Ординатура / Офтальмология / Английские материалы / Contact Lenses in Ophthalmic Practice_Mannis, Zadnik. Coral-Ghanem, Kara-Jose_2003

280 C. Coral-Ghanem and D.A. Berntsen

3.Ghormley NR. Rigid EW lenses: complications. Int Contact Lens Clin. 1987; 14:219.

4.Carrell BA, Bennett ES, Henry VA, Grohe RM. The effect of rigid gaspermeable lens cleaners on lens parameter stability. J Am Optom Assoc. 1992; 63:193–198.

5.Grohe RM, Caroline PJ, Norman CW. Rigid gas-permeable surface cracking. Part I: clinical syndrome. Contact Lens Spectrum. 1987;2:37–45.

6.Grohe RM, Caroline PJ. RGP non-wetting syndrome. Contact Lens Spectrum. 1989;4:32–44.

7.Henry VA, Bennett ES, Forrest JF. Clinical investigation of the Paraperm EW rigid gas-permeable contact lenses. Am J Optom. 1987;64:313–320.

8.Schnider CM. Rigid gas-permeable extended wear. Contact Lens Spectrum. 1990;5:101–106.

9.Bennett ES. How to manage the rigid lens wearer. Rev Optom. 1986;123: 102–110.

10.Grohe RM, Lebow KA. Vascularized limbal keratitis. Int Contact Lens Clin. 1989;16:197–209.

11.Miller WL. Rigid gas-permeable surface defects associated with an isolated case of vascularized limbal keratitis. Int Contact Lens Clin. 1995;22:201–212.

12.Schnider CM, Terry RB, Holden BA. Effects of lens design on peripheral corneal desiccation. J Am Optom Assoc. 1997;68:163–170.

13.Bennett ES. Rigid gas-permeable lens problem solving. In: Bennett ES, Henry VA, eds. Clinical Manual of Contact Lenses. Philadelphia: Lippincott Williams & Wilkins, 2000:181–210.

14.Wilson SE, Lin DTC, Klyce SD, et al. Rigid contact lens decentration: a risk factor for corneal warpage. CLAO J. 1990;16:177–182.

15.Kikkawa Y, Salmon TO. Rigid lens tear exchange and the tear mucous layer.

Contact Lens Forum. 1990;15:17–24.

16.Schnider CM, Bennett ES, Grohe RM. Rigid extended wear. In: Bennett ES, Weissman BA, eds. Clinical Contact Lens Practice. Philadelphia: JB Lippincott, 1991:1–14.

17.Hill RM, Brezinski SD. The center thickness factor. Contact Lens Spectrum. 1987;2:52–54.

18.Kalin NS, Maeda N, Klyce SD, et al. Automated topographic screening for keratoconus in refractive surgery candidates. CLAO J. 1996;22:164–167.

19.Ruiz-Montenegro J, Mafra CH, Wilson SE, et al. Corneal topographic alterations in normal contact lens wearers. Ophthalmology. 1993;100:128–134.

20.Weinstock FJ. Contact Lens Fitting: A Clinical Text Atlas. New York: JB Lippincott, 1989;11:10–11.

24

Lid and Conjunctival Complications Associated with Contact Lens Use

Cleusa Coral-Ghanem,

Newton Kara-Jose´,

and LeVelle Jenkins

1.Why does ptosis occur in contact lens users, and how is it managed?

Ptosis generally occurs in association with inflammatory conditions related to blepharitis or meibomianitis, which leads to subclinical lid edema. Ptosis is most common in rigid contact lens users, principally in those whose contact lenses have a large diameter or a thick edge. One study by van der Bosch and Lemij1 demonstrated that rigid contact lens users, when compared with a control group, had an overall 0.5-mm decrease in superior lid height. Ptosis has also been described in patients whose contact lenses were ‘‘lost’’ and remained for a period of time in the superior cul-de-sac.2 In this position, the ‘‘lost’’ contact lens produced chronic irritation and subsequent ptosis. For this reason, whenever a patient has a history of contact lens use and the subsequent development of ptosis, the conjunctival fornices and tarsi should be carefully examined and stained with fluorescein. This may sometimes reveal the lost lens.

