should be inspected to ensure that they are clean with no deposit formation. Dried mucus on a lens is very abrasive.

Raised nodular scars

Keratoconus patients may develop raised nodular scars that cause lens intolerance and pain, and which do not resolve when lens wear ceases. They may be removed by superficial keratectomy, in which the epithelium is peeled off and the raised stroma beneath is removed by dissection,15 or by excimer laser phototherapeutic keratectomy.16 After both procedures it is possible to resume lens wear after a month. These procedures may reduce the need for penetrating keratoplasty.

Discomfort

Because of the localized ectasia the fit of the lens is often less than perfect. The small lenses fitted on small cones may lie interpalpebrally and cause discomfort as the eyelids bump the lenses with the blink. Large flat lenses may have too great an edge lift if fitted on small or moderate cones. Because of the corneal astigmatism, lenses may decenter and cause discomfort or loss. Lens fit should be examined in all positions of gaze to ensure an adequate fit.

1.Kenney MC, Brown DJ, Rajeev B. The elusive causes of keratoconus: a working hypothesis. CLAO J 2000;26:10–13.

2.Goundhowiardjo TD, van Haeringen NJ. Corneal aldehyde dehydrogenase, glutathione reductase, and glutathione S-transferase in pathologic corneas. Cornea 1993;12:310–314.

3.Wilson SE, Kim WJ. Keratocyte apoptosis: implications on corneal wound healing, tissue organisation, and disease. Invest Ophthalmol Vis Sci 1998;39:220–226.

4.Tretter T, Rabinowitz YS, Young H, et al. Aetiological factors in keratoconus. Ophthalmology 1995; 102(Suppl.):156.

5.Karseras AG, Ruben M. Aetiology of keratoconus. Br J Ophthalmol 1976;60:522–525.

6.Mannis MJ, Morrison TL, Zadnik K, Holland EJ, Krachmer JH. Personality trends in keratoconus – an analysis. Arch Ophthalmol 1987;105: 798–800.

7.Swartz NG, Cohen EJ, Scott DG, et al. Personality and keratoconus. CLAO J 1990;16:62–64.

8.Szczotka LB, Thomas J. Comparison of axial and instantaneous videokeratographic data in keratoconus and utility in contact lens curvature prediction. CLAO J 1998;24:22–28.

9.Zadnik K, Barr JT. Biomicroscopic signs and disease severity in keratoconus. Collaborative Longitudinal Evaluation of Keratoconus (CLEK) Study Group.

Cornea 1996;15:139–146.

10.Edrington TB, Szczotka LB, Barr JT, et al. Rigid contact lens fitting relationships in keratoconus. Collaborative Longitudinal Evaluation of