Cornea

Cornea


4.1 SUPERFICIAL PUNCTATE KERATOPATHY


Symptoms


Pain, photophobia, red eye, foreign body sensation, mildly decreased vision.


Signs


(See Figure 4.1.1.)




FIGURE 4.1.1. Superficial punctate keratopathy with fluorescein.


Critical. Pinpoint corneal epithelial defects that stain with fluorescein. May be confluent if severe. Staining pattern may allude to etiology. Pain is relieved by the instillation of anesthetic drops.


NOTE: Relief of pain with the instillation of anesthetic drops (e.g., proparacaine) strongly suggests corneal epithelial disease as the etiology of pain. Although anesthetic drop instillation is an essential part of the ocular examination, patients should NEVER be prescribed topical anesthetic drops and the clinician should ensure the patient does not take anesthetic drops from the office. When used chronically, these drops inhibit epithelial healing and may cause ring corneal ulcers.


Other. Conjunctival injection, watery discharge.


Etiology


Superficial punctate keratopathy (SPK) is nonspecific but is most commonly seen in the following disorders, which may be associated with a specific staining pattern:


Superior staining


—Contact lens-related disorder: e.g., chemical toxicity, tight lens syndrome, contact lens overwear syndrome, giant papillary conjunctivitis. See 4.21, Contact Lens-Related Problems.


—Foreign body under the upper eyelid: Typically linear SPK, fine epithelial defects arranged vertically.


—Floppy eyelid syndrome: Extremely loose upper eyelids that evert easily. See 6.6, Floppy Eyelid Syndrome.


—Superior limbic keratoconjunctivitis (SLK): Superior bulbar conjunctival inflammation. See 5.4, Superior Limbic Keratoconjunctivitis.


—Vernal conjunctivitis: Atopy, large conjunctival papillae under the upper eyelid and/or limbus. See 5.1, Acute Conjunctivitis.


Interpalpebral staining


—Dry-eye syndrome: Poor tear lake, decreased tear break-up time, decreased Schirmer test. See 4.3, Dry-Eye Syndrome.


—Neurotrophic keratopathy: May progress to corneal ulceration. See 4.6, Neurotrophic Keratopathy.


—Ultraviolet burn/photokeratopathy: Often in welders or from sun lamps. See 4.7, Thermal/Ultraviolet Keratopathy.


Inferior staining


—Blepharitis: Erythema, telangiectasias, or crusting of the eyelid margins, meibomian gland dysfunction. See 5.8, Blepharitis/
Meibomitis.


—Exposure keratopathy: Poor eyelid closure with failure of eyelids to cover the entire globe. See 4.5, Exposure Keratopathy.


—Topical drug toxicity: e.g., neomycin, gentamicin, trifluridine, atropine, any drops with preservatives, including artificial tears, or any frequently used drop.


—Conjunctivitis: Discharge, conjunctival injection, eyelids stuck together on awakening. See 5.1, Acute Conjunctivitis, and 5.2, Chronic Conjunctivitis.


—Trichiasis/distichiasis: One or more eyelashes rubbing against the cornea (superior SPK if misdirected lashes from upper eyelid). See 6.5, Trichiasis.


—Entropion or ectropion: Eyelid margin turned in or out (superior SPK if upper eyelid abnormality). See 6.3, Ectropion, and 6.4, Entropion.


Other


—Trauma: Can occur from relatively mild trauma, such as chronic eye rubbing.


—Mild chemical injury: See 3.1, Chemical Burn.


—Thygeson SPK: Bilateral, recurrent epithelial keratitis (raised epithelial staining lesions, not SPK) without conjunctival injection. See 4.8, Thygeson Superficial Punctate Keratopathy.


NOTE: Presence of underlying inflammation and infiltrates indicates punctate epithelial keratitis, which appears as granular opalescent devitalized epithelial cells that stain relatively poorly with fluorescein. May stain with rose bengal. May indicate a viral etiology.


Work-Up


1. History: Trauma? Contact lens wear? Eye drops? Discharge or eyelid matting? Chemical or ultraviolet light exposure? Time of day when worse? Snoring or sleep apnea?


2. Evaluate the cornea, eyelid margin, and tear film with fluorescein. Evert the upper and lower eyelids. Check eyelid closure, position, and laxity. Look for inward-growing lashes.


3. Inspect contact lenses for fit (if still in the eye) and for the presence of deposits, sharp edges, and cracks.


NOTE: A soft contact lens should be removed before placing fluorescein in the eye.


Treatment


See the appropriate section to treat the underlying disorder. SPK is often treated nonspecifically as follows:


1. Noncontact lens wearer with a small amount of SPK


—Artificial tears q.i.d., preferably preservative free.


—Can add a lubricating ointment q.h.s.


2. Noncontact lens wearer with a large amount of SPK


—Preservative-free artificial tears q2h.


—Antibiotic (e.g., bacitracin/polymyxin B or erythromycin ointment q.i.d. for 3 to 5 days).


—Consider a cycloplegic drop (e.g., cyclopentolate 1% to 2% t.i.d., or scopolamine 0.25% b.i.d.) for relief of pain and photophobia.


3. Contact lens wearer with a small amount of SPK


—Discontinue contact lens wear.


—Artificial tears four to six times per day, preferably preservative free.


—Can add a lubricating ointment q.h.s.


4. Contact lens wearer with a large amount of SPK


—Discontinue contact lens wear.


—Antibiotic: Fluoroquinolone (e.g., gatifloxacin, moxifloxacin, or besifloxacin) or tobramycin drops four to six times per day, and tobramycin, ciprofloxacin, or bacitracin/polymyxin B ointment q.h.s. If confluent SPK, consider bacitracin/polymyxin B, ciprofloxacin, or tobramycin ointment four to six times per day.


—Consider a cycloplegic drop (e.g., cyclopentolate 1% to 2% t.i.d.) for relief of pain and photophobia.


NOTE: DO NOT patch contact lens-related SPK or epithelial defects because they can quickly develop into severe infectious ulcers.


Follow-Up


1. Non-contact lens wearers with SPK are not seen again solely for the SPK unless the patient is a child or is unreliable. Reliable patients are told to return if their symptoms worsen or do not improve within 2 to 3 days. When underlying ocular disease is responsible for the SPK, follow-up is in accordance with the guidelines for the underlying problem.


2. Contact lens wearers with a large amount of SPK are seen daily until significant improvement is demonstrated. Contact lenses are not to be worn until the condition clears. Antibiotics may be discontinued when the SPK resolves. The patient’s contact lens regimen (e.g., wearing time, cleaning routine) must be corrected or the contact lenses changed if either is thought to be responsible (see 4.21, Contact Lens-Related Problems). Contact lens wearers with a small amount of SPK are rechecked in several days to 1 week, depending on their symptoms and degree of SPK.


