4.1 Superficial Punctate Keratopathy


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


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 corneal ulceration.

Other. Conjunctival injection, watery discharge.

Figure 4.1.1 Superficial punctate keratopathy stained with fluorescein.


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 4.20, 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: Decreased corneal sensation. May progress to corneal ulceration. SEE 4.6, NEUROTROPHIC KERATOPATHY.

    • Ultraviolet burn/photokeratopathy: Often in welders or from sunlamps. SEE 4.7, 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, as well as any drop 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: SPK can occur from relatively mild trauma, such as chronic eye rubbing.

    • Mild chemical injury: SEE 3.1, CHEMICAL BURN.

    • Thygeson keratitis: Bilateral, recurrent epithelial keratitis (raised epithelial staining lesions, not SPK) without conjunctival injection. SEE 4.8, THYGESON SUPERFICIAL PUNCTATE KERATITIS.


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

  • 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 or misdirected lashes.

  • 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 instillation of fluorescein.


  • Noncontact 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.

  • Contact lens wearers with a large amount of SPK are seen every day or two 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 4.20, CONTACT LENS-RELATED PROBLEMS). Contact lens wearers with a small amount of SPK are rechecked in several days to 1 week, depending on symptoms and degree of SPK.

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

4.2 Recurrent Corneal Erosion


Recurrent attacks of acute ocular pain, photophobia, foreign body sensation, and tearing. The pain may awaken patients from sleep or occur immediately upon eye opening. There is often a history of prior corneal abrasion in the involved eye.


Critical. Localized irregularity and mobility of the corneal epithelium (fluorescein dye may outline the area with negative or positive staining) or a corneal abrasion. Epithelial changes may resolve within hours of the onset of symptoms so abnormalities may be subtle or absent when the patient is examined.

Other. Corneal epithelial dots or small cysts (microcysts), a fingerprint pattern, or map-like lines may be seen in both eyes if epithelial basement membrane (map–dot–fingerprint) dystrophy is present. These findings may also be seen unilaterally and focally in any eye that has recurrent erosions.


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

  • Anterior corneal dystrophy: Epithelial basement membrane (most common), Reis–Bücklers, Thiel–Behnke, 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, cataract surgery, or any surgery in which the corneal epithelium is removed (either therapeutically or for visualization).


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

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


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. It is important to educate patients that persistent use of lubricating ointment (5% sodium chloride or tear ointment) for 3 to 6 months following the initial healing process reduces the chance of recurrence.

4.3 Dry Eye Syndrome


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 (e.g., when working on a computer that results in decreased blink rate). Usually bilateral and chronic (although patients sometimes are seen with recent onset in one eye). Discomfort often out of proportion to clinical signs.



  • Scanty or irregular tear meniscus seen at the inferior eyelid margin: The normal meniscus should be at least 0.5 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



  • Idiopathic: Commonly found in menopausal and postmenopausal women.

    • Evaporative: Lipid layer tear deficiency; often associated with blepharitis or meibomian gland dysfunction. Symptoms may be worse in the morning with complaints of visual blurring upon waking.

    • Aqueous deficient: Aqueous layer tear deficiency; aqueous production decreases with age. Symptoms frequently worse later in the day or after extensive use of the eyes.

    • Combination: Evaporative and aqueous deficiency often occurs together. May also include a 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, granulomatosis with polyangiitis [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, antispasmodics, tricyclic antidepressants, beta blockers, diuretics, retinoids, selective serotonin reuptake inhibitors, chemotherapy).

  • Infiltration of the lacrimal glands (e.g., sarcoidosis, tumor).

  • Postradiation fibrosis of the lacrimal glands.

  • Vitamin A deficiency: Usually from malnutrition, intestinal malabsorption, or bariatric surgery. SEE 13.7, VITAMIN A DEFICIENCY.