In the hydrophilic contact lens wearer, ptosis is most commonly due to giant papillary conjunctivitis in an advanced phase. Unilateral cases are diagnosed earlier because of the obvious difference between the two upper lids.

When a patient with ptosis wants contact lenses, it is better to correct the lid abnormality prior to the fitting, and, whenever possible, to opt for a hydrophilic lens.

24. Lid and Conjunctival Complications 283

the contact lens, producing a decrease in visual acuity and decreasing lens tolerance. The contact lens exacerbates the inflammation of the lid margins. In these cases, different factors may be involved:

●Mechanical irritation by the edge of the contact lens with blinking

●Chemical irritation from the contact lens material or maintenance solutions

●Deposits on the contact lens

Management

1.Stop contact lens use.

2.Perform lid massage and meibomian gland expression when there is an excess of lipids. If the exudate is milky white instead of clear, the bacteria have infected the gland itself, and an oral antibiotic is warranted.

3.Use warm compresses to increase the fluidity of the secretions.

4.Cleanse the upper and lower lid margins with diluted baby shampoo or commercial solutions. This treatment removes eyelash and skin debris laden with bacteria.

5.Treat with topical antibiotic in mixed forms of seborrheic blepharitis associated with staphylococcal disease or meibomianitis. Antibiotics are less effective in patients with pure seborrheic blepharitis.7,10

6.Prescribe systemic antibiotics such as doxycycline or tetracycline. In patients with meibomianitis who do not also have acre rosacea, the antibiotic dose can be diminished or discontinued after 3 months of treatment. The use of lipophilic antibiotics diminishes the production of bacterial lipases. Moreover, tetracycline reduces the production of cholesterol esters necessary for the development of blepharitis and inhibits the activity of collagenase, preventing corneal vascularization.11

7.A mild topical corticosteroid can be used for a short period of time in cases of severe inflammation and discomfort.

8.After regression of lid inflammation, one can refit the lens with the causative factors eliminated.

3.How does contact lens–induced superior limbic keratoconjunctivitis manifest itself; why does it occur; and how is it treated (Color Plate 27)?

Symptoms and Signs

●Photophobia

●Burning

●Excessive tearing

●Mild lid swelling

●Pseudoptosis

●Blepharospasm

24. Lid and Conjunctival Complications 285

●Burning

●Foreign body sensation

●Punctate keratopathy and/or corneal erosion

●Fluorescein staining (generally in the paracentral cornea concentric to the limbus)

Causes

An improper lens–cornea relationship due to a large contact lens, a tight lens, a lens with surface deposits, poor centration, and lid eversion or inversion.

●Alterations in the material. Alterations in the material with breakage or deterioration of the contact lens can cause mechanical irritation.

●Impurities. Impurities within the contact lens may cause an immediate and intense conjunctival reaction as well as keratitis.

●Deposits. Deposits on the surface of the contact lens may make it rough or excessively tight and may accordingly diminish visual acuity as well as oxygen transmissibility to the cornea.

●Contamination. The surface of the lens can be contaminated by fungi or bacteria and can provoke an irritative conjunctivitis that disappears with removal of the contact lens.

An ocular infection can occur if there is a corneal abrasion. The hydrophilic contact lens for aphakia is the most susceptible to invasion with fungi.

Management

1.Refit with a new contact lens.

2.Remove the deposits with the help of an enzymatic cleaner.

3.Employ specific treatment in cases of compromise of the corneal surface.

6.How and why does mucoprotein conjunctivitis occur in the contact lens user, and what is its management?

Symptoms and Signs

●Ocular irritation

●Discharge

●Blurring of vision because of deposits

●Decreased contact lens tolerance

Causes

●Mucoprotein deposits on the contact lens surface

●Sensitivity to preservatives in contact lens maintenance solutions

286 C. Coral-Ghanem et al.

Management

1.Have the patient temporarily discontinue contact lens wear.

2.Start steroid and antibiotic drops.

3.Remove deposits or exchange contact lenses.

4.Change the method of contact lens maintenance.