NOTE: Contact lens wearers should be told not to wear their lenses when their eyes feel irritated.


4.2 RECURRENT CORNEAL EROSION


Symptoms


Recurrent attacks of acute ocular pain, photophobia, foreign body sensation, and tearing. Typically occur at the time of awakening, when the eyelids are rubbed or opened. There is often a history of prior corneal abrasion in the involved eye. The unpredictability of recurrent erosions may cause patients intense anxiety.


Signs


Critical. Localized roughening of the corneal epithelium (fluorescein dye may lightly outline the area) or a corneal abrasion. Epithelial changes may resolve within hours of the onset of symptoms so that an abnormality is difficult to detect or absent when the patient is examined.


Other. Corneal epithelial dots or small cysts (microcysts), a fingerprint pattern, or maplike lines may be seen in both eyes if epithelial basement membrane (map–dot–fingerprint) dystrophy is present.


Etiology


Damage to the corneal epithelium or epithelial basement membrane from one of the following:


Anterior corneal dystrophy: e.g., epithelial basement membrane (most common), Reis–Bücklers, and Meesmann dystrophies.


Previous traumatic corneal abrasion: Injury may have been years before the current presentation.


Stromal corneal dystrophy: Lattice, granular, and macular dystrophies.


Corneal degeneration: Band keratopathy, Salzmann nodular degeneration.


Keratorefractive, corneal transplant, or cataract surgery.


Work-Up


1. History: History of a corneal abrasion? Ocular surgery? Family history (corneal dystrophy)?


2. Slit-lamp examination with fluorescein staining (visualization of abnormal basement membrane lines may be enhanced by staining the tear film thickly with fluorescein and looking for areas of rapid tear break-up, referred to as “negative staining”).


Treatment


1. Acute episode: Cycloplegic drop (e.g., cyclopentolate 1%) and antibiotic ointment (e.g., erythromycin, bacitracin) four to six times daily. Can use 5% sodium chloride ointment q.i.d. in addition to antibiotic ointment. If the defect is large, a pressure patch or bandage contact lens and topical antibiotic drops q.i.d. may be placed (NEVER patch contact lens wearers). Oral analgesics as needed.


2. Never prescribe topical anesthetic drops for home use.


3. After epithelial healing is complete, artificial tears four to eight times per day and artificial tear ointment q.h.s. for at least 3 to 6 months, or 5% sodium chloride drops four times per day and 5% sodium chloride ointment q.h.s. for at least 3 to 6 months.


4. If the corneal epithelium is loose or heaped and is not healing, consider epithelial debridement. Apply a topical anesthetic (e.g., proparacaine) and use a sterile cotton-tipped applicator or cellulose sponge to gently remove the loose epithelium.


5. For erosions not responsive to the preceding treatment, consider the following:


—Prophylactic medical treatment with 5% sodium chloride ointment q.h.s. or oral doxycycline (matrix metalloproteinase inhibitor) 50 mg b.i.d. with or without a short course of topical corticosteroid drops (e.g., fluorometholone 0.1% b.i.d. to q.i.d. for 2 to 4 weeks).


—Extended-wear bandage soft contact lens for several months with a topical antibiotic until epithelial adhesion is obtained.


—Anterior stromal puncture can be applied to localized erosions, often after trauma, outside the visual axis in cooperative patients. It can be performed with or without an intact epithelium. Stromal puncture may be applied manually at the slit lamp or more recently with a Nd:YAG laser. This treatment may cause small permanent corneal scars that are usually of no visual significance.


—Epithelial debridement with diamond burr polishing of Bowman membrane. Effective for large areas of epithelial irregularity and lesions in the visual axis.


—Phototherapeutic keratectomy (PTK): Excimer laser ablation of the superficial stroma is successful in up to 90% of patients with recurrent erosions. Diamond burr polishing is at least as effective.


—Other treatment options may include alcohol delamination of the corneal epithelium and autologous serum drops.


Follow-Up


Every 1 to 2 days until the epithelium has healed, and then every 1 to 3 months, depending on the severity and frequency of the episodes.


4.3 DRY-EYE SYNDROME


Symptoms


Burning, dryness, foreign body sensation, mildly to moderately decreased vision, excess tearing. Often exacerbated by smoke, wind, heat, low humidity, or prolonged use of the eye (commonly when working on a computer). May worsen later in the day. Usually bilateral and chronic (although patients sometimes are seen with recent onset in one eye). Discomfort often out of proportion to clinical signs.


Signs


Critical.


Scanty or irregular tear meniscus seen at the inferior eyelid margin: The normal meniscus should be at least 1 mm in height and have a convex shape.


Decreased tear break-up time (measured from a blink to the appearance of a tear film defect, by using fluorescein stain): Less than 10 seconds indicates tear film instability.


NOTE: Tear film defects must be randomly located, as isolated areas of repeated early tear break-up may indicate a focal corneal surface irregularity.


Other. Punctate corneal or conjunctival fluorescein, rose bengal, or lissamine green staining; usually inferiorly or in the interpalpebral area. Excess mucus or debris in the tear film and filaments on the cornea may be found in severe cases.


Differential Diagnosis


See 4.1, Superficial Punctate Keratopathy.


Etiology


Idiopathic: Commonly found in menopausal and postmenopausal women.


—Evaporative: Outer lipid layer tear deficiency; often associated with blepharitis or meibomian gland dystrophy.


—Hyposecretory: Middle aqueous layer tear deficiency; production decrease with age.


—Combination: Often an inner mucin layer tear deficiency.


Lifestyle related: Arid climate, allergen exposure, smoking, extended periods of reading/computer work/television viewing.


Connective tissue diseases: e.g., Sjögren syndrome, rheumatoid arthritis, Wegener granulomatosis, systemic lupus erythematosus.


Conjunctival scarring: e.g., ocular cicatricial pemphigoid, Stevens–Johnson syndrome, trachoma, chemical burn.


Drugs: e.g., oral contraceptives, anticholinergics, antihistamines, antiarrhythmics, antipsychotics, antispasmotics, tricyclic antidepressants, beta blockers, diuretics, retinoids, selective serotonin reuptake inhibitors, chemotherapy.


Infiltration of the lacrimal glands: e.g., sarcoidosis, tumor.


Post-radiation fibrosis of the lacrimal glands.


Vitamin A deficiency: Usually from malnutrition, intestinal malabsorption, or bariatric surgery. See 13.7, Vitamin A Deficiency.


After laser in situ keratomileusis (LASIK): Likely secondary to disruption of corneal nerves and interference with normal reflex tearing.