  • After corneal refractive surgery such as photorefractive keratectomy (PRK) and laser in situ keratomileusis (LASIK): Likely secondary to disruption of corneal nerves and interference with normal reflex tearing.


  • History and external examination to detect underlying etiology.

  • Slit lamp examination with fluorescein stain to examine the ocular surface and tear break-up time. May also use rose bengal or lissamine green stain to examine the cornea and conjunctiva. Tear meniscus is best examined prior to the instillation of eye drops.

  • 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.

  • Other potentially helpful in-office tests include measurement of tear osmolarity and level of matrix metalloproteinase-9 (MMP-9); elevation of these factors suggests dryness and inadequate tear film. Tear lactoferrin can also be measured; low levels suggest aqueous deficient dry eye disease.

  • Consider screening for Sjögren syndrome.


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

NOTE: Patients with significant dry eye should be discouraged from contact lens wear and corneal refractive surgery such as PRK and LASIK. 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


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


Critical. Short fluorescein-staining strands of degenerated epithelial cells surrounding a mucus core adherent to anterior surface of cornea.

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


  • Severe ocular dryness: Most common cause. SEE 4.3, DRY EYE SYNDROME.

  • SLK: Filaments are located in the superior cornea, in association with superior conjunctival injection, superior punctate fluorescein staining, and superior corneal pannus. SEE 5.4, SUPERIOR LIMBIC KERATOCONJUNCTIVITIS.

  • Recurrent corneal erosions: Recurrent spontaneous corneal abrasions often occurring upon waking. 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) or ptosis.

  • Neurotrophic keratopathy: SEE 4.6, NEUROTROPHIC KERATOPATHY.


  • History, especially for the previously mentioned conditions.

  • Slit lamp examination with fluorescein staining.


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


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


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).

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

Figure 4.5.1 Exposure keratopathy with fluorescein.


  • 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, eyelid surgery such as excisional procedure, chemical burn, or herpes zoster ophthalmicus).

  • 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 (e.g., Parkinson disease, neurotrophic cornea).


  • History: Previous Bell palsy or eyelid surgery? Thyroid disease?

  • 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.

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

  • 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).

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


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


Foggy or blurry vision, red eye, foreign body sensation, swollen eyelid.


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


  • Early: Perilimbal injection and intrapalpebral corneal punctate epithelial defects or a frank nonhealing epithelial defect with rolled edges, stromal edema, and Descemet folds. Typically located inferior to the visual axis.

  • Late: Corneal ulcer usually without infectious infiltrate, although concomitant infectious keratitis may occur. 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. Progressive thinning may occur rapidly and lead to a descemetocele (corneal stromal loss down to Descemet membrane) or perforation.

Differential Diagnosis



Occurs in eyes with diminished or absent corneal sensation. Denervation causes the corneal epithelium and tear film to become abnormal and unstable. May occur with any of the following conditions:

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

  • Following ocular surgery, particularly after corneal incisional or laser surgery (e.g., keratoplasty, LASIK, PRK).

  • Tumor (especially an acoustic neuroma, where both the fifth and seventh cranial nerves may
    be affected) or any neurologic insult/disease of the fifth cranial nerve (e.g., brainstem stroke, trauma, multiple sclerosis, Riley–Day syndrome).

  • Chronic contact lens wear.

  • Diabetic neuropathy.

  • Extensive panretinal photocoagulation: May damage the long ciliary nerves (these patients often have concurrent diabetic neuropathy).

  • Complication of trigeminal nerve or dental surgery.

  • Complication of radiation therapy to the eye or an adnexal structure.

  • Chronic topical medications (e.g., timolol, topical NSAIDs).

  • Topical anesthetic abuse.

  • 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.

  • Chemical injury or exposure to hydrogen sulfide or carbon disulfide (used in manufacturing).


  • History: Previous episodes of a red and painful eye? Prior herpes infection, cold sores, or shingles rash around the eye and/or forehead? Diabetes? History of irradiation, stroke, or hearing problem? Previous refractive procedure or other eye surgery? Chemical exposure? Smoking history? Topical medications?