5.Refit with rigid gas permeable (RGP) lenses or lower water content soft lenses.

If the patient tends to be a deposit former, check for abnormalities in the tear film and the meibomian glands.

Mucoprotein conjunctivitis is most common in hydrophilic lens wearers, principally those using high-water-content lenses.

7.How does giant papillary conjunctivitis (GPC) manifest, and what are the causes?

Symptoms and Signs

Initial symptoms include decreased lens tolerance or loss of tolerance to contact lens wear, increased itching after lens removal, increased mucus discharge in the morning, and photophobia. Vision can be interrupted because of the deposits on the lens itself or the displacement of the lens due to superior lid papillary hypertrophy.

Contact Lens Deposits

There are a variety of morphologic characteristics of these deposits. They may be classified by their microscopic appearance as granular, trabecular, cellular, or mixed.15 The higher the water content, the larger the amount of deposits and the more difficult it is to keep the contact lens clean.16 It appears that there is no predisposition for the appearance of a specific type of protein deposit on the lens surface.17,18 Although a deposit-coated contact lens does not necessarily lead to the occurrence of GPC,19 patients with GPC characteristically have deposits on the lens surface.

Giant Papillae on the Superior Tarsus (Color Plates 35 and 36).

From 0.3 to 2 mm in diameter, tarsal papillae may frequently exceed 1 mm in diameter and are almost always found on the superior tarsus, their size generally reflecting the stage of the disease.20 The initial presentation of giant papillae appears to be related to the type of contact lens used. The use of a rigid contact lens is associated initially with papillae at the lid margin, which then increase in the direction of the superior tarsus. The use of hydrophilic contact lenses is often associated with the opposite pattern, in which the papillae are generally seen at the superior tarsus and advance in the direction of the palpebral margin.21,22 Fluorescein staining of the papillae occurs when the endothelial cells are mechanically damaged or when the apex is flattened in the form of a crater.22,23 The patient with giant papillary conjunctivitis may

24. Lid and Conjunctival Complications 287

have minimal or no symptoms, but the papillae may enlarge anew when exposed to the suspected allergic stimulus, specifically protein deposits on the surface of the contact lens.24,25 Total regression of giant papillae may take months to years.26 In the advanced stages, giant papillary conjunctivitis may cause ptosis of the lid.27

Causes of GPC

Giant papillary conjunctivitis is likely a delayed hypersensitivity response of a cutaneous basophilic type. The hypothesis is that the principal causes inciting antigen and disease are deposits on the contact lens or the lens material. In the majority of cases, a decrease in the reaction occurs with a new contact lens, even if it is the same material. The contact lens coated with deposits causes conjunctival trauma with liberation of neutrophilic chemotactic factors. The trauma is related also to the development of GPC encountered in patients submitted to surgery when the nylon suture remains exposed, causing mechanical irritation to the superior tarsal conjunctiva. One encounters similar manifestations in patients with prostheses, extrusion of scleral implants, keratinized dermoid cysts, and cyanoacrylate adhesives. Other forms of trauma include the edge of the contact lens that comes into contact with the superior tarsus. Chronic trauma predisposes the conjunctiva to a major absorption of antigen. The trauma is followed by hypersensitivity reaction of types I and IV. The histologic findings are similar to those in vernal conjunctivitis.28

8.What is the treatment of giant papillary conjunctivitis?

In early GPC with mild signs and symptoms, decreased wearing time is recommended; alternatively, disposable contact lenses with daily removal can be employed.

In patients with moderate signs and symptoms, it is advisable to discontinue use for 1 to 4 weeks, especially if there is fluorescein staining at the apices of the papillae. With the removal of the contact lens, the symptoms disappear almost immediately or within 4 to 5 days.29 Removal of the traumatic agent produces an improvement in the clinical picture.30 The papillae retain their form for weeks or months and very slowly become less elevated, eventually transforming into flattened disks approximately 1 mm in diameter.