Work-Up


1. History and external examination to detect underlying etiology.


2. Slit-lamp examination with fluorescein stain to examine the tear meniscus and tear break-up time. May also use rose bengal or lissamine green stain to examine the cornea and conjunctiva.


3. Schirmer test. Technique: After drying the eye of excess tears, Schirmer filter paper is placed at the junction of the middle and lateral one-third of the lower eyelid in each eye for 5 minutes. Eyes are to remain open with normal blinking.


—Unanesthetized: Measures basal and reflex tearing. Normal is wetting of at least 15 mm in 5 minutes.


—Anesthetized: Topical anesthetic (e.g., proparacaine) is applied before drying the eye and placing the filter paper. Measures basal tearing only. Abnormal is wetting of 5 mm or less in 5 minutes. Less than 10 mm may be considered borderline. We prefer the less irritating anesthetized method.


Treatment


Mild Dry Eye


Artificial tears q.i.d.


Moderate Dry Eye


1. Increase the frequency of artificial tear application up to q1–2h; use unit dose preservative-free artificial tears.


2. Add a lubricating ointment or gel q.h.s.


3. Lifestyle modification (e.g., humidifiers and smoking cessation).


4. Cyclosporine 0.05% b.i.d. is effective for patients with chronic dry eye and decreased tears secondary to ocular inflammation. Cyclosporine often burns with application for the first several weeks and takes 1 to 3 months for significant clinical improvement. To hasten improvement and lessen side effects, consider treating patients concomitantly with a mild topical corticosteroid drop (e.g., loteprednol 0.5%) b.i.d. to q.i.d. for 1 month while beginning cyclosporine therapy.


5. If these measures are inadequate or impractical, consider punctal occlusion. Use collagen inserts (temporary) or silicone or acrylic plugs (reversible). Be sure any inflammatory component including blepharitis is treated prior to punctal occlusion.


Severe Dry Eye


1. Cyclosporine 0.05%, as described earlier.


2. Punctal occlusion, as described earlier (both lower and upper puncta if necessary), and preservative-free artificial tears up to q1–2h as needed. Consider permanent occlusion by thermal cautery if plugs fall out.


3. Add lubricating ointment or gel b.i.d. to q.i.d., p.r.n.


4. Moisture chamber (plastic film sealed at orbital rim) or goggles with lubrication at night.


5. If mucus strands or filaments are present, remove with forceps and consider 10% acetylcysteine q.i.d.


6. Other therapies may include oral flaxseed oil, oral omega-3 fatty acids, autologous serum tears, topical vitamin A, bandage contact lens, or a scleral lens.


7. Consider a permanent lateral tarsorrhaphy if all of the previous measures fail. A temporary adhesive tape tarsorrhaphy (to tape the lateral one-third of the eyelid closed) can also be used, pending a surgical tarsorrhaphy.



NOTE:


1. In addition to treating the dry eye, treatment for contributing disorders (e.g., blepharitis, exposure keratopathy) should be instituted if these conditions are present.


2. Always use preservative-free artificial tears if dosing is more frequent than q.i.d. to prevent preservative toxicity.


3. If the history suggests the presence of a connective tissue disease (e.g., history of arthritic pain, dry mouth), referral should be made to an internist or rheumatologist for further evaluation.


Follow-Up


In days to months, depending on the severity of the drying changes and the symptoms. Anyone with severe dry eyes caused by an underlying chronic systemic disease (e.g., rheumatoid arthritis, sarcoidosis, ocular pemphigoid) may need to be monitored more closely.



NOTE: Patients with significant dry eye should be discouraged from contact lens wear and LASIK surgery. However, daily disposable contact lenses can be successful if fit loosely and combined with cyclosporine 0.05% and plugs, if needed.


Patients with Sjögren syndrome have an increased incidence of lymphoma and mucous membrane problems and may require internal medicine, rheumatologic, dental, and gynecologic follow-up.


4.4 FILAMENTARY KERATOPATHY


Symptoms


Moderate-to-severe pain, red eye, foreign body sensation, photophobia.


Signs


Critical. Short fluorescein-staining strands of epithelial cells and mucus attached to the anterior surface of the cornea at one end of the strand.


Other. Conjunctival injection, poor tear film, punctate epithelial defects.


Etiology


Dry-eye syndrome: Most common cause. See 4.3, Dry-Eye Syndrome.


Superior limbic keratoconjunctivitis: Filaments are located in the superior cornea, in association with superior conjunctival injection and fluorescein staining, and with superior corneal pannus. See 5.4, Superior Limbic Keratoconjunctivitis.


Recurrent corneal erosions: Recurrent spontaneous corneal abrasions often occurring upon awakening. See 4.2, Recurrent Corneal Erosion.


Adjacent to irregular corneal surface (e.g., postoperative, near a surgical wound).


Patching: e.g., postoperative, after corneal abrasions.


Neurotrophic keratopathy: See 4.6, Neurotrophic Keratopathy.


Chronic bullous keratopathy: See 4.28, Aphakic Bullous Keratopathy/Pseudophakic Bullous Keratopathy.


Work-Up


1. History, especially for the previously mentioned conditions.


2. Slit-lamp examination with fluorescein staining.


Treatment


1. Treat the underlying condition.


2. Consider debridement of the filaments. After applying topical anesthesia (e.g., proparacaine), gently remove filaments at their base with fine forceps or a cotton-tipped applicator. This gives temporary relief, but the filaments will recur if the underlying etiology is not treated.


3. Lubrication with one of the following regimens:


—Preservative-free artificial tears six to eight times per day and lubricating ointment q.h.s.


—Punctal occlusion.


—Acetylcysteine 10% q.i.d.


NOTE: Acetylcysteine is not commercially available as a drop but can be made by a compounding pharmacy.


4. If the symptoms are severe or treatment fails, then consider a bandage soft contact lens (unless the patient has severe dry eyes). Extended-wear bandage soft contact lenses may need to be worn for weeks to months. Consider concomitant topical antibiotic use.


Follow-Up


In 1 to 4 weeks, if the condition is not improved, consider repeating the filament removal or applying a bandage soft contact lens. Long-term lubrication must be maintained if the underlying condition cannot be eliminated.


4.5 EXPOSURE KERATOPATHY


Symptoms


Ocular irritation, burning, foreign body sensation, and redness of one or both eyes. Usually worse in the morning.


Signs


Critical. Inadequate blinking or closure of the eyelids, leading to corneal drying. Punctate epithelial defects are found in the lower one-third of the cornea or as a horizontal band in the region of the palpebral fissure (see Figure 4.5.1).




FIGURE 4.5.1. Exposure keratopathy with fluorescein.


Other. Conjunctival injection and chemosis, corneal erosion, infiltrate or ulcer, eyelid deformity, or abnormal eyelid closure.


