Ординатура / Офтальмология / Английские материалы / Clinical Ocular Pharmacology 5th edition_Bartlett, Jaanus_2008

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Figure 26-19 Using a mounted bovine eye, the techniques of corneal foreign body removal are illustrated. (A) Spud is directed tangentially to the cornea, and the edge is used to lift the foreign body. (B) The tip of a sterile 25-gauge needle is used to lift the foreign body. Note that the bevel of the needle is positioned away from the cornea.

A small crater-like depression results after removal of a corneal foreign body and any accompanying rust ring. Once the foreign body is removed, the management is similar to treating a corneal abrasion. If the corneal disruption is minimal and accompanying symptoms are not significant, then broad-spectrum antibiotics, such as 0.5% moxifloxacin drops during the day and 0.3% ciprofloxacin ointment at bedtime, are used until the corneal tissue heals (Figure 26-22). NSAIDs, such as

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Figure 26-21 Corneal rust ring removal. Introduced tangentially to the cornea (A), the Alger brush is used to remove rust-containing epithelial cells gently (B). (From Casser L, Fingeret M, Woodcome HT. Corneal rust ring removal. In: Atlas of primary eyecare procedures, ed. 2. Norwalk, CT:Appleton & Lange, 1997: 170–173.)

topical 0.1% diclofenac, provide pain relief, especially after corneal rust ring removal. Therapeutic soft contact lenses can aid in reducing pain by protecting the corneal nerve endings. NSAIDs and prophylactic antibiotics are instilled four times a day with the lens in place.Eye patching provides no benefit in healing time or pain. If an anterior

uveitis is present, cycloplegic agents such as 5% homatropine should be instilled.

A follow-up examination is performed 24 hours later. During follow-up examinations it is important to monitor for signs of secondary bacterial keratitis, secondary fungal keratitis, or an intraocular foreign body that may have

502 CHAPTER 26 Diseases of the Cornea

Figure 26-23 Small Coat’s white ring (arrow) noted during routine examination of an asymptomatic patient. (Courtesy of Pat Caroline.)

been overlooked initially. Most epithelial defects left after foreign body removal heal within 24 to 48 hours.

If the foreign body disrupted Bowman’s membrane and the anterior stroma, a small, usually circular, corneal opacity results after the healing process. Even when located on the visual axis, these small opacities tend not to significantly affect visual acuity and often are noted during routine eye examinations. If a metallic foreign body and rust ring had been present, the resultant opacity often retains a light brown tinge. It also is not uncommon to note a Coat’s white ring during routine slit-lamp examination in an asymptomatic patient. This granular white ring opacity is believed to represent residual iron deposits at the site of a prior corneal foreign body (Figure 26-23).

Once the acute episode related to a corneal foreign body has resolved, it is important to provide patient education about the value of protective eyewear to help prevent future corneal foreign bodies. This is especially important if the patient is monocular, exhibits multiple corneal opacities from past foreign bodies, or is engaged in an occupation in which the likelihood of debris striking the eyes is great.

Lamellar Lacerations and Penetrating Injuries

Etiology

Any sharp object that injures the eye with sufficient force can cause a corneal laceration in which the stroma is penetrated to any depth. Corneal penetration occurs if the object or foreign body passes completely through the cornea. Objects that may cause lacerating or penetrating

injuries include glass, knives, thorns, darts, pencils, wire, or high-velocity foreign bodies from striking or grinding metal. Penetrating injuries caused by metal wire can be associated with intraocular cilia (eyelashes), which may be difficult to detect. Severe ocular injuries occur most commonly in young adult males, with an average age of 25 to 34 years.

One obvious concern in the event of a lamellar laceration or corneal penetration is the insult to the regularity and clarity of the corneal surface and the potential impact on visual acuity.This issue also affects the method chosen for repair. In the case of corneal penetration, there is also concern about intraocular foreign bodies, damage to intraocular structures, and, most importantly, the risk of polymicrobial endophthalmitis.