Exchange of the contact lens for a new one of a different material and a different design is recommended. If possible, it is advisable to switch to disposable, frequent planned-replacement, or RGP lenses. One-day or 1- to 2-week disposable contact lenses are desirable in this situation because they can be disposed of frequently. The daily use of disposable contact lenses requires the daily use of a surfactant cleaner and daily disinfection, as with conventional hydrophilic lenses. Hydrogen peroxide is a disinfection solution without preservative that

288 C. Coral-Ghanem et al.

will eliminate the possibility of additional intolerance to preservative, and its use, together with enzymatic cleaner, is also beneficial.

Management

1.Increase the use of enzymatic agents to keep lens clean.

2.Discourage continuous wear because it favors greater deposit formation.

Topical Corticosteroids

Corticosteroids can be used in the initial phase of treatment. The limited use of topical steroids is suggested in cases of severe GPC to minimize the hyperproduction of mucus, extreme hyperemia, cellular infiltrates, and inflammatory mediators present in the lacrimal area in stage IV GPC, for which conventional therapy can be used. Corticosteroids do not treat the cause of GPC but rather reduce or eliminate the symptoms by controlling the inflammatory reaction. The patient should be alerted to the risk of prolonged use of corticosteroids, principally the development of secondary glaucoma or steroid-induced cataract.

Histamines and other vasoactive substances in the surrounding tissue require 2 weeks to be metabolized or destroyed by enzymes. In this interim, to alleviate symptoms, the patient can use vasoconstrictor substances, combined medicines such as olopatadine 0.1% drops, or corticosteroids.

Mast Cell Stabilizers

The use of these substances is an attempt to interfere with the cellular response to the antigenic stimulus.

Disodium Cromoglycate (2% to 4%)

Cromoglycate sodium stabilizes the membrane of mast cells, thereby avoiding the release of histamine and other biochemical mediators. When applied topically in stage I or II GPC, sodium cromoglycate prevents the signs and symptoms associated with type I allergic reactions, including GPC.31

The side effects of sodium cromoglycate are minimal. They include burning or stinging with application of the drops.32 Two to four drops a day are recommended while the patient is using contact lenses.

Lodoxamide 0.1%

Lodoxamide 0.1% (Alomide ) acts to inhibit the degranulation of mast cells and the migration of eosinophils. It alleviates itching, photophobia, and decreases secretions. The recommended dose is four times per day for 3 months. It generally takes 7 to 14 days for significant effect, and it may be used with vasoconstrictors and antihistamines.

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Mast Cell Stabilizer Plus Antihistamine

Olopatadine Chlorhydrate 0.1% (Patanol )

Olopatadine acts to block H1 receptors, inhibiting the release of histamine and alleviating itching. It inhibits inflammatory mediators [triptase and prostaglandin D2 (PGD2)]. It stabilizes mast cell membranes, diminishing the recurrences. It also decreases hyperemia through its decongestant activity. Two drops daily are recommended at intervals of 6 to 8 hours.

The treatment of GPC in rigid contact lens users is similar to that in hydrophilic lens users. The difference is that one can use a polish on rigid lenses to eliminate deposits without exchanging the lens. Thin and smooth-edged designs are less likely to incite mechanical lid irritation and the deposit of debris. There is an inverse relation between the oxygen permeability (Dk) of the material in an RGP lens and the time of onset of giant papillary conjunctivitis.33 It may be necessary to change the design and the material of the RGP or move to a polymethylmethacrylate lens.

9.What are the principal causes of conjunctival hyperemia?

●Changes in tear film

●Changes in contact lens material

●Air conditioning

●Eye rubbing

●Insufficient blinking

●Contact lens deposits

●Corneal hypoxia

●Insufficient lubrication of contact lens

●Poor contact lens–cornea relationship

●Environmental pollution

●Allergic reactions to preservatives in solutions

●Toxic reactions to lens care solutions

●Traumatic insertion or removal of the contact lenses

10.How and why does acute early-morning red eye occur (Color Plate 30)?

Symptoms and Signs

●Unilateral ocular pain in the morning upon arising

●Intense photophobia and tearing

●Limbal and bulbar conjunctival injection

●Subepithelial or anterior stromal infiltrates a few millimeters from the limbus

●Absence of superficial punctate keratitis