Etiology


Seventh nerve palsy: Orbicularis oculi weakness (e.g., Bell palsy). See 10.9, Isolated Seventh Nerve Palsy.


Sedation or altered mental status.


Eyelid deformity: e.g., ectropion or eyelid scarring from trauma, chemical burn, or herpes zoster ophthalmicus (HZO).


Nocturnal lagophthalmos: Failure to close the eyes during sleep.


Proptosis: e.g., due to an orbital process, such as thyroid eye disease. See 7.1, Orbital Disease.


After ptosis repair or blepharoplasty procedures.


Floppy eyelid syndrome: See 6.6, Floppy Eyelid Syndrome.


Poor blink from Parkinson disease.


Work-Up


1. History: Previous Bell palsy or eyelid surgery? Thyroid disease?


2. Evaluate eyelid closure and corneal exposure. Ask the patient to close his or her eyes gently (as if sleeping). Assess Bell phenomenon (the patient is asked to close the eyelids forcefully against resistance; abnormal when the eyes do not rotate upward). Check for eyelid laxity.


3. Check corneal sensation before instillation of anesthetic drops. If sensation is decreased, there is greater risk for corneal complications.


4. Slit-lamp examination: Evaluate the tear film and corneal integrity with fluorescein dye. Look for signs of secondary infection (e.g., corneal infiltrate, anterior chamber reaction, severe conjunctival injection).


5. Investigate any underlying disorder (e.g., etiology of seventh nerve palsy).


Treatment


Prevention is critical. All patients who are sedated or obtunded are at risk for exposure keratopathy and should receive lubrication as recommended in the following.


In the presence of secondary corneal infection, see 4.11, Bacterial Keratitis.


1. Correct any underlying disorder.


2. Preservative-free artificial tears q2–6h. Punctal occlusion with plugs may also be considered.


3. Lubricating ointment q.h.s. or q.i.d.


4. Consider eyelid taping or patching q.h.s. to maintain the eyelids in the closed position. If severe, consider taping the lateral one-third of the eyelids closed (leaving the visual axis open) during the day. Taping is rarely definitive but may be tried when the underlying disorder is thought to be temporary.


5. When maximal medical therapy fails to prevent progressive corneal deterioration, one of the following surgical procedures may be beneficial:


—Partial tarsorrhaphy (eyelids sewn together).


—Eyelid reconstruction (e.g., for ectropion).


—Eyelid gold weight implant (e.g., for seventh nerve palsy).


—Orbital decompression (e.g., for proptosis).


—Conjunctival flap or amniotic membrane graft (for severe corneal decompensation if the preceding fail).


Follow-Up


Reevaluate every 1 to 2 days in the presence of corneal ulceration. Less frequent examinations (e.g., in weeks to months) are required for less severe corneal disease.


4.6 NEUROTROPHIC KERATOPATHY


Symptoms


Red eye, foreign body sensation, swollen eyelid.


Signs


Critical. Loss of corneal sensation, epithelial defects with fluorescein staining.


Other.


Early: Perilimbal injection progressing to corneal punctate epithelial defects or a frank nonhealing epithelial defect with rolled edges, stromal edema, and Descemet folds.


Late: Corneal ulcer with associated iritis. The ulcer often has a gray, heaped-up epithelial border, tends to be in the lower one-half of the cornea, and is horizontally oval. A descemetocele (corneal stromal loss down to Descemet membrane) or perforation may occur.


Differential Diagnosis


See 4.1, Superficial Punctate Keratopathy.


Etiology


Postinfection with varicella zoster virus (VZV) or herpes simplex virus (HSV).


Post-LASIK (or other refractive) eye surgery.


Chronic contact lens wear.


Stroke, multiple sclerosis, Riley–Day syndrome.


Diabetic neuropathy.


Extensive panretinal photocoagulation: may damage the long ciliary nerves.


Complication of trigeminal nerve or dental surgery.


Complication of irradiation to the eye or an adnexal structure.


Tumor (especially an acoustic neuroma).


Topical anesthetic abuse.


Chronic topical medications (e.g., timolol, diclofenac, sulfacetamide).


Crack keratopathy: Often bilateral. Take careful history for crack cocaine smoking or potential exposure. Often helpful to admit patient and remove them from their environment.


Work-Up


1. History: Previous episodes of a red and painful eye (herpes)? Previous ocular shingles rash? Diabetes? Previous irradiation, stroke, or hearing problem? Previous refractive procedure or other eye surgery?


2. Prior to anesthesia instillation, test corneal sensation bilaterally with a sterile cotton wisp.


3. Slit-lamp examination with fluorescein staining of cornea and conjunctiva.


4. Check the skin for herpetic lesions or scars from a previous herpes zoster infection.


5. Look for signs of a corneal exposure problem (e.g., inability to close an eyelid, seventh nerve palsy, absent Bell phenomenon).


6. If suspicious of a central nervous system lesion, obtain a computed tomography (CT) or magnetic resonance imaging (MRI) of the brain.


Treatment


1. Mild-to-moderate punctate epithelial staining: Preservative-free artificial tears q2–4h and artificial tear ointment q.h.s. Consider punctal plugs.


2. Small corneal epithelial defect: Antibiotic ointment (e.g., erythromycin or bacitracin) four to eight times per day for 3 to 5 days or until resolved. Usually requires prolonged artificial tear treatment, as described previously.


3. Corneal ulcer: See 4.11, Bacterial Keratitis, for the work-up and treatment of an infected ulcer. Antibiotic ointment q2h without patching may be used. Alternatively, if the ulcer is sterile, apply antibiotic ointment, cycloplegic drop, and a pressure patch and re-evaluate in 24 hours. Repeat procedure daily until healed. Collagenase inhibitors (e.g., topical acetylcysteine, oral tetracyclines) may promote re-epithelization. A tarsorrhaphy (eyelids sewn together), bandage soft contact lens, conjunctival flap, amniotic membrane graft, or keratoprosthesis may be required. Autologous serum, albumin, or umbilical cord serum eye drops may also be beneficial.


NOTE: Patients with neurotrophic keratopathy and corneal exposure often do not respond to treatment unless a tarsorrhaphy is performed. A temporary adhesive tape tarsorrhaphy (the lateral one-third of the eyelid is taped closed) may be beneficial, pending more definitive treatment.


Follow-Up


1. Mild-to-moderate epithelial staining: In 3 to 14 days.


2. Corneal epithelial defect: Every 1 to 3 days until improvement demonstrated, and then every 5 to 7 days until resolved.


3. Corneal ulcer: Daily until significant improvement is demonstrated. Hospitalization may be required for severe ulcers (see 4.11, Bacterial Keratitis).


