Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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5Monitoring of IOP is performed during the early postoperative period with a Tono-Pen® because Goldmann applanation tonometry is unreliable.

6Removal of sutures when the graft-host junction has healed. This is usually after 12–18 months, although in elderly patients it may take much longer. Removal of broken or loose individual sutures is performed as soon as identified, to avoid promoting rejection.

7Rigid contact lenses may be required to optimize visual acuity in eyes with astigmatism.

Postoperative complications

1Early complications include persistent epithelial defects, irritation by protruding sutures (Fig. 7.4A) which may give rise to papillary hypertrophy (Fig. 7.4B), wound leak, flat anterior chamber, iris prolapse, uveitis, elevation of intraocular pressure, traumatic graft rupture (rare – Fig. 7.5A), microbial keratitis (Fig. 7.5B) and endophthalmitis (Fig. 7.5C). A rare complication is a fixed dilated pupil (Urrets-Zavalia syndrome).

2Late complications include astigmatism, recurrence of initial disease process, late wound separation, retrocorneal membrane formation, glaucoma and cystoid macular oedema.

Fig. 7.4 (A) Protruding suture; (B) giant papillary conjunctivitis

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Fig. 7.5 Early postoperative complications. (A) Traumatic graft rupture and extrusion of IOL; (B) microbial keratitis; (C) endophthalmitis

(Courtesy of R Bates – fig. A; S Tuft – fig. C)

Corneal graft rejection

Allograft rejection can occur following penetrating keratoplasty and, less commonly, lamellar grafting. Rejection of any layer of the cornea can occur. Endothelial rejection is the most common and most serious as it can lead to endothelial cell loss and decompensation. Stromal rejection and epithelial rejection are less frequent and respond readily to topical steroid treatment, with fewer long-term consequences. Elements of the different types of rejection can coexist. Late graft failure through decompensation can also occur in the absence of rejection, although rejection is a common contributory factor.

1Pathogenesis. The normal cornea is immunologically privileged due to multiple factors including the absence of blood vessels and lymphatics and the presence of relatively few antigen-presenting cells. This privilege can be lost by inflammation and neovascularization, such that rejection is able to occur. Other important predisposing factors for rejection include eccentric or larger grafts (over 8 mm in diameter), infection (particularly herpetic), glaucoma and previous keratoplasty. If the host becomes sensitized to the major or minor histocompatibility antigens present in the donor cornea type IV hypersensitivity can develop against the graft, and rejection may result. Antigen-presenting cells in the donor cornea may initiate this process. HLA matching has a small beneficial effect on graft survival.

2Symptoms of graft rejection include blurred vision, redness, photophobia, a dull periocular ache and often grittiness. However, many cases are asymptomatic until rejection is well-established. The time of onset is very variable, occurring from days to years after grafting.

3Signs vary depending on type of graft; the following description applies principally to PKP.

•Ciliary injection and anterior uveitis is an early manifestation (Fig. 7.6A).

•Epithelial rejection may be accompanied by an elevated line of abnormal epithelium (Fig. 7.6B) in a quiet or mildly inflamed eye, occurring at an average of 3 months; increased treatment may not be required.

•Subepithelial rejection is characterized by subepithelial infiltrates, reminiscent of adenoviral infection (Krachmer spots) on the donor cornea (Fig. 7.6C), with deeper oedema and infiltrative opacification.

•Stromal rejection is characterized by deeper haze. It can be chronic or hyperacute, the latter in association with endothelial rejection.

•Endothelial rejection is characterized by a linear pattern of keratic precipitates (Khodadoust line) associated with an area of inflammation at the graft margin (Fig. 7.6D).

•Stromal oedema is indicative of endothelial failure.

4Management. Early treatment is essential as this greatly improves the chances of reversing the rejection episode. The most aggressive treatment is generally required for endothelial rejection, followed in order of severity by stromal, subepithelial and epithelial.

