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

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Fig. 6.32 Terrien marginal degeneration. (A) Peripheral stromal opacification; (B) circumferential thinning; (C) pseudopterygia

Treatment

•Safety spectacle lenses (polycarbonate as a minimum) if thinning is significant.

•Contact lenses for astigmatism. Scleral lenses, or even soft lenses with rigid gas permeable ‘piggybacking’, are likely to be necessary.

•Surgery, involving either crescent-shaped excision of the gutter with suturing of the margins or peripheral lamellar transplantation, gives variable results.

•'Tectonic’ corneal grafting for perforation or threatened perforation.

•Topical lubricants or weak topical steroids for inflammatory episodes, the latter with caution because of the risk of promoting thinning.

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Neurotrophic keratopathy

Pathogenesis

Neurotrophic keratopathy occurs when there is loss of the trigeminal innervation to the cornea resulting in partial or complete anaesthesia.

The loss of neural influences results in intracellular oedema, exfoliation of epithelial cells, impairment of epithelial healing and loss of goblet cells, culminating in epithelial breakdown and persistent ulceration. Loss of acetylcholine, substance P, and growth factors from the epithelium appear to be important.

Causes

1Acquired damage to the 5th cranial nerve or trigeminal ganglion following surgical ablation for trigeminal neuralgia (tic doloureux), stroke, aneurysm, multiple sclerosis or tumour (acoustic neuroma or neurofibroma).

2Systemic disease such as diabetes and leprosy.

3Ocular disease such as herpes simplex and herpes zoster keratitis, abuse of topical anaesthetic, chemical burn and refractive corneal surgery.

4Congenital causes include familial dysautonomia (Riley–Day syndrome), Möbius syndrome, Goldenhar syndrome, anhidrotic ectodermal dysplasia and hereditary sensory neuropathy.

Diagnosis

The severity of signs can vary during the course of disease. Some patients develop serious lesions early while others only develop problems after many years.

1Corneal sensation is tested with a wisp of cotton or an anasthesiometer (<5 mm is clinically significant).

2Signs

•Interpalpebral punctate keratopathy in which the epithelium appears irregular (Fig. 6.33A).

•Slightly epithelial opacification, oedema and small defects (Fig. 6.33B).

•Persistent epithelial defect in which the epithelium at the edge of the lesion appears rolled and thickened, and is poorly attached (Fig. 6.33C).

•Enlargement of epithelial defect with stromal oedema and infiltration.

•Stromal corneal melting (Fig. 6.33D) that may be virtually asymptomatic.

•Perforation is uncommon but can occur rapidly, especially if there is secondary infection.

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Fig. 6.33 Neurotrophic keratopathy. (A) Early central epithelial changes; (B) small epithelial defect and stromal oedema; (C) large epithelial defect; (D) stromal infiltration and melting

(Courtesy of S Tuft – fig. C; S Bonini – fig. D)

Treatment

1Discontinuation, if possible, of potentially toxic medications already in use.

2Topical lubricants (non-preserved) for associated dry eye or corneal exposure. Topical insulin-like growth factor-1, substance P, and neurogenic growth factor have been evaluated but are not commercially available.

3Protection of the ocular surface by the following:

a Simple taping of the lids, particularly at night, may provide temporary protection.

bBotulinum toxin injection to induce a protective ptosis.

cTarsorrhaphy may be temporary or permanent, and lateral or central, according to the underlying pathology and visual potential.

d Therapeutic silicone contact lenses may be fitted provided the eye is carefully monitored for infection.

eAmniotic membrane patch with temporary central tarsorrhaphy.

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Exposure keratopathy

Pathogenesis

Exposure keratopathy is the result of incomplete lid closure (lagophthalmos). Lagophthalmos may only be present on blinking or gentle lid closure, but absent on forced lid closure. The result is drying of the cornea despite normal tear production.

Causes

1Neuroparalytic, especially facial nerve palsy which may be idiopathic or the result of surgery for an acoustic neuroma or parotid tumour.

2Reduced muscle tone as in coma or parkinsonism.

3Mechanical

•Eyelid scarring associated with cicatricial pemphigoid, burns and trauma.

•Tight facial skin due to eczema, solar keratosis, xeroderma pigmentosum and following blepharoplasty.

4Abnormality of globe position

•Severe proptosis due to thyroid eye disease or orbital tumour.

•Severe enophthalmos.