Diagnosis

A careful history helps to reveal the etiology of the traumatic event, although the possibility of corneal laceration or penetration may not be determined definitively from the history alone. Patient symptomatology associated with deep corneal injuries may vary widely. In the event of a small corneal penetration that has self-sealed,associated symptomatology may be relatively minor. More extensive involvement may produce symptoms of pain, photophobia, tearing, or blepharospasm.

If the history or examination indicates that deep laceration or penetration is present, care must be taken to avoid undue pressure on the globe (Figure 26-24). The use of topical or regional anesthesia helps to minimize blepharospasm as a cause of pressure on the globe. If this is the case, it is best to apply a Fox shield and refer the patient to a cornea specialist.There is no need for further examination and potentially exacerbate the injury.

In the event of a large object impaled into the eye, such as a nail or fishhook (Figure 26-25), the etiology of the corneal wound is obvious. Otherwise, careful slitlamp examination is needed to determine the extent of

Figure 26-24 Corneal laceration (arrow). (Courtesy of Pat Caroline.)

Figure 26-25 Corneal penetration secondary to imbedded fishhook. (Courtesy of Pat Caroline.)

the injury. An optic section at the site of the wound should be evaluated under high magnification to determine the depth of the laceration. A full-thickness corneal “track” suggests that penetration has occurred. Evaluating for Seidel’s sign at the site of the wound also helps to determine whether corneal penetration has occurred (see Chapter 30). It is possible, however, that small lacerations or puncture wounds will self-seal so that Seidel’s sign is negative even after penetration. An anterior chamber reaction, abnormally shaped pupil, cataract, prolapsed black uveal tissue, shallowing of the anterior chamber, iris transillumination defects, vitreous hemorrhage, and dramatic lowering of IOP indicate a corneal penetrating injury.

It is important to examine thoroughly for retained foreign material that may have entered the eye. When indicated, orbital radiographs, B-scans, and/or computed tomography should be obtained to aid in identifying and localizing the object. Magnetic resonance imaging is contraindicated when a metallic intraocular foreign body is suspected.

Management

Small, shallow, nonpenetrating corneal lacerations may be treated the same as corneal abrasions (Figure 26-26). Small self-sealing corneal penetration with no sign of active aqueous loss may be treated conservatively with topical antibiotic prophylaxis, systemic antibiotic prophylaxis to prevent endophthalmitis, and pupillary dilation and cycloplegia. Larger lacerations with tissue loss and obvious corneal penetration require aggressive treatment by a corneal specialist (Figure 26-27).Taping a metal Fox shield over the eye to prevent further injury is appropriate while the patient is transported (Figure 26-28). Corneal suturing, penetrating keratoplasty, tissue adhesives, and conjunctival flaps are among the treatment options that may be used by the corneal specialist.

After surgical repair of a corneal laceration, visual rehabilitation may be obtained with the fitting of a contact lens, even with prominent central scarring and sutures intact. This is especially necessary to help retain binocularity and

Figure 26-26 During routine examination, a small fullthickness corneal scar was noted from prior corneal injury (arrow).The patient also exhibited an iris sphincter tear and small rosette cataract but denied a prior traumatic ocular event.

prevent amblyopia in pediatric patients who have had corneal laceration repair. A positive visual outcome with a contact lens may preclude the need for penetrating keratoplasty in these patients.

Penetrating keratoplasty may restore functional vision when posttraumatic corneal scars are dense and

Figure 26-27 Full-thickness corneal scar secondary to a full thickness penetrating injury. (Courtesy of Pat Caroline.)

504 CHAPTER 26 Diseases of the Cornea

Figure 26-28 If a patient is referred for consultation due to a suspected corneal penetrating injury, it is appropriate to tape a metal Fox shield over the eye to protect from further trauma during transportation. Tape is placed over the edge of the Fox shield to enhance patient comfort (here shown partially completed).

centrally located. Although emergency penetrating keratoplasty may be needed in the event of a large traumatic corneal penetration, the chances of obtaining a clear graft after penetrating keratoplasty improve if the procedure is delayed for at least 3 months.