  • Prior to anesthetic instillation, test corneal sensation bilaterally with a sterile cotton wisp.

  • Slit lamp examination with fluorescein staining of cornea and conjunctiva.

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

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

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


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

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

  • Corneal ulcer: Daily until significant improvement is demonstrated. Hospitalization may be required for severe ulcers (SEE 4.11, BACTERIAL KERATITIS).

4.7 Ultraviolet Keratopathy


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 worsen 6 to 12 hours after the exposure. Usually bilateral.


Critical. Dense, confluent punctate epithelial defects in an interpalpebral distribution highlighted 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).

  • Thermal burn/keratopathy: Often from contact with curling iron, boiling fluid, fire ember, or flame. Injury usually limited to corneal epithelium; may have marked superficial corneal opacification or eschar. Treat with possible debridement of involved area, and then as for corneal abrasion. SEE 3.2, CORNEAL ABRASION.

  • 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.


  • History: Welding? Sunlamp use? Topical medications? Chemical exposure? Prior episodes? Use of protective eyewear?

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

  • If chemical exposure suspected, check pH of tear lake in upper and lower conjunctival fornices. If not neutral (6.8 to 7.5), treat as chemical burn. SEE 3.1, CHEMICAL BURN.


  • If a bandage soft contact lens was placed, the patient is seen in 1 to 2 days.

  • Reliable patients without a bandage contact lens are asked to assess their own symptoms after 24 hours (if a patch was placed, it is removed at this time).

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

  • If still significantly symptomatic, reevaluate. If significant punctate staining is present, retreat with a cycloplegic, antibiotic, and possible pressure patch, as discussed previously.

  • Unreliable patients or those with an unclear etiology should not be patched and should not have a bandage contact lens placed. Such patients should be reexamined in 1 to 2 days.

4.8 Thygeson Superficial Punctate Keratitis


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


Critical. Coarse stellate gray-white corneal epithelial opacities that are often central, slightly elevated, and stain lightly with fluorescein. Underlying
subepithelial infiltrates may be present. (see Figure 4.8.1).

Figure 4.8.1 Thygeson superficial punctate keratitis.

Other. Minimal to no conjunctival injection, corneal edema, anterior chamber reaction, or eyelid abnormalities.

Differential Diagnosis



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


Irritation, redness, decreased vision; may be asymptomatic.


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

  • Pterygium: Wing-shaped fold of fibrovascular tissue arising from the interpalpebral conjunctiva and extending onto the cornea. There is no associated thinning of the cornea below these lesions. Usually nasal in location (see Figure 4.9.1).

  • 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.

Figure 4.9.1 Pterygium.

Differential Diagnosis

  • Conjunctival intraepithelial neoplasia (CIN): Unilateral papillomatous jelly-like, velvety, or leukoplakic (white) mass, often elevated and vascularized. May not be in a wing-shaped configuration and not necessarily 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. 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. There is often associated underlying corneal thinning.

  • 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.


Elastotic degeneration of deep conjunctival layers resulting in fibrovascular tissue proliferation. Related to sunlight exposure and chronic irritation. More common in individuals from equatorial regions.


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.


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

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

  • 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 a limited duration if recurrent inflammation occurs. A topical antihistamine ± mast cell stabilizer can be used as needed (e.g., bepotastine, ketotifen, olopatadine).

4.10 Band Keratopathy


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


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. (See Figure 4.10.1.).

Other. May have other signs of chronic eye disease.


More Common. Chronic uveitis (e.g., JIA), interstitial keratitis (IK), corneal edema, 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.


  • History: Chronic eye disease? Previous ocular surgery? Chronic exposure to environmental irritants or ocular medications? Systemic disease?

    Figure 4.10.1 Band keratopathy.

  • Slit lamp examination.

  • 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.