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aTopical steroids (dexamethasone phosphate 0.1% or prednisolone acetate 1%) preservative-free hourly for 24 hours are the mainstay of therapy. The frequency is reduced gradually over several weeks. Steroid ointment can be used at bedtime as a regimen is tapered. High risk patients should be maintained on the highest tolerated topical dose (e.g. prednisolone acetate 1% four times daily).

b Topical cycloplegics such as atropine 1% once or twice daily. A milder agent can be used if inflammation is slight.

cTopical ciclosporin 0.05% to 2% may be of benefit.

dSystemic steroids (oral prednisolone 1 mg/kg/day in divided doses, or intravenous methylprednisolone 500 mg daily for up to 3 days) may help to reverse rejection and prevent further rejection episodes but only if given within 8 days of onset.

eSubconjunctival steroids (betamethasone 2–3 mg) may be useful.

fOther systemic immunosuppressants such as ciclosporin, tacrolimus or azathioprine.

5Differential diagnosis includes graft failure (no inflammation), infective keratitis including fungal and herpetic, uveitis, sterile suture reaction, raised IOP and epithelial ingrowth.

Fig. 7.6 Allograft rejection. (A) Ciliary injection in pre-rejection; (B) elevated epithelial line in epithelial rejection; (C) Krachmer spots in stromal rejection; (D) endothelial rejection

(Courtesy of S Tuft – figs A, B and C)

Superficial lamellar keratoplasty

This involves partial thickness excision of the corneal epithelium and stroma so that the endothelium and part of the deep stroma are left behind.

1Indications

•Opacification of the superficial one-third of the corneal stroma not caused by potentially recurrent disease.

•Marginal corneal thinning or infiltration as in recurrent pterygium, Terrien marginal degeneration, and limbal dermoids or other tumours.

•Localized thinning or descemetocele formation.

2Technique is similar to penetrating keratoplasty except that only a partial thickness of the cornea is grafted.

Deep anterior lamellar keratoplasty

Deep anterior lamellar keratoplasty (DALK) is a relatively new technique in which all opaque corneal tissue is removed almost to the level of Descemet membrane. The theoretical advantage is the decreased risk of rejection because the endothelium, a major target for rejection, is not transplanted. The major technical difficulty lies in judging the depth of the corneal dissection as close as possible to Descemet membrane without perforation, and unless this is achieved visual outcome is likely to be compromised.

1Indications

•Disease involving the anterior 95% of corneal thickness with a normal endothelium and absence of breaks or scars in Descemet membrane (e.g. keratoconus without a history of acute hydrops).

•Chronic inflammatory disease such as atopic keratoconjunctivitis which carries an increased risk of graft rejection.

2Advantages

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•No risk of endothelial rejection although epithelial/subepithelial/stromal rejection may occur.

•Less astigmatism and a structurally stronger globe as compared with penetrating keratoplasty.

•Increased availability of graft material since endothelial quality is irrelevant.

3Disadvantages

•Difficult and time-consuming with a high risk of perforation particularly in older patients.

•Interface haze may limit best final visual acuity.

4Postoperative management is similar to penetrating keratoplasty except that lower intensity topical steroids are needed and sutures can be usually removed after 6 months.

Descemet stripping endothelial keratoplasty

Descemet stripping endothelial keratoplasty (DSEK) involves removal only of diseased endothelium along with Descemet membrane (descemetorhexis), through a corneoscleral or corneal incision. Folded donor tissue is introduced through the same small (about 5 mm) incision. A version of this procedure, Descemet stripping (automated) endothelial keratoplasty, DSAEK, in which donor preparation involves an automated microkeratome, has been widely adopted by specialist corneal surgeons.

1Indications include endothelial disease such as pseudophakic bullous keratopathy.

2Advantages

•Relatively little refractive change and a structurally essentially intact globe.

•Faster visual rehabilitation than PKP.

•The corneal incision is sutured, but there are no graft sutures.