4.7 THERMAL/ULTRAVIOLET KERATOPATHY


Symptoms


Moderate-to-severe ocular pain, foreign body sensation, red eye, tearing, photophobia, blurred vision; often a history of welding or using a sunlamp without adequate protective eyewear. Symptoms typically worse 6 to 12 hours after the exposure. Usually bilateral.


Signs


Critical. Confluent punctate epithelial defects in an interpalpebral distribution, seen with fluorescein staining.


Other. Conjunctival injection, mild-to-moderate eyelid edema, mild-to-no corneal edema, relatively miotic pupils that react sluggishly, and mild anterior chamber reaction.


Differential Diagnosis


Toxic epithelial keratopathy from exposure to a chemical (e.g., solvents, alcohol) or drug (e.g., neomycin, gentamicin, antiviral agents).


Exposure keratopathy: Poor eyelid closure. See 4.5, Exposure Keratopathy.


Floppy eyelid syndrome: Loose upper eyelids that evert easily during sleep. See 6.6, Floppy Eyelid Syndrome.


Work-Up


1. History: Welding? Sunlamp use? Topical medications? Chemical exposure? Prior episodes?


2. Slit-lamp examination: Use fluorescein stain. Evert the eyelids to search for a foreign body.


3. If chemical exposure suspected, check pH of tear lake in lower conjunctival fornix. If not neutral (6.8 to 7.5), treat as chemical burn. See 3.1, Chemical Burn.


Treatment


1. Cycloplegic drop (e.g., cyclopentolate 1%).


2. Antibiotic ointment (e.g., erythromycin or bacitracin) four to eight times per day.


3. Consider a pressure patch for the more affected eye for 24 hours in reliable patients.


4. Oral analgesics as needed.


Follow-Up


1. Reliable patients are asked to assess their own symptoms after 24 hours (if a patch was placed, it is removed at this time).


2. If much improved, the patient continues with topical antibiotics (e.g., erythromycin or bacitracin ointment q.i.d.).


3. If still significantly symptomatic, the patient should return for re-evaluation. If significant punctate staining is still present, the patient is retreated with a cycloplegic, antibiotic, and possible pressure patch, as discussed previously.


4. Unreliable patients or those with an unclear etiology should not be patched and should be re-examined in 24 to 48 hours.


4.8 THYGESON SUPERFICIAL PUNCTATE KERATOPATHY


Symptoms


Mild-to-moderate foreign body sensation, photophobia, and tearing. No history of red eye. Usually bilateral with a chronic course of exacerbations and remissions.


Signs


Critical. Coarse stellate gray-white corneal epithelial opacities that are often central, slightly elevated, stain lightly with fluorescein, with or without underlying subepithelial infiltrates (see Figure 4.8.1).




FIGURE 4.8.1. Thygeson superficial punctate keratopathy.


Other. No conjunctival injection, corneal edema, anterior chamber reaction, or eyelid abnormalities.


Differential Diagnosis


See 4.1, Superficial Punctate Keratopathy.


Treatment


Mild


1. Artificial tears four to eight times per day.


2. Artificial tear ointment q.h.s.


3. Consider therapeutic soft contact lens.


4. Treatment based more on patient symptoms than corneal appearance.


Moderate to Severe


1. Mild topical steroid (e.g., fluorometholone 0.1% or loteprednol 0.2% to 0.5% q.i.d.) for 1 to 4 weeks. Then taper very slowly. May need prolonged low-dose topical steroid therapy.


2. If no improvement with topical steroids, a therapeutic soft contact lens can be tried.


3. Cyclosporine 0.05% drops q.d. to q.i.d. may be an alternative or adjunctive treatment, especially in patients with side effects from steroids.


Follow-Up


Weekly during an exacerbation, then every 3 to 6 months. Patients receiving topical steroids require intraocular pressure (IOP) checks every 4 to 12 weeks.


4.9 PTERYGIUM/PINGUECULA


Symptoms


Irritation, redness, decreased vision; may be asymptomatic.


Signs


Critical. One of the following, almost always located at the 3- or 9-o’clock position at the limbus.


Pterygium: Wing-shaped fold of fibrovascular tissue arising from the interpalpebral conjunctiva and extending onto the cornea. Usually nasal in location (see Figure 4.9.1).




FIGURE 4.9.1. Pterygium.


Pinguecula: Yellow-white, flat or slightly raised conjunctival lesion, usually in the interpalpebral fissure adjacent to the limbus, but not involving the cornea.


Other. Either lesion may be highly vascularized and injected or may be associated with SPK or delle (thinning of the adjacent cornea secondary to drying). An iron line (Stocker line) may be seen in the cornea just beyond the leading edge of a pterygium.


Differential Diagnosis


Conjunctival intraepithelial neoplasia (CIN): Unilateral papillomatous jelly-like, velvety, or leukoplakic (white) mass, often elevated, vascularized, not in a wing-shaped configuration, not in the typical 3- or 9-o’clock location of a pterygium or pinguecula. See 5.12, Conjunctival Tumors.


NOTE: Atypical pterygia require biopsy to rule out CIN or melanoma.


Limbal dermoid: Congenital rounded white lesion, usually at the inferotemporal limbus. May be a manifestation of Goldenhar syndrome if accompanied by preauricular skin tags or vertebral skeletal defects. See 5.12, Conjunctival Tumors.


Other conjunctival tumors: e.g., papilloma, nevus, melanoma; see 5.12, Conjunctival Tumors.


Pseudopterygium: Conjunctival tissue adherent to the peripheral cornea. May appear in location of previous trauma, corneal ulceration, or cicatrizing conjunctivitis.


Pannus: Blood vessels growing into the cornea, often secondary to chronic contact lens wear, blepharitis, ocular rosacea, herpes keratitis, phlyctenular keratitis, atopic disease, trachoma, trauma, and others. Usually at the level of Bowman membrane with minimal to no elevation.


Sclerokeratitis: See 5.7, Scleritis.


Etiology


Elastotic degeneration of deep conjunctival layers, related to sunlight exposure and chronic irritation. More common in individuals from equatorial regions.


Work-Up


Slit-lamp examination to identify the lesion and evaluate the adjacent corneal integrity and thickness. Check for corneal astigmatism in the axis of the pterygium.


Treatment


1. Protect eyes from sun, dust, and wind (e.g., sunglasses or goggles if appropriate).


2. Lubrication with artificial tears four to eight times per day to reduce ocular irritation.


3. For an inflamed pterygium or pinguecula:


—Mild: Artificial tears q.i.d.