Diagnosis

1 Symptoms are those of a dry eye.

2Signs

•Mild punctate epithelial changes involving the inferior third of the cornea, particularly with nocturnal lagophthalmos.

•Epithelial breakdown (Fig. 6.34A).

•Stromal melting (Fig. 6.34B), which may result in perforation.

•Secondary infection may supervene (Fig. 6.34C).

•Inferior fibrovascular change with Salzmann degeneration may develop over time.

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Fig. 6.34 Exposure keratopathy. (A) Inferior epithelial defect; (B) stromal melting; (C) secondary bacterial infection

(Courtesy of S Tuft – fig. C)

Treatment

Treatment depends on the severity of exposure and whether recovery is anticipated.

1Reversible exposure

•Artificial tears during the day and ointment at night.

•Taping the lid closed at night may be an alternative to ointment.

•Bandage silicone rubber or scleral contact lenses.

•Temporary tarsorrhaphy or Frost suture.

2Permanent exposure

•Permanent tarsorrhaphy.

•Gold weights inserted in the upper lid for facial nerve palsy.

•Permanent central tarsorrhaphy and conjunctival flap may be required for severe cases.

•Management of proptosis by orbital decompression if necessary.

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Thygeson superficial punctate keratitis is an uncommon, usually bilateral, idiopathic condition characterized by exacerbations and remissions. It most commonly affects young adults but may occur at any age and recurrences can continue for decades.

Diagnosis

1Symptoms consist of recurrent attacks of irritation, photophobia, blurred vision and watering.

2Signs

•Mainly central, coarse, distinct, granular, greyish, slightly elevated epithelial lesions (Fig. 6.36A) that stain with fluorescein.

•A mild subepithelial haze may be present (Fig. 6.36B), especially if topical antivirals have been used.

•The conjunctiva is uninvolved and the eye is not hyperaemic.

3Differential diagnosis includes post-adenoviral keratitis.

Fig. 6.36 (A) Thygeson superficial punctate keratitis; (B) associated subepithelial haze

(Courtesy of R Curtis – fig. B)

Treatment

1Topical

•Lubricants may suffice in mild cases.

•Steroids (fluorometholone 0.1% or loteprednol 0.2–0.5% b.d.) initially with gradual tapering. In some cases higher intensity treatment may be needed.

•Ciclosporin 0.05% is a good alternative to steroids, particularly in patients requiring long-term therapy.

2 Contact lenses (extended wear or daily disposable soft) may be considered if steroids are contraindicated or as an alternative.

3Phototherapeutic keratectomy brings short term relief but recurrence is likely.

Filamentary keratopathy

Pathogenesis

Filamentary keratopathy is a common condition that can cause considerable discomfort. It is thought that a loose area of epithelium acts as a focus for deposition of mucus and cellular debris. The causes are shown in Table 6.6.

Table 6.6 -- Causes of filamentary keratopathy

•Aqueous deficiency (keratoconjunctivitis sicca)

•Excessive contact lens wear

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•Corneal epithelial instability (recurrent erosion syndrome, corneal graft, cataract surgery, refractive surgery and drug toxicity)

•Superior limbic keratoconjunctivitis

•Bullous keratopathy

•Neurotrophic keratopathy

•Prolonged or frequent eye closure

Diagnosis

1Symptoms consist of discomfort with foreign body sensation, redness and sometimes photophobia.

2Signs

•Strands of degenerated epithelial cells and mucus (Fig. 6.37 and see Figs. 4.4B and C) that move with blinking, attached at one end to the cornea.

•Filaments stain well with rose bengal and to a lesser extent with fluorescein.

•A small epithelial defect may be present at the base of a filament.

•Chronic filaments may form plaques.

Fig. 6.37 Corneal filaments

(Courtesy of S Tuft)

Management

1General

•Any underlying cause such as dry eye should be treated (see Ch. 4).

•All unnecessary medications should be stopped.

2Specific treatment for filaments.

•Mechanical removal for short-term symptomatic relief.

•Mucolytic agents such as 5% or 10% acetylcysteine drops.

•Non-steroidal anti-inflammatory drops such as diclofenac.

•Hypertonic 5% saline (drops q.i.d., ointment at bedtime) to encourage adhesion of loose epithelium.

•Bandage soft contact lenses of high oxygen permeability to protect the cornea from the shearing action of the lids.