•Overall similar complication rate and risks to PKP, and most complications are readily treatable; reported posterior graft dislocation rate is up to 80%, though with a mean of only 15%.

3Disadvantages

•New technique with significant learning curve.

•Investment in expensive new equipment required for the automated method.

•Endothelial rejection can still occur (mean 10%).

•Eventual visual outcome may not be quite as good as PKP.

•Long-term results not yet known.

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Keratoprostheses

Keratoprostheses are artificial corneal implants used in patients unsuitable for keratoplasty. The modern osteoodontokeratoprosthesis consists of the patient's own tooth root and alveolar bone which supports the central optical cylinder. This is usually covered with a buccal mucous membrane graft. Surgery is difficult and time consuming and is performed in two stages, 2–4 months apart.

1Indications

•Patients with bilateral blindness with visual acuity of hand movements or less but normal optic nerve and retinal function.

•Severe, debilitating but inactive anterior segment disease with no realistic chance of success from conventional keratoplasty such as Stevens−Johnson syndrome, ocular cicatricial pemphigoid (Fig. 7.7A), chemical burns or trachoma.

•Multiple previous failed corneal grafts or other types of ocular surface reconstruction such as amniotic membrane or stem cell grafting.

•Normal intraocular pressure with or without medication.

•Absence of active ocular surface inflammation.

•Good patient motivation.

2Complications include glaucoma, retroprosthesis membrane formation, tilting or extrusion of the cylinder (Fig. 7.7B), retinal detachment and endophthalmitis.

3Results. Approximately 80% of patients experience visual improvement which varies from CF to 6/12 or even better. Poor visual outcome is often associated with pre-existing optic nerve or retinal dysfunction.

Fig. 7.7 (A) Keratoprosthesis; (B) extrusion

(Courtesy of R Bates – fig. A)

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Refractive procedures

Introduction

Refractive surgery encompasses a range of procedures aimed at changing the refraction of the eye by altering the cornea or lens, the principal refracting components. Myopia, hypermetropia (hyperopia) and astigmatism can all be addressed, though correction of presbyopia is yet to be achieved on a consistently satisfactory basis.

Correction of myopia

1Photorefractive keratectomy (PRK – see below)

2 Laser epithelial keratomileusis (LASEK - see below).

3Laser in situ keratomileusis (LASIK – see below).

4Clear lens extraction gives very good visual results but carries a small risk of retinal detachment.

5Iris clip (‘lobster claw’) implant is attached to the iris (Fig. 7.8A). Complications include subluxation, an oval pupil, endothelial cell loss, cataract, pupillary-block glaucoma and retinal detachment.

6Phakic posterior chamber implant (implantable contact lens, ICL) is inserted behind the iris and in front of the lens (Fig. 7.8B), and supported in the ciliary sulcus. The lens is composed of material derived from collagen (Collamer) with a power of −3 D to −20.50 D. Visual results are promising but the procedure may be associated with uveitis, pupillary-block glaucoma, endothelial cell loss, cataract formation and retinal detachment.

Fig. 7.8 Phakic intraocular implants for correction of myopia. (A) Anterior chamber ‘lobster claw’ implant; (B) posterior chamber implant is injected between the iris and anterior lens capsule

(Courtesy of Krachmer, Mannis and Holland, from Cornea, Mosby 2005 – fig. B)

Correction of hypermetropia (hyperopia)

1 PRK and LASEK can correct low degrees of hypermetropia.

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2LASIK can correct up to 4 D.

3Conductive keratoplasty (CK) involves the application of radiofrequency energy to the corneal stroma and can correct low to moderate hypermetropia and hypermetropic astigmatism. Burns are placed in one or two rings in the corneal periphery using a probe. The resultant thermally-induced stromal shrinkage is accompanied by an increase in central corneal curvature. Significant regression may occur but the procedure can be repeated. CK may also be helpful for presbyopia (see below). Complications are infrequent.