—Moderate to severe: A mild topical steroid (e.g., fluorometholone 0.1% q.i.d., or loteprednol 0.2% to 0.5% q.i.d.). A nonsteroidal anti-inflammatory drop (e.g., ketorolac 0.4% to 0.5%) may be used two to four times per day to decrease symptoms.


4. If a delle is present, then apply artificial tear ointment q2h. See 4.24, Dellen.


5. Surgical removal is indicated when:


—The pterygium progresses toward the visual axis.


—The patient is experiencing excessive irritation not relieved by the aforementioned treatment.


—The lesion is interfering with contact lens wear.


NOTE: Pterygia can recur after surgical excision. Bare sclera dissection with a conjunctival autograft or amniotic membrane graft reduces the recurrence rate. Intraoperative application of an antimetabolite (5-fluorouracil or mitomycin-C) also reduces recurrence. Complications are reduced if no bare sclera remains.


Follow-Up


1. Asymptomatic patients may be checked every 1 to 2 years.


2. Pterygia should be measured periodically (every 3 to 12 months, initially) to determine the rate at which they are growing toward the visual axis.


3. If treating with a topical steroid, check after a few weeks to monitor inflammation and IOP. Taper and discontinue the steroid drop over several weeks once the inflammation has abated. A nonsteroidal drop may be used periodically for short times for recurrent inflammation.


4.10 BAND KERATOPATHY


Symptoms


Decreased vision, foreign body sensation, corneal whitening; may be asymptomatic.


Signs


(See Figure 4.10.1.)




FIGURE 4.10.1. Band keratopathy.


Critical. Anterior corneal plaque of calcium at the level of Bowman membrane, typically within the interpalpebral fissure, and separated from the limbus by clear cornea. Lucid spaces are often present in the plaque, giving it a Swiss cheese appearance. The plaque usually begins at the 3- and 9-o’clock positions, adjacent to the limbus, and can extend across the cornea.


Other. May have other signs of chronic eye disease.


Etiology


More Common. Chronic uveitis (e.g., juvenile idiopathic arthritis), interstitial keratitis (IK), corneal edema, repeated trauma, phthisis bulbi, long-standing glaucoma, dry eye, ocular surgery (especially retinal detachment repair with silicone oil), idiopathic.


Less Common. Hypercalcemia (may result from hyperparathyroidism, renal failure, sarcoidosis, multiple myeloma, Paget disease of bone, vitamin D excess, etc.), hyperphosphatemia, gout, corneal dystrophy, myotonic dystrophy, long-term exposure to irritants (e.g., mercury fumes), and other causes.


Work-Up


1. History: Chronic eye disease? Previous ocular surgery? Chronic exposure to environmental irritants? Systemic disease?


2. Slit-lamp examination.


3. If no signs of chronic anterior segment disease or long-standing glaucoma are present and the band keratopathy cannot be accounted for, then consider the following work-up:


—Serum calcium, albumin, magnesium, and phosphate levels. Blood urea nitrogen and creatinine. Uric acid level if gout is suspected.


Treatment


Mild (e.g., Foreign Body Sensation)


Artificial tears four to six times per day and artificial tear ointment q.h.s. or q.i.d., p.r.n. Consider bandage contact lens for comfort.


Severe (e.g., Obstruction of Vision, Irritation not Relieved by Lubricants, Cosmetic Problem)


Removal of the calcium may be performed at the slit lamp or under the operating microscope by chelation using disodium ethylenediamine tetraacetic acid (EDTA):


1. Dilute a solution of 15% EDTA to create a 3% mixture by mixing in a 1.0-mL tuberculin syringe, 0.2 mL of 15% EDTA with 0.8 mL of 0.9% normal saline.


2. Anesthetize the eye with a topical anesthetic (e.g., proparacaine) and place an eyelid speculum.


3. Debride the corneal epithelium with a sterile scalpel or a sterile cotton-tipped applicator dipped in topical anesthetic or EDTA solution.


4. Wipe a cellulose sponge or cotton swab saturated with the 3% disodium EDTA solution over the band keratopathy until the calcium clears (which may take 10 to 30 minutes).


5. Irrigate with normal saline, place an antibiotic ointment (e.g., erythromycin), a cycloplegic drop (e.g., cyclopentolate 1% to 2%), and a pressure patch on the eye for 24 hours. (A bandage soft contact lens or an amniotic membrane may be used to cover the epithelial defect.)


6. Consider giving the patient an analgesic (e.g., acetaminophen with codeine).


Follow-Up


1. If surgical removal has been performed, the patient should be examined every 1 to 2 days with repatching (optional), frequent antibiotic ointment, and a cycloplegic until the epithelial defect heals.


2. Residual anterior stromal scarring may be amenable to excimer laser PTK to improve vision. PTK may also be used to try to improve the ocular surface and prevent recurrent erosions.


3. The patient should be checked every 3 to 12 months, depending on the severity of symptoms. Surgical removal can be repeated if the band keratopathy recurs.


4.11 BACTERIAL KERATITIS


Symptoms


Red eye, moderate-to-severe ocular pain, photophobia, decreased vision, discharge, acute contact lens intolerance.


Signs


(See Figure 4.11.1.)




FIGURE 4.11.1. Bacterial keratitis.


Critical. Focal white opacity (infiltrate) in the corneal stroma. An ulcer exists if there is also stromal loss with an overlying epithelial defect that stains with fluorescein.


NOTE: An examiner using a slit beam cannot see through an infiltrate or ulcer to the iris, whereas stromal edema or mild anterior stromal scars are more transparent.


Other. Epithelial defect, mucopurulent discharge, stromal edema, anterior chamber reaction with or without hypopyon formation (which, in the absence of globe perforation, usually represents sterile inflammation), conjunctival injection, corneal thinning, folds in Descemet membrane, upper eyelid edema. Posterior synechiae, hyphema, and increased IOP may occur in severe cases.


Differential Diagnosis


Fungal: Must be considered after any traumatic corneal injury, particularly from vegetable matter (e.g., a tree branch), which may lead to filamentous fungal keratitis. Contact lens wear is another risk factor. Infiltrates commonly have feathery borders and may be surrounded by satellite lesions. Candida infections generally occur in eyes with pre-existing ocular surface disease and look like bacterial ulcers. See 4.12, Fungal Keratitis.


Acanthamoeba: This protozoan causes an extremely painful epithelial keratitis and/or stromal infiltrate. It usually occurs in daily-wear soft contact lens wearers who may or may not practice poor lens hygiene, have a history of swimming while wearing contact lenses, or a history of trauma. In the early stages, the slit-lamp appearance typically looks more like HSV keratitis than a bacterial ulcer. In the late stages (3 to 8 weeks), the infiltrate often becomes ring shaped. See 4.13, Acanthamoeba Keratitis.