A lacerating or penetrating injury will likely result in a dense corneal scar (see Figure 26-27). Other complications include anterior synechia, cataracts, and irregular astigmatism. Lacerations more than 4 mm in length have a higher incidence of residual astigmatism. Factors that predict the visual outcome are visual acuities at the time of injury;the presence of hyphema,uveal prolapse,cataract, vitreous loss, vitreous hemorrhage, or retinal detachment; length of the laceration; time duration between the injury and surgical care; and an injury located posterior to the rectus muscle insertion.

Patient education in the use of protective eyewear may help prevent corneal injuries and is particularly important in the monocular patient. Tetanus immunization is recommended following significant corneal injuries.

Recurrent Corneal Erosion

Etiology

RCEs are reoccurring episodes of spontaneous breakdown or sloughing of the epithelial layer of the cornea. RCEs are caused by poor adhesion complexes between the epithelial basement membrane and Bowman’s layer.

Ultrastructural changes include abnormalities in the epithelial basement membrane, defective or absent hemidesmosomes, and decreased anchoring fibrils. The condition may occur after superficial corneal trauma, in conjunction with ABMD, or may be idiopathic.

Approximately 42% to 64% of RCEs occur after superficial trauma to the cornea. Fingernail injuries are reported to be the most common cause of traumatic RCE. Other causes of traumatic RCE include injuries from paper, cardboard, vegetative material, contact lenses, foreign body removal, and trauma to the epithelium during LASIK.

Approximately 16% to 46% of RCEs are associated with ABMD. Other corneal dystrophies associated with RCE include Fuchs’, Reis-Bücklers, lattice, and granular. Dystrophic RCEs are typically bilateral and less severe.

There are many other causes of RCE, but they occur much less frequently.Among these causes are chemical or thermal burns, herpes simplex keratitis, neuroparalytic keratitis, bullous keratopathy, severe dry eyes, nocturnal lagophthalmos, diabetes mellitus, meibomian gland dysfunction, ocular rosacea, and Alport syndrome. Approximately 5% to 30% of RCEs occur spontaneously without any known predisposing factor.

After RCE, the epithelial lesion heals rapidly, usually within 5 days with no visible sequelae.At some later time the symptoms suddenly recur. The mean time to recurrence in one study of 80 patients was 18 months. Although the time from initial injury to recurrence was reported to range from 2 days to 16 years, 63% of recurrences were noted within the first 4 months. Although RCEs can start at any age, depending on the underlying corneal etiology, early adulthood to middle age is the common age at onset.

Diagnosis

The most common symptom of RCE is acute pain on awakening. Other common symptoms include photophobia, tearing, blurred vision, redness, burning, blepharospasm, and foreign body sensation. These symptoms, which can cause great anxiety and lifestyle disruption, tend to recur in cycles of days, weeks, or months.

RCEs can be classified into two main groups. Macroform RCEs may last several days, have large epithelial defects, and involve severe pain. Microform RCEs typically result in milder symptoms that last 30 minutes to several hours,and the epithelium may appear intact at the time of the slit-lamp examination. Most erosions occur in the lower third of the cornea in the approximate location of most Hudson-Stähli lines (Figure 26-29). Investigators believe that RCEs occur in this location because epithelial stem cells derive from the limbus, and healing of central corneal lesions is accomplished by centripetal movement of peripheral epithelial cells.

In addition to a frank epithelial defect that stains with NaFl, epithelial edema, microcysts, and poor epithelial attachment may be seen in acute cases of RCE. If the

Figure 26-29 Recurrent corneal erosion in the inferior third of the cornea (arrow) exhibits positive NaFl staining centrally. Note the surrounding punctate positive and negative stains.

epithelium is loose but still in position, it may appear as a slightly wavy or irregular area with surrounding edema. Negative NaFl staining will be seen in the area of loose or elevated epithelium (Figure 26-30). Perilimbal injection, upper eyelid edema, and blepharospasm are possible in severe cases.

An ABMD may be evident. Classic findings of ABMD include intraepithelial geographic opacities, microcysts, and concentric refractile lesions that resemble fingerprints. The use of retroillumination is helpful in viewing the epithelial defects with the slit-lamp biomicroscope.

Figure 26-30 Negative NaFl staining over an area of raised epithelium. (Courtesy of Pat Caroline.)