4Laser thermal keratoplasty with a holmium laser can correct low hypermetropia. Laser burns are placed in one or two rings in the corneal mid-periphery (Fig. 7.9A). As with CK, thermally-induced stromal shrinkage is accompanied by increased corneal curvature. This change decays over time but treatment can be repeated.

5Other modalities include intracorneal inlays, and clear lens extraction and phakic lens implants as described above for myopia.

Fig. 7.9 Refractive laser procedures. (A) Appearance following thermal keratoplasty; (B) photorefractive keratectomy; (C) laser in situ keratomileusis

(Courtesy of H Nano Jr – fig. A; C Barry – fig. B; Eye Academy – fig. C)

Correction of astigmatism

1Limbal relaxing incisions/arcuate keratotomy involves making paired arcuate incisions on opposite sides of the cornea in the axis of the correcting ‘plus’ cylinder (the steep meridian). The resultant flattening of the steep meridian coupled with a smaller steepening of the flat meridian at 90° to the incisions reduces astigmatism. The desired result can be controlled by varying the length and depth of the incisions, and their distance from the optical centre of the cornea. Arcuate keratotomy may be combined with compression sutures placed in the perpendicular meridian, when treating large degrees of astigmatism such as may occur following penetrating keratoplasty.

2 PRK and LASEK can correct up to 3 D.

3LASIK can correct up to 5 D.

4Lens surgery involves using a ‘toric’ intraocular implant incorporating an astigmatic correction. Postoperative rotation of the implant away from the desired axis occurs in a significant minority.

5Conductive keratoplasty (see ‘hypermetropia’ above).

Correction of presbyopia

1Lens extraction, either to treat cataract or for purely refractive purposes with the insertion of a multifocal/bifocal or ‘accommodating’ implant can optically restore some reading vision, though dissatisfaction occurs in a significant minority and reading glasses may still have to be worn for some tasks. Acronyms used include clear lens exchange (CLE), refractive lens exchange (RLE) and presbyopic lens exchange (PreLEx). Much research effort is being applied to the development of effective accommodating IOLs.

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2Conductive keratoplasty (see ‘hypermetropia’ above); there is some evidence that CK may impart a degree of multifocal functionality to the cornea.

3Laser-induced monovision refers to the use of laser refractive surgery to induce ‘monovision’, in which one eye is set for emmetropia and the other for low myopia, in order to facilitate both good distance and near vision with the eyes used together.

4Corneal multifocality. Several different approaches are under development utilizing laser (e.g. LASIK) to alter the shape of the cornea such that a bifocal or transitional effect is induced.

5Scleral expansion surgery. Results have been inconsistent and unpredictable and this technique has not achieved sustained popularity.

6Intracorneal inlays have shown benefit for presbyopia in trials, though the biocompatibility of some materials has been relatively poor, requiring explantation.

7Laser to the crystalline lens using femtosecond pulses to improve elasticity is in early development but shows some promise.

Laser refractive procedures

To settle any contact lens-induced corneal distortion prior to definitive keratometry, soft contact lenses should probably be discontinued for 2 weeks and hard/rigid gas permeable lenses for at least 3 weeks (some surgeons suggest 1 week for each year of wear to date).

Photorefractive keratectomy

Photorefractive keratectomy (PRK) is performed with the excimer laser, which can accurately ablate corneal tissue to an exact depth with minimal disruption of surrounding tissue. Myopia is treated by ablating the central anterior corneal surface so that it becomes flatter; approximately 10 µm of ablation will correct 1 D of myopia. Hypermetropia is treated by ablation of the periphery so that the centre becomes steeper. PRK is able to correct myopia up to 6 D, astigmatism up to 3 D and low hypermetropia.

1Technique

a The visual axis is marked and the corneal epithelium removed.

bThe patient fixates on the aiming beam of the laser.

cThe laser is applied to ablate only Bowman layer and anterior stroma (Fig. 7.9B). This usually takes 30–60 seconds.

The cornea usually heals within 48–72 hours aided by a bandage contact lens. A subepithelial haze invariably develops within 2 weeks and persists for 1–6 months. It rarely causes diminished visual acuity but may give nocturnal glare.

2Complications include slow-healing epithelial defects, corneal haze and haloes, poor night vision and regression of refractive correction. Uncommon problems include decentred ablation, scarring, abnormal epithelial healing, irregular astigmatism, hypoaesthesia, sterile infiltrates, infection and acute corneal necrosis.

Laser epithelial keratomileusis

Laser epithelial keratomileusis (LASEK) is an adaptation of PRK. In LASEK the epithelium is first detached and peeled back, laser applied and then the flap repositioned. It is associated with less pain, less haze and more rapid visual recovery than PRK. LASEK works well with low corrections and for patients who are unsuitable for LASIK such as those with very thin corneas. The technique is as follows:

a Alcohol 20% is applied for 30–40 seconds and an epithelial sheet is cleaved at the basement membrane.

bLaser is applied.

cThe epithelial flap is re-positioned.

Functional vision is usually achieved within 4–7 days and the procedure has a low risk of serious complications. The main disadvantage compared with LASIK is variable epithelial healing with unpredictability of postoperative pain.

Laser in situ keratomileusis

Laser in situ keratomileusis (LASIK) is a very commonly-performed refractive procedure. It is more versatile than PRK and LASEK and can correct hypermetropia of up to 4 D, astigmatism of up to 5 D and myopia of up to 12 D depending on corneal thickness. To decrease the risk of subsequent ectasia, a residual corneal base of at least 250 µm thickness must remain after the flap has been cut and tissue ablated. The amount of tissue removed and the total treatment is therefore limited by the original corneal thickness. The thickness of the flap can be varied but thinner flaps are more difficult to handle and more prone to wrinkling.

1Technique

aA suction ring is applied to the globe; this raises the intraocular pressure to over 65 mmHg, and may temporarily occlude the central retinal artery and extinguish vision.

b The ring is centred on the cornea and provides a guide track into which an automated microkeratome is inserted. c The keratome is mechanically advanced across the cornea to create a thin flap, which is reflected (Fig. 7.9C).

dSuction is released and the bed is treated with the excimer laser as for PRK.

eThe flap is repositioned and allowed to settle undisturbed for 30 seconds.

Compared to LASEK, the procedure offers the advantages of minimal discomfort, faster visual rehabilitation, rapid stabilization of refraction and minimal stromal haze.

2Operative complications include buttonholing of the flap, flap amputation, incomplete or irregular flap creation, and rarely corneal perforation.

3Postoperative

•Tear instability is almost universal and may require treatment.

•Wrinkling (Fig. 7.10A), distortion or dislocation of the flap.

•Subepithelial haze (Fig. 7.10B) with resultant glare especially at night.

•Epithelial defects that may predispose to epithelial ingrowth under the flap (Fig. 7.10C).

•Diffuse lamellar keratitis ('sands of Sahara’) may develop 1–7 days following LASIK. It is characterized by granular deposits at the flap interface (Fig. 7.10D). Treatment is with intensive topical antibiotics and steroids.

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•Bacterial keratitis is rare (Fig. 7.10E).

•Ectasia is a well-recognized complication. ‘Forme fruste’ (occult/mild) keratoconus and a low post-ablation corneal thickness are the major risk factors. Treatment options include corneal grafting, intrastromal inlays, and collagen crosslinking.

Fig. 7.10 Complications of LASIK. (A) Wrinkling of the flap; (B) subepithelial haze; (C) epithelial ingrowth; (D) diffuse lamellar keratitis; (E) bacterial keratitis

(Courtesy of S Tuft – figs A and D; H Nano Jr – fig. B; R Fogla – fig. C; R Bates – fig. E)

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