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

kanski 7th

Fig. 6.69 Complications of contact lens wear. (A) Epithelial microcysts fromacute hypoxia; (B) lipid deposition fromchronic hypoxia; (C) marginal infiltrates in immune response keratitis; (D) vascularization and scarring in chronic toxic keratitis

(Courtesy of S Tuft – figs A and B; J Dart – fig. D)

Immune response keratitis

1Pathogenesis. A hypersensitivity response to bacterial antigen or the chemicals used in lens care can lead to the development of sterile marginal corneal infiltrates; the mechanism is thought to be similar to that of marginal keratitis.

2Signs. Mildly red eye associated with marginal infiltrates with no or minimal epithelial defects (Fig. 6.69C).

3Treatment involves cessation of lens wear until resolution occurs. Topical antibiotics and steroids may be used in some cases, but if the diagnosis is uncertain treatment should be that of bacterial keratitis.

Toxic keratitis

1Pathogenesis. Acute chemical injury may be caused by inadvertently placing a contact lens on the eye without first neutralizing toxic cleaning agents such as hydrogen peroxide. Chronic toxicity can result from long-term exposure to disinfecting preservatives such as thiomersal or benzalkonium chloride.

2Signs

•Acute pain, redness, and chemosis on lens insertion, which may take 48 hours to resolve completely.

•Vascularization and scarring of the cornea and limbal conjunctiva in chronic cases (Fig. 6.69D).

3Treatment may involve switching to daily disposable lenses or using a non-preserved disinfectant such as hydrogen peroxide.

Suppurative keratitis

Contact lens wear is the greatest risk factor for the development of bacterial keratitis; the risk is probably least for rigid contact lenses. Bacteria in the tear film are normally unable to bind to the corneal epithelium, but following an abrasion and in association with hypoxia, bacteria can attach and penetrate the epithelium with the potential to cause infection. Bacteria and protozoa may also be introduced onto the corneal surface by poor lens hygiene or the use of tap water to rinse lenses.

Contact lens-associated giant papillary conjunctivitis

See Chapter 5.

Copyright © 2011 Elsevier Inc.All rights reserved. Read our Terms and Conditions of Use and our PrivacyPolicy.

If you find this useful please saythanks in your way: dramroo

309 / 1137

kanski 7th

Congenital anomalies of the cornea and globe

Microcornea

Microcornea is a rare AD unilateral or bilateral condition.

1Signs

•The adult horizontal corneal diameter is 10 mm or less (Fig. 6.70A).

•Hypermetropia, shallow anterior chamber but other dimensions are normal.

2Ocular associations include glaucoma (closed and open angle), congenital cataract, leukoma (Fig. 6.70B), cornea plana, Rieger anomaly, microphakia and optic nerve hypoplasia.

3Syndromic systemic associations include fetal alcohol, Ehlers–Danlos, Weill–Marchesani, Waardenburg, Nance Horan and Cornelia de Lange syndromes.

Fig. 6.70 (A) Severe microcornea; (B) microcornea and corneal opacity

(Courtesy of S Fogla – fig. A)

Megalocornea

Megalocornea is a rare, bilateral, non-progressive condition thought to be due to defective growth of the optic cup.

1Inheritance is usually X-linked recessive so that 90% of affected individuals are males. The condition maps to Xq21.3-q22.

2Signs

•Normal intraocular pressure.

•Large corneal diameter is 13 mm or over and a very deep anterior chamber (Fig. 6.71A).

•High myopia and astigmatism but normal visual acuity.

•Pigment dispersion with Krukenberg spindle, trabecular hyperpigmentation (Fig. 6.71B) and iris

310 / 1137

kanski 7th

transillumination.

•Lens subluxation may occur due to zonular stretching.

3Systemic associations include Alport syndrome, Marfan syndrome, Ehlers–Danlos syndrome, Down syndrome, osteogenesis imperfecta, progressive facial hemiatrophy, renal carcinoma and megalocornea-mental retardation syndrome.

Fig. 6.71 (A) Megalocornea; (B) trabecular hyperpigmentation due to pigment dispersion

Sclerocornea

Sclerocornea is a very rare, usually bilateral, condition that may be associated with cornea plana (see below).

1Inheritance of the milder form is AD and the more severe is AR, although sporadic cases are probably more common.

2Signs. Peripheral corneal opacification and vascularization that makes the cornea appear small (Fig. 6.72A). Occasionally the entire cornea is involved (Fig. 6.72B).

311 / 1137

kanski 7th

Fig. 6.72 Sclerocornea. (A) mild; (B) severe

Cornea plana

This is a rare bilateral condition.

1 Signs. Flat cornea, and a corresponding reduction in refractive power resulting in high hypermetropia; there are two types:

aCornea plana 1 (CNA1) is AD with reduced corneal refractive power to 38–42 D.

bCornea plana 2 (CNA2) is AR AD with reduced corneal refractive power to 23–35 D (Fig. 6.73).