Negative NaFl staining may be present in areas where the epithelium is elevated and not adhering well.

Rarely, sterile anterior stromal infiltrates may develop late in RCE.These lesions are typically less than 2 mm in diameter and located paracentrally. They are usually culture negative and most likely represent an inflammatory reaction.

Between episodes, the most common signs of RCE are epithelial microcysts, surface irregularities, and subepithelial scarring. A pseudodendrite appearance is possible due to apposition of the loose and well-attached epithelium. Reports indicate corneal topography may also exhibit well-delineated areas that are more than 2 diopters flatter than the surrounding corneal tissue. These areas, called corneal topographic lagoons, measure less than 2 mm and are more commonly seen in patients with RCE than in control patients.

Management

Treatment generally focuses on decreasing symptoms and encouraging regrowth and reanchoring of the epithelium. It is important to warn the patient of the recurrent nature of the condition and to continue treatment for some time after the cornea appears to be healed.

During acute episodes a broad-spectrum topical prophylactic antibiotic ointment, such as 0.3% tobramycin or 0.5% moxifloxacin, protects the cornea from secondary infection while it heals. The use of a therapeutic contact lens and topical NSAIDs, such as diclofenac sodium 0.1% solution or ketorolac 0.5% solution, provide symptomatic relief.The therapeutic soft contact lens also protects the regenerating epithelium and temporarily provides epithelial stability. A cycloplegic agent, such as 5% homatropine, should be instilled to decrease ciliary spasm and pain. Oral analgesics can be prescribed as needed (see Chapter 7). The eye should be examined in 24 hours and the therapy continued until the epithelial defect is healed.

If the epithelium is not healing or if the patient presents with grossly loose and elevated epithelium, the area should be debrided. First, a topical anesthetic is instilled to anesthetize the cornea and loosen the epithelium. A dry cellulose ophthalmic sponge or moistened sterile cotton-tipped applicator can be used to gently remove the epithelium (see Figure 26-15). Debriding too aggressively must be avoided, because this could damage the basement membrane and increase healing time. Debridement should be followed by the use of a broadspectrum topical prophylactic antibiotic, a topical NSAID, a therapeutic soft contact lens, and a cycloplegic agent. Debridement facilitates the healing process but does not affect the incidence of recurrences.

Once the epithelial defect is healed, artificial tears should be used four to eight times daily, and hypertonic agents, such as 5% sodium chloride ointment, should be administered at bedtime for 3 to 6 months. Patients should continue using hypertonic agents for several months after

506 CHAPTER 26 Diseases of the Cornea

symptoms have resolved because there is a tendency for recurrence of the erosion if the hypertonic therapy is withdrawn prematurely. Hypertonic agents decrease eyelid adhesion and also may create an osmotic gradient that draws fluid from the epithelium, keeping it apposed to Bowman’s membrane and thereby promoting adherence.

Although some clinicians believe bland ointment may be just as effective, studies have shown that artificial tears and steroids are not as effective as hypertonic ointment for controlling recurrences. It has been reported that 80% to 90% of patients with symptomatic RCEs experience some improvement in symptoms with the use of hypertonic ointment.

Topical ophthalmic corticosteroids and oral tetracyclines have been shown to decrease the frequency of RCEs by inhibiting matrix metalloproteinase enzymes. Metalloproteinase enzymes, which have an increased concentration and activity after RCE, have been shown to degrade the epithelial basement membrane and anchoring fibrils. In seven patients who did not respond to conventional therapy, oral doxycycline 50 mg two times a day for 2 months and topical steroids two or three times a day for 3 weeks resulted in rapid healing and no recurrences over an average follow-up period of 22 months. The therapeutic effect of topical corticosteroids and oral tetracyclines may also be due to decreased inflammation or improved meibomian gland secretion. Because meibomian gland dysfunction is thought to play a role in recalcitrant RCEs, treating the meibomian gland dysfunction may contribute to healing.

Autologous serum, obtained from a blood sample and instilled topically, has been shown to considerably reduce the recurrences of RCE without side effects such as allergic reactions. Autologous serum supplies the eye with substances such as fibronectin, vitamin A, lysozyme, epidermal growth factor, transforming growth factor-β, and other cytokines, which are essential for repairing damaged epithelium.