HSV: May have eyelid vesicles or corneal epithelial dendrites. A history of recurrent unilateral eye disease or known ocular herpes is common. Bacterial superinfections may develop in patients with chronic herpes simplex keratitis. It is unusual for HSV to have a staining infiltrate; if present, one needs to rule out a superinfection. See 4.15, Herpes Simplex Virus.


Atypical mycobacteria: Usually follows ocular injuries with vegetable matter or ocular surgery, such as cataract extraction, corneal grafts, and refractive surgery (especially LASIK). It has a more indolent course. Culture plates (on Lowenstein Jensen media) must be kept for 8 weeks. An acid-fast bacillus smear is very helpful.


Sterile corneal thinning and ulcers: Usually less painful, minimal or no discharge, iritis, or corneal edema, no infiltrates, and negative cultures. The melting is caused by the associated disease. See 4.23, Peripheral Corneal Thinning/Ulceration.


Staphylococcal hypersensitivity: Peripheral corneal infiltrates, sometimes with an overlying epithelial defect, usually multiple, often bilateral, with a clear space between the infiltrate and the limbus. Conjunctival injection is localized rather than diffuse, and there is less pain. There is minimal-
to-no anterior chamber reaction. Often with coexisting blepharitis. See 4.19, Staphylococcal Hypersensitivity.


Sterile corneal infiltrates: Typically from an immune reaction to contact lens solutions or hypoxia. Usually multiple small, often peripheral, subepithelial infiltrates with an intact overlying epithelium and minimal or no anterior chamber reaction. Usually a diagnosis of exclusion after ruling out an infectious process. Similar lesions can occur after adenoviral conjunctivitis, but these are often more central and more gray. See 5.1, Acute Conjunctivitis.


Residual corneal foreign body or rust ring: History of foreign body injury. May be accompanied by corneal stromal inflammation, edema, and sometimes, a sterile infiltrate. There may be a mild anterior chamber reaction. The infiltrate and inflammation usually clear after the foreign body and rust ring are removed, but a superinfection may occur.


Topical anesthetic abuse: A type of neurotrophic ulcer that should be suspected when there is poor response to appropriate therapy. In the late stages of anesthetic abuse, the corneal appearance may mimic an infectious process despite negative cultures. A large ring opacity, edema, and anterior chamber reaction are characteristic. Crack cocaine keratopathy has a similar appearance. Healing, with or without scarring, typically occurs when the exposure to anesthetic is stopped.


Etiology


Bacterial organisms are the most common cause of infectious keratitis. In general, corneal infections are assumed to be bacterial until proven otherwise by laboratory studies or until a therapeutic trial of topical antibiotics is unsuccessful. At the Wills Eye Institute, the most common causes of bacterial keratitis are Staphylococcus, Pseudomonas, Streptococcus, Moraxella, and Serratia species. Clinical findings vary widely depending on the severity of disease and on the organism involved. The following clinical characteristics may be helpful in predicting the organism involved. However, clinical impression should never take the place of broad-
spectrum initial treatment and appropriate laboratory evaluation. See Appendix 8, Corneal Culture Procedure.


Staphylococcal ulcers typically have a well-defined, gray-white stromal infiltrate that may enlarge to form a dense stromal abscess.


Streptococcal infiltrates may be either very purulent or crystalline (see 4.14, Crystalline Keratopathy). Severe anterior chamber reaction and hypopyon formation are common in the former, and the latter tends to occur in patients on chronic topical steroids.


Pseudomonas typically presents as a rapidly progressive, suppurative, necrotic infiltrate associated with a hypopyon and mucopurulent discharge in the setting of soft contact lens use (see Figure 4.11.2).




FIGURE 4.11.2. Pseudomonal keratitis.


Moraxella may cause infectious keratitis in patients with preexisting ocular surface disease and in patients who are immunocompromised. Infiltrates are typically indolent, located in the inferior portion of the cornea, and have a tendency to be full-thickness and may perforate.


Work-Up


1. History: Contact lens wear and care regimen should always be discussed. Sleeping in contact lenses (this greatly increases the risk of bacterial keratitis and should be strongly discouraged)? Daily or extended-wear lenses? Conventional, frequent replacement, or single use? Disinfecting solutions used? Recent changes in routine? Swimming or hot tub use with lenses? Trauma or corneal foreign body? Corneal surgery? History of refractive surgery? Eye care before visit (e.g., antibiotics or topical steroids)? Previous corneal disease? Systemic illness?


2. Slit-lamp examination: Stain with fluorescein to determine if there is epithelial loss overlying the infiltrate; document the size, depth, and location of the corneal infiltrate and epithelial defect; assess the anterior chamber reaction and look for a hypopyon; and measure the IOP by Tono-Pen.


3. Corneal scrapings for smears and cultures if appropriate. We routinely culture infiltrates larger than 1 to 2 mm, in the visual axis, unresponsive to initial treatment, or if we suspect an unusual organism based on history or examination. See Appendix 8, Corneal Culture Procedure.


4. In contact lens wearers suspected of having an infectious ulcer, the contact lenses and case are cultured, if possible. Explain to the patient that the cultured contact lenses will be discarded.


Treatment


Ulcers and infiltrates are initially treated as bacterial unless there is a high index of suspicion of another form of infection. Initial therapy needs to be broad spectrum.


1. Cycloplegic drops for comfort and to prevent synechiae formation (e.g., scopolamine 0.25% t.i.d.). Use atropine 1% t.i.d. when a hypopyon is present.


2. Topical antibiotics according to the following algorithm:


Low Risk of Visual Loss


Small, nonstaining peripheral infiltrate with at most minimal anterior chamber reaction and no discharge:


—Noncontact lens wearer: Broad-spectrum topical antibiotics [e.g., fluoroquinolone (moxifloxacin, gatifloxacin, besifloxacin, levofloxacin) drops q1–2h].


—Contact lens wearer: Fluoroquinolone (e.g., gatifloxacin, moxifloxacin, ciprofloxacin, besifloxacin, levofloxacin) drops q1–2h; can add tobramycin or ciprofloxacin ointment q.h.s. If using ointment more than q.i.d., use ciprofloxacin ointment.


Borderline Risk of Visual Loss


Medium size (1- to 1.5-mm diameter) peripheral infiltrate, or any smaller infiltrate with an associated epithelial defect, mild anterior chamber reaction, or moderate discharge:


—Fluoroquinolone (e.g., moxifloxacin, gatifloxacin, besifloxacin, levofloxacin) q1h around the clock. Consider starting with a loading dose of q5 min for five doses and then q30 min until midnight then q1h. Moxifloxacin has better Gram-positive coverage. Gatifloxacin and ciprofloxacin have better Pseudomonas and Serratia coverage.


Vision Threatening


Our current practice at Wills Eye is to start fortified antibiotics for most ulcers larger than 1 to 2 mm, in the visual axis, or unresponsive to initial treatment. See Appendix 9, Fortified Topical Antibiotics/Antifungals, for directions on making fortified antibiotics.


—Fortified tobramycin or gentamicin (15 mg/mL) q1h, alternating with fortified cefazolin (50 mg/mL) or vancomycin (25 mg/mL) q1h. This means that the patient will be placing a drop in the eye every one-half hour around the clock. Vancomycin drops should be reserved for resistant organisms, patients at risk for resistant organisms (e.g., due to hospital or antibiotic exposure, unresponsive to initial treatment), and for patients who are allergic to penicillin or cephalosporins. An increasing number of methicillin-resistant Staphylococcus aureus (MRSA) infections are now community acquired. If the ulcer is severe and pseudomonas is suspected, start fortified tobramycin every 30 minutes and fortified cefazolin q1h; in addition, consider fortified ceftazidime q1h.


NOTE: All patients with borderline risk of visual loss or severe vision-threatening ulcers are initially treated with loading doses of antibiotics using the following regimen: One drop every 5 minutes for five doses, then every 30 to 60 minutes around the clock.


3. In some cases, topical corticosteroids are added after the bacterial organism and sensitivities are known, the infection is under control, and severe inflammation persists. Infectious keratitis may worsen significantly with topical corticosteroids, especially when caused by fungus, atypical mycobacteria, or Pseudomonas.


4. Eyes with corneal thinning should be protected by a shield without a patch (a patch is never placed over an eye thought to have an infection). The use of an antimetalloproteinase (e.g., doxycycline 100 mg b.i.d.) may help to suppress connective tissue breakdown and prevent the perforation of the cornea.


5. No contact lens wear.


6. Oral pain medication as needed.


7. Oral fluoroquinolones (e.g., ciprofloxacin 500 mg p.o. b.i.d.; moxifloxacin 400 mg p.o. q.d.) penetrate the cornea well. These may have added benefit for patients with scleral extension or for those with frank or impending perforation. Ciprofloxacin is preferred for Pseudomonas and Serratia.


8. Systemic antibiotics are also necessary for Neisseria and Haemophilus infections [e.g., ceftriaxone 1 g intravenously (i.v.) if corneal involvement, or intramuscularly (i.m.) q12–24h if there is only conjunctival involvement]. Oral fluoroquinolones have been used for Neisseria gonorrhea, but there is increasing resistance in some locations and in men who have sex with men.


9. Admission to the hospital may be necessary if:


—Infection is sight threatening.


—Patient has difficulty administering the antibiotics at the prescribed frequency.


—High likelihood of noncompliance with drops or daily follow-up.


—Suspected topical anesthetic abuse.


—Intravenous antibiotics are needed (e.g., corneal perforation, scleral extension of the infection, gonococcal conjunctivitis with corneal involvement).


10. For atypical mycobacteria, consider prolonged treatment (q1h for 1 week, then gradually tapering) with one of the following topical agents: fluoroquinolones [e.g., moxifloxacin or gatifloxacin), amikacin (15 mg/mL), clarithromycin (1% to 4%), or tobramycin (15 mg/mL)]. Consider oral treatment with clarithromycin 500 mg b.i.d. Previous LASIK has been implicated as a risk factor for atypical mycobacteria infections (although recently, Staphylococcal infections have been more common post-LASIK).


11. Bacterial coinfection may occasionally complicate fungal (especially candidal) and Acanthamoeba keratitis. Mixed bacterial infections can also occur.


Follow-Up


1. Daily evaluation at first, including repeated measurements of the size of the infiltrate and epithelial defect. The most important criteria in evaluating treatment response are the amount of pain, the epithelial defect size, the size and depth of the infiltrate, and the anterior chamber reaction. The IOP must be checked and treated if elevated (see 9.7, Inflammatory Open-Angle Glaucoma). Reduced pain is often the first sign of a positive response to treatment.


2. If improving, the antibiotic regimen is gradually tapered but is never tapered past the minimum dose to inhibit the emergence of resistance (usually t.i.d. to q.i.d. depending on the agent). Otherwise, the antibiotic regimen is adjusted according to the culture and sensitivity results.


3. If cultures were not taken or the cultures were negative and the infiltrate or ulcer does not respond or subsequently worsens, then new cultures (without stopping treatment), stains, and treatment with fortified antibiotics are needed. Treatment is modified based on the culture results. Hospitalization may be recommended. See Appendix 8, Corneal Culture Procedure.


4. A corneal biopsy may be required if the condition is worsening and infection is still suspected despite negative cultures.


5. For an impending or a complete corneal perforation, a corneal transplant or patch graft is considered. Cyanoacrylate tissue glue may also work in a treated corneal ulcer that has perforated despite infection control. Due to concern about drug penetration, antibiotics are often given for 1 to 2 days prior to glue application over an active area of infection.


NOTE: Outpatients are told to return immediately if the pain increases, vision decreases, or they notice an increase in the size of the ulcer when they look in the mirror.


4.12 FUNGAL KERATITIS


Symptoms


Pain, photophobia, red eye, tearing, discharge, foreign body sensation. Often history of minor trauma particularly with vegetable matter (e.g., a tree branch), contact lens wear, chronic eye disease, and/or a history of poor response to conventional antibacterial therapy. Usually more indolent than bacterial keratitis.


Signs


Critical.


Filamentous fungi: Corneal stromal gray-white opacity (infiltrate) with a feathery border. The epithelium over the infiltrate may be elevated above the remainder of the corneal surface, or there may be an epithelial defect with stromal thinning (ulcer).


Nonfilamentous fungi: A yellow-white stromal infiltrate similar to a bacterial ulcer.


Other. Satellite lesions surrounding the primary infiltrate, conjunctival injection, mucopurulent discharge, anterior chamber reaction, hypopyon. The infiltrate is more likely to extend beyond the epithelial defect than in bacterial ulcers.


Differential Diagnosis


See 4.11, Bacterial Keratitis.


Etiology


Filamentous fungi (e.g., Fusarium or Aspergillus species most commonly): Usually from trauma with vegetable matter in previously healthy eyes. There was a Fusarium keratitis epidemic in contact lens wearers associated with Bausch & Lomb’s ReNu with MoistureLoc solution (recalled May 2006).


Nonfilamentous fungi (e.g., Candida species): Usually in previously diseased eyes, e.g., dry eyes, herpes simplex or zoster keratitis, exposure keratopathy, and chronic use of corticosteroid drops (see Figure 4.12.1).




FIGURE 4.12.1. Candida fungal keratitis.

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Oct 2, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Cornea
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