2Associations include shallow anterior chamber with predisposition to angle-closure glaucoma, scleroderma, microcornea and microphthalmos, Peters anomaly, and iris abnormalities including irido-corneal adhesions.

Fig. 6.73 Cornea plana

312 / 1137

kanski 7th

(Courtesy of R Visser)

Keratectasia

Keratectasia is a very rare, usually unilateral, condition thought to be the result of intrauterine keratitis and perforation. It is characterized by protuberance between the eyelids or a severely opacified and sometimes vascularized cornea (Fig. 6.74). It is often associated with raised intraocular pressure.

Fig. 6.74 Keratectasia

Posterior keratoconus

Posterior keratoconus is an uncommon, sporadic, unilateral, non-progressive increase in curvature of the posterior corneal surface. The anterior surface is normal and visual acuity unimpaired because of the similar refractive indices of the cornea and aqueous humour. Two types are recognized:

1Generalis, in which there is an increase in curvature of the entire posterior corneal surface.

2Conscriptus, which is characterized by a localized paracentral or central posterior corneal indentation (Fig. 6.75).

Fig. 6.75 Posterior keratoconus

(Courtesy of S Johns)

Microphthalmos

Microphthalmos is a developmental arrest of ocular growth, defined as total axial length (TAL) at least two standard deviations below agesimilar controls. The TAL is reduced because of stunted growth of the anterior or posterior segment, or both. The condition is typically sporadic and may be unilateral or bilateral.

1 Simple microphthalmos is not associated with other major ocular malformations (Fig. 6.76A).

313 / 1137

kanski 7th

2Complex (colobomatous) microphthalmos is associated with coloboma, usually of the iris (Fig. 6.76B).

3Microphthalmos with cyst is caused by failure of the optic fissure to close, leading to the formation of an orbital cyst that communicates with the eye. The extent of the cystic component is best delineated on MR or CT (Fig. 6.76C).

4Posterior microphthalmos is a rare subset of microphthalmos in which TAL is reduced in the setting of normal corneal diameter, resulting in high hypermetropia and papillomacular retinal fold. This differs from nanophthalmos, which is described as eyes with microphthalmos, microcornea and a tendency toward uveal effusions.

Fig. 6.76 (A) Left simple microphthalmos; (B) left microphthalmos and bilateral iris colobomas; (C) axial CTshows right microphthalmos with cyst

(Courtesy of L MacKeen – fig. C)

Anophthalmos

1Simple anophthalmos is caused either by complete failure of budding of the optic vesicle or early arrest in its development. It is associated with other abnormalities such as absence of extraocular muscles, a short conjunctival sac and microblepharon (Fig. 6.77A).

2Anophthalmos with cyst (congenital cystic eyeball) is a condition in which the globe is replaced by a cyst (Fig. 6.77B).

314 / 1137

kanski 7th

Fig. 6.77 (A) Bilateral simple anophthalmos; (B) anophthalmos with cyst

(Courtesy of U Raina – fig. B)

Copyright © 2011 Elsevier Inc.All rights reserved. Read our Terms and Conditions of Use and our PrivacyPolicy.

If you find this useful please saythanks in your way: dramroo

315 / 1137

kanski 7th

Chapter 7 – Corneal and Refractive Surgery

KERATOPLASTY 240

Introduction 240 Penetrating keratoplasty 241

Superficial lamellar keratoplasty 244 Deep anterior lamellar keratoplasty 244

Descemet stripping endothelial keratoplasty  244

KERATOPROSTHESES 245 REFRACTIVE PROCEDURES 245

Introduction 245

Laser refractive procedures  247

Keratoplasty

Introduction

Corneal transplantation or grafting is an operation in which abnormal corneal host tissue is replaced by healthy donor cornea. A corneal graft may consist of (a) partial-thickness (anterior or posterior lamellar) or (b) full-thickness (penetrating) keratoplasty (PKP).

General indications

1Optical keratoplasty is performed to improve vision. Important indications include pseudophakic bullous keratopathy, keratoconus, dystrophies (Fig. 7.1A), degenerations and scarring.

2Tectonic grafting may be carried out to restore or preserve corneal integrity in eyes with severe structural changes such as severe thinning with descemetocele (Fig. 7.1B).

3 Therapeutic corneal transplantation may afford removal of infected corneal tissue in eyes unresponsive to antimicrobial therapy. 4 Cosmetic grafting may be performed to improve the appearance of the eye, but is a rare indication.

316 / 1137

kanski 7th

Fig. 7.1 (A) Optical penetrating keratoplasty for macular dystrophy; (B) tectonic patch graft for descemetocele

(Courtesy of S Tuft – fig. B)

Donor tissue

Donor tissue should be removed within 12–24 hours of death. Corneas from infants (3 years and under) are used only very occasionally, even for paediatric transplants, as they are associated with surgical, refractive and rejection problems. There is an attempt to age-match donors and recipients. Most corneas are stored in coordinating ‘eye banks’ prior to transplantation, where pre-release evaluation includes medical history review and donor blood screening to exclude contraindications, and microscopic examination of the cornea including endothelial cell count determination. Corneas are preserved in hypothermic storage (up to 7–10 days) or organ culture medium (4 weeks) until needed; culture allows extended testing for infective contamination. Contraindications to ocular tissue donation are set out below, though there is international variation and the list is not exhaustive:

•Death of unknown cause.

•Certain systemic infections such as HIV, viral hepatitis, syphilis, congenital rubella, tuberculosis, septicaemia and active malaria.

•Prior high-risk behaviour for HIV and hepatitis such as sex with someone HIV positive, men who have sex with men, intravenous drug abuse and prostitution.

•Infectious and possibly infectious diseases of the CNS such as Creutzfeldt–Jakob disease, systemic sclerosing panencephalitis, progressive multifocal leucoencephalopathy, encephalitis, Alzheimer disease and other dementias, Parkinson disease, multiple sclerosis and motor neurone disease.

•Receipt of a transplanted organ.

•Receipt of human pituitary-derived growth hormone.

•Brain or spinal surgery before 1992.

•Most haematological malignancies.

•Ocular disease such as inflammation and disease likely to compromise graft outcome, some malignant ocular tumours (e.g. retinoblastoma) and corneal refractive surgery.

Recipient prognostic factors

The following host factors may adversely affect the prognosis of a corneal graft and should therefore be addressed prior to surgery. In general, the most favourable cases are keratoconus, localized scars and dystrophies.

•Severe stromal vascularization, absence of corneal sensation, extreme thinning at the proposed host-graft junction and active corneal inflammation.

•Abnormalities of the eyelids such as blepharitis, ectropion, entropion and trichiasis; these should be addressed before surgery.

•Recurrent or progressive forms of conjunctival inflammation, such as atopic conjunctivitis and ocular cicatricial pemphigoid.

•Tear film dysfunction.

317 / 1137

kanski 7th

•Anterior synechiae.

•Uncontrolled glaucoma.

•Uveitis.

Penetrating keratoplasty

Although component layer grafting of the cornea is available, PKP remains the most commonly performed corneal transplantation procedure, largely because lamellar surgery is difficult and time-consuming, and because interface irregularity can limit visual outcome. Indications include:

•Disease involving all layers of the cornea.

•Specific common indications are keratoconus, pseudophakic bullous keratopathy, Fuchs endothelial and other dystrophies.

Technique

1Determination of graft size is done preoperatively with a variable slit beam, and operatively by trial placement of trephines with different diameters or by measurement with a calliper. Grafts of diameter 8.5 mm or more are prone to postoperative anterior synechiae formation, vascularization and increased intraocular pressure. An ideal size is 7.5 mm; grafts smaller than this may give rise to high astigmatism.

2Excision of donor cornea should always precede that of host cornea. Donor tissue is usually prepared by trephining a previously excised corneoscleral button, endothelial side up in a concave Teflon block. The donor button is usually trephined to be about 0.25 mm larger in diameter than the planned diameter of the host opening, to facilitate watertight closure, minimize postoperative flattening and reduce the possibility of postoperative glaucoma. A mechanically-guided trephination is standard, although newer laser techniques are more accurate and are preferred by some surgeons where available.

3Excision of diseased host tissue is then carried out, taking care not to damage the iris and lens (Fig. 7.2A–F). Recipient trephining can be performed freehand or with suction trephine systems such as the Hessburg–Barron which stabilize the globe and ensure that the angle of trephination is perpendicular to the surface. Motorized and laser systems are also in use.

4Fixation of donor button with 10-0 monofilament nylon (Fig. 7.3A–F).

Fig. 7.2 Excision of host tissue. (A) Partial-thickness trephination; (B) anterior chamber is entered with a knife; (C, Dand E) excision is completed with scissors; (F) injection of viscoelastic

(Courtesy of R Fogla)

Fig. 7.3 Fixation of donor button. (A and B) Donor button is placed onto the viscoelastic bed; (C) initial cardinal suture is placed at 12 o’clock; (D) four interrupted cardinal sutures in place; (E) additional radial sutures; (F) continuous running suture

(Courtesy of R Fogla)

Postoperative management

1Topical steroids are used to decrease the risk of immunological graft rejection. After initial administration 2-hourly and then reducing to four times daily, the dose may be further tapered, depending on the condition of the eye. Steroids are, however, usually continued long-term at low intensity, such as once daily for a year or more.

2Other immunosuppressants such as oral azathioprine and topical and systemic ciclosporin may be used for prevention of rejection, but are usually reserved for high-risk patients.

3Mydriatics b.d. for two weeks, or longer if uveitis persists.

4 Oral aciclovir may be used in the context of pre-existing herpes simplex keratitis to minimize the risk of recurrence.

318 / 1137