If erosions are occurring more frequently than once monthly and diffuse areas are involved, long-term use of a therapeutic soft contact lens may aid in reforming the adhesion complexes. A large-diameter therapeutic contact lens should be fitted to allow minimal movement. Such lenses are used in an attempt to protect the epithelium from eyelid trauma during blinking and adhering to the tarsal conjunctiva. The lenses tend to increase patient comfort and decrease the severity and frequency of recurrences, but they do not always prevent recurrences. Besides erosions occurring underneath the contact lens, other problems associated with contact lens wear may develop, including contact lens loss, discomfort, deposits, vascularization, stromal infiltrates, and infection. It is suggested that the patient be examined 24 hours after a therapeutic contact lens is dispensed, 1 week later, and each month subsequently to monitor for these complications. If the patient is tolerating the lens well, it should be

left in place for 2 months after the erosion has healed. This regimen typically results in 3 to 6 months of wearing time.When lens wear is discontinued, the patient should be instructed to instill 5% sodium chloride ointment into the conjunctival sac at bedtime for several months.

During corneal healing it is important to monitor for any signs of corneal infiltrate or anterior uveitis.Although most corneal infiltrates associated with RCE have been shown to be sterile, the clinical appearance of these infiltrates is not definitive in differentiating infectious from immune causes. For this reason any infiltrates that develop should initially be treated with antibiotic drops as if they were infectious.

Up to 95% of patients with symptomatic RCEs experience some improvement in symptoms with the use of medical therapy. If the patient experiences more than one erosion per month despite medical therapy, invasive treatment is indicated. These treatment options include anterior corneal stromal puncture with a needle or an Nd:YAG laser, PTK, and superficial epithelial keratectomy.

Anterior stromal puncture stimulates the production of collagen and fibronectin, which improve the attachment of the epithelium and basement membrane to the anterior stroma.A bent-tipped 23to 25-gauge needle is used to puncture through loose epithelium and Bowman’s layer into the anterior stroma (Figure 26-31). Enough pressure should be applied to indent the cornea one-fourth to one-third the depth of the anterior chamber, which should cause approximately 50% stromal thickness penetration. The bent tip prevents accidental penetration and controls the penetration depth. These punctures are placed approximately 0.5 mm apart over the entire area of loose epithelium and about 1 mm outside the area delineated by NaFl. Although scarring from anterior stromal puncture with a needle is minimal enough to cause no apparent effect on visual acuity, it is typically avoided in the visual axis due to the risk of decreased vision and glare. Stromal puncture with an Nd:YAG laser is less likely to produce scarring. However, one major disadvantage of the laser procedure is the need, in some cases, to debride the corneal epithelium before the treatment is administered. This makes the procedure more painful for the patient and prolongs the recovery time. The rate of recurrence after anterior stromal puncture is 14% to 40%.Anterior stromal puncture is not the treatment of choice in patients with an ABMD that is not well defined.

Patients with chronic RCE and widespread ABMD benefit from therapeutic modalities that treat larger areas of the cornea. PTK has been shown to be an effective treatment for these patients, resulting in decreased symptoms and increased visual acuity. PTK is useful for corneal erosions that affect the visual axis, and it can be combined with photorefractive keratectomy. One drawback of PTK is the expensive equipment required to perform the procedure. PTK removes superficial tissue of Bowman’s layer to allow the formation of a new basement

membrane with stronger adhesion complexes. The rate of recurrence after one PTK procedure is 0 to 27%. Retreatment with PTK has been successful, with a recurrence rate of 0 to 20%. A mild corneal haze that may cause visual symptoms occurs 3 to 7 weeks after the procedure in 36% to 80% of patients. This haze typically requires no treatment. Although there is a trend toward hyperopia,most studies showed no statistically significant refractive error shift as long as the ablation depth was less than 10 mcm.