Recurrent corneal epithelial erosions

Pathogenesis

Recurrent corneal epithelial erosion is the tendency for minor trauma to precipitate significant corneal epithelial disturbances. The condition is caused by an abnormally weak attachment between the basal cells of the corneal epithelium and their basement membrane. Minor trauma, such as eyelid-corneal interaction during sleep, can be sufficient to detach the epithelium. Erosions may be associated with previous trauma or corneal surgery, and with certain corneal dystrophies (see below).

Diagnosis

1Presentation is with severe pain, photophobia, redness, blepharospasm, and watering waking the patient during the night or present on awaking in the morning. There is usually (but not invariably) a prior history of corneal abrasion, sometimes years

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previously, and this may have been minor compared to the recurrent symptoms.

2Signs

•An epithelial defect may be present, usually in the inferior interpalpebral zone (Fig. 6.38).

•Healing of a defect can often be very rapid (hours), but the extent of loose epithelium may be highlighted by areas of pooling of fluorescein and rapid tear film breakup.

Fig. 6.38 Corneal erosion

Treatment

1Acute symptoms

•Antibiotic ointment q.i.d. and cyclopentolate 1% b.d.

•Pressure patching should not be used as it may impair healing and does not improve comfort.

•In severe cases a bandage contact lens alleviates pain but may not improve healing.

•Debridement of heaped/scrolled areas of epithelium with a cellulose sponge may enhance healing.

•Topical diclofenac 0.1% reduces pain.

•Topical anaesthetic dramatically relieves pain but should not be dispensed for patient use.

•Hypertonic sodium chloride 5% drops q.i.d. and ointment at bedtime may improve epithelial adhesion.

•Following resolution, some authorities advise using a prophylactic topical lubricant such as carbomer gel q.i.d. for several months.

2Recurrent symptoms

•Topical lubricant gel or ointment instilled at bedtime used long-term may be sufficient.

•Simple debridement of epithelium of involved areas which may be followed by smoothing of Bowman layer with a diamond burr or an excimer laser.

•Long-term extended-wear bandage contact lenses.

•Anterior stromal puncture for localized areas off the visual axis may reduce the recurrence rate; it may not be necessary to remove the epithelium prior to the procedure.

Xerophthalmia

Pathogenesis

Vitamin A is essential for the maintenance of the body's epithelial surfaces, for immune function and for the synthesis of retinal photoreceptor proteins. Xerophthalmia refers to the spectrum of ocular disease caused by lack of vitamin A, and is a late manifestation of severe deficiency. Lack of vitamin A in the diet may be caused by malnutrition, malabsorption, chronic alcoholism or by highly selective dieting. The risk in infants is increased if their mothers are malnourished and by coexisting diarrhoea or measles.

Diagnosis

1 Symptoms are night blindness (nyctalopia), discomfort and loss of vision.

2Conjunctiva

•Xerosis is characterized by dryness of the conjunctiva in the interpalpebral zone with loss of goblet cells, squamous metaplasia and keratinization.

•Bitot spots are triangular patches of foamy keratinized epithelium in the interpalpebral zone (Fig. 6.39A) thought to be caused by Corynebacterium xerosis.

3Cornea

•Lustreless appearance due to secondary xerosis.

•Bilateral punctate corneal epithelial erosions in the interpalpebral zone can progress to epithelial defects but are reversible with treatment.

•Keratinization.

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•Sterile corneal melting by liquefactive necrosis (keratomalacia) which may result in perforation (Fig. 6.39B).

4Retinopathy, characterized by yellowish peripheral dots, may occur in advanced cases and is associated with decreased electroretinogram amplitude.

Table 6.7 -- WHO grading of Xerophthalmia

XN = night blindness

X1 = conjunctival xerosis (X1A) with Bitot spot (X1B)

X2 = corneal xerosis

X3 = corneal ulceration, less than one-third (X3A); more than one-third (X3B)

XS = corneal scar

XF = xerophthalmic fundus

Fig. 6.39 Xerophthalmia. (A) Bitot spot; (B) keratomalacia and perforation

(Courtesy of N Rogers – fig. A; S Kumar Puri – fig. B)

Treatment

Keratomalacia is an indicator of very severe vitamin A deficiency and should be treated as a medical emergency due to the risk of death, particularly in infants.

1Systemic treatment involves oral (oil-based 200 000 IU) or intramuscular vitamin A (aqueous-based 100 000 IU) for keratomalacia. Multivitamin supplements and dietary sources of vitamin A are also administered.

2Local

•Intense lubrication.

•Topical retinoic acid may promote healing but is not sufficient without systemic supplements.

•Corneal perforation is addressed surgically as necessary.

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