  • If surgical removal has been performed, the patient should be examined every few days until the epithelial defect has healed.

  • 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.

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

4.11 Bacterial Keratitis


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


Critical. Focal white opacity (infiltrate) in the corneal stroma associated with an epithelial defect and underlying stromal thinning/tissue loss.

NOTE: An examiner using a slit beam cannot see clearly 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, folds in Descemet membrane, anterior chamber reaction, endothelial fibrin/cell deposition with or without hypopyon formation (which, in the absence of globe perforation, usually represents sterile inflammation), conjunctival injection, upper eyelid edema. Posterior synechiae, hyphema, and increased IOP may occur in severe cases.

Figure 4.11.1 Bacterial keratitis.

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 may mimic the clinical picture of bacterial ulcers. SEE 4.12, FUNGAL KERATITIS.

  • Acanthamoeba: This protozoan classically causes an extremely painful keratitis and/or stromal infiltrate; is associated with perineural invasion. It usually occurs in daily-wear soft contact lens wearers who may or may not practice poor lens hygiene. History of trauma or history of swimming and/or hot tubbing while wearing contact lenses may be elicited. In the early stages, the epithelial abnormality may look 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. If a staining infiltrate develops in a patient with stromal herpetic keratitis, one needs to rule out bacterial 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: Minimal or no discharge, mild iritis, peripheral stromal infiltration with overlying staining and adjacent vascularization, and negative cultures. Corneal melting may be associated with various systemic diseases. SEE 4.22, 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/meibomitis. SEE 4.18, STAPHYLOCOCCAL HYPERSENSITIVITY.

  • Sterile corneal infiltrates: Typically from an immune reaction to contact lens solutions or hypoxia related to contact lens wear. Usually multiple small, often peripheral, subepithelial infiltrates with little overlying staining and minimal anterior chamber reaction. Usually a diagnosis of exclusion after ruling out an infectious process. Similar lesions can occur after adenoviral conjunctivitis, but these tend to be more central and less dense with a preceding history of conjunctivitis. 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 such as Acanthamoeba or herpes simplex stromal keratitis. 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 after the exposure to anesthetic is stopped.


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 Wills Eye, 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). Acute fulminant onset with severe anterior chamber reaction and hypopyon formation are common in the former, while the latter tends to have a more indolent course and occurs in patients often on chronic topical steroids (e.g., corneal transplant patients).

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

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

Figure 4.11.2 Pseudomonal keratitis.


  • History: Contact lens wear and care regimen should always be discussed. Sleeping in contact lenses? Daily or extended-wear lenses? Conventional, frequent replacement, or single use? Disinfecting solutions used? Recent changes in routine? Water exposure (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?

  • 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. Measure the IOP, preferably with a Tono-Pen.

  • Corneal scrapings for smears and cultures if appropriate and if culture media are available. We routinely culture infiltrates if they are larger than 1 to 2 mm, in the visual axis, unresponsive to initial treatment, or if there is suspicion for an unusual organism based on history or examination. SEE APPENDIX 8, CORNEAL CULTURE PROCEDURE.

  • In contact lens wearers suspected of having an infectious ulcer, the contact lenses and case are cultured, if available. Explain to the patient that the cultured contact lenses will be discarded. A positive culture from a contact lens or contact lens case should be interpreted with clinical judgment. While a contaminant can be misleading, a result that supports the examination findings can be helpful.


  • Daily evaluation at first, including repeat 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 (which may initially increase because of scraping for cultures and smears), 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.

  • 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.

  • Consider new or repeat cultures and stains (without stopping treatment) in the setting of non-responsive or worsening infiltrate/ulcer. Treat with fortified antibiotics and modify based on culture results and the clinical course. Hospitalization may be recommended. SEE APPENDIX 8, CORNEAL CULTURE PROCEDURE.

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

  • 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


Pain, photophobia, redness, 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.



  • 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 gray-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



Oct 20, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Cornea

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