Superficial epithelial keratectomy with a variablespeed diamond burr or Amoils epithelial scrubber has also been shown to be safe and effective in treating larger erosion areas and areas that affect the visual axis. No significant difference was found in corneal haze, recurrence of erosions, or best-corrected visual acuity in patients treated with superficial epithelial keratectomy with diamond burr polishing and patients undergoing PTK. Both treatment options are safe and effective. However, treatment with a diamond burr is simpler and less expensive.

After anterior stromal puncture, PTK, or superficial keratectomy, broad-spectrum topical prophylactic ophthalmic antibiotic drops such as 0.3% tobramycin, 0.3% ciprofloxacin, or one of the newer generation fluoroquinolones, moxifloxacin or gatifloxacin, should be instilled three to four times daily, along with a broadspectrum antibiotic ointment such as 0.3% tobramycin or 0.3% ciprofloxacin instilled into the conjunctival sac at bedtime. NSAIDs such as diclofenac sodium 0.1% solution

or ketorolac 0.5% solution and a therapeutic soft contact lens should be instituted. A cycloplegic agent and/or oral analgesic may also be helpful in controlling pain.The patient should be examined each day until the epithelium is healed. The antibiotic solution should be continued for 1 week after the procedure. Patients should instill hypertonic ointment into the conjunctival sac at bedtime for several months and should be examined at 1-week and 2-month intervals after the epithelium is healed.

Corneal delamination with 20% alcohol has been described for RCE treatment. After the application of 20% alcohol for 40 seconds, 73% of patients were free of symptoms over an average period of 23 months’ follow-up. No patients had decreased visual acuity after the procedure.The successful use of substance P–derived peptide and botulinum toxin injections has also been described to treat RCE, but no controlled studies have been performed. Other interventions, such as microdiathermy and surface cautery or diathermy, are used primarily for symptom relief if there is no visual potential.

Exposure Keratopathy

Etiology

Numerous neurologic and mechanical factors may result in chronic corneal drying due to infrequent or incomplete blinking or inadequate eyelid closure (lagophthalmos). The resultant irritation to the corneal tissue is known as exposure keratopathy.

508 CHAPTER 26 Diseases of the Cornea

Ectropion is an example of an eyelid abnormality that may result in exposure keratopathy. Bell’s palsy involves disrupted innervation to the orbicularis oculi muscle.The resultant retraction of the lower eyelid together with reduced blink capability of the upper lid may result in exposure keratopathy. Graves’ disease is an example of a systemic condition that can produce exophthalmos (see Figure 32-5) and accompanying exposure keratopathy. Patients who have had cosmetic lid or facial surgery, such as CO2 laser cosmetic skin resurfacing or blepharoplasty, and patients under deep sedation are more likely to have lagophthalmos and exposure keratopathy. Nocturnal lagophthalmos, in which the eyelids do not close fully during sleep, is a relatively common cause of exposure keratopathy.

Diagnosis

Patients with exposure keratopathy typically present with symptoms of foreign body sensation, burning, stinging, photophobia, tearing, and redness. The symptomatology may be more pronounced in the morning after a night of corneal desiccation, particularly in the case of nocturnal lagophthalmos. In the less frequent event of secondary corneal ulceration or infection, the symptoms are more pronounced and consistent with these conditions.

Depending on the patient’s eyelid configuration, slit-lamp examination reveals punctate epithelial erosions in the interpalpebral or inferior areas of the cornea. These lesions stain prominently with NaFl and, often, rose bengal (Figure 26-32). Corresponding conjunctival injection is common. In more severe long-standing cases inferior micropannus, scarring, or corneal thinning may be noted.

Patients with exposure keratopathy may develop filamentary keratitis.The dry eye can cause corneal irregularities and increased mucin, which promotes the formation of fine epithelial and mucous strands that are attached to

Figure 26-32 Patient with exposure keratopathy exhibits staining inferiorly/intrapalpebrally with rose bengal. (Courtesy of Pat Caroline.)

Figure 26-33 Corneal filaments with lissamine green staining. (Courtesy of Pat Caroline.)

the cornea.These corneal filaments stain with rose bengal or lissamine green (Figure 26-33).

A thorough history along with other observed ocular, facial, or systemic findings assists in determining the etiology of exposure keratitis.The potential for lagophthalmos can be assessed by asking the patient to gently close his or her eyes and inspecting for incomplete lid closure and exposure of the globe. In patients with lagophthalmos a portion of the globe is visible through the incompletely closed fissure (see Figure 24-17). If the patient has a normal Bell’s reflex, the bulbar conjunctival-scleral portion of the globe is visible; if the patient has a poor Bell’s reflex, the cornea is visible through the incompletely closed fissure, and exposure keratopathy results. Friends or family members can observe the patient’s eyelids during sleep to help determine whether nocturnal lagophthalmos is present. It is essential that eyelid apposition be evaluated carefully in patients under deep sedation to avoid exposure keratopathy.

Management

If exposure keratopathy is the result of an ocular or systemic abnormality, the underlying condition should be addressed. Patients with exposure keratopathy resulting from Bell’s palsy or Graves’ disease often are comanaged by a physician caring for the systemic problem together with the eye care practitioner attending to the ocular complications.

Management of exposure keratopathy is directed toward lubrication of the globe and cornea as long as the lagophthalmos is present. These measures typically include ocular lubricating drops during the day and bland ophthalmic lubricating ointment instilled into the conjunctival sac at bedtime. If lubrication is not sufficient, and often as an interim measure, the eyelids may be closed with hypoallergenic tape to prevent corneal exposure during sleep.Moreover,several types of plastic shields are available to reduce tear evaporation and resultant corneal desiccation.

If an underlying lid abnormality such as ectropion is the cause of exposure keratitis, then an oculoplastics consultation is appropriate. In extreme cases of exposure, a tarsorrhaphy may be performed to preserve corneal health. In the event that exposure keratitis has become complicated by secondary infection, appropriate treatment must be initiated.

If filamentary keratitis is present, treatment should include the use of nonpreserved ocular lubricating drops during the day, bland ophthalmic lubricating ointment instilled into the conjunctival sac at bedtime, and punctal occlusion.Topical medications, including hypertonic solution (5% NaCl), mucolytic agents such as acetylcysteine, steroids, NSAIDs, aid in the resolution of the corneal filaments.The filaments typically resolve within 1 to 4 weeks after initiating treatment. NSAIDs such as 0.1% diclofenac instilled four times per day for 3 to 4 weeks have been shown to improve clinical symptoms such as foreign body sensation, itching, and pain in addition to eliminating the filaments. Some advocate the mechanical removal of the filaments with jeweler’s forceps; however, this may cause further surface damage and slow the resolution of the filamentary keratitis. Silicone hydrogel contact lenses that are approved for therapeutic use protect the compromised epithelium from sheering effects of the eyelids, allowing the epithelium to reattach to the basement membrane. Maintenance treatment for filamentary keratitis may be necessary, including nonpreserved ocular lubricating drops during the day, bland ophthalmic lubricating ointment at bedtime, punctal occlusion, and NSAIDs for acute flare-ups.

Chemical and Thermal Burns

Etiology

Thermal and chemical burns account for 8% to 19% of traumatic eye injuries. Most burns are mild; however, burns can potentially cause severe cosmetic and visual impairment. Most ocular burn victims are males with an average age of 28 to 36 years. Alkali injuries are more frequent than acid or thermal injuries and are typically the most damaging.

Alkali injuries to the eye represent true medical emergencies because the impact on ocular tissue, including the cornea, may be devastating. The chemical composition of alkaline substances promotes rapid penetration through all corneal layers without neutralization of the substance. Calcium hydroxide (in lime, plaster, cement, mortar, and whitewash) is the most common cause of alkali burns. It forms precipitates that can be retained in the fornix. These precipitates can cause severe damage if not recognized and removed. Other common alkali agents that may cause ocular burns include ammonia (a common cleaning agent), sodium hydroxide (in lye, drain cleaners, or caustic soda), potassium hydroxide (in caustic potash), and magnesium hydroxide (a component of flares and fireworks).

Burns secondary to acid solutions result in coagulation of proteins. This reaction forms a barrier of precipitated tissue, which tends to limit ocular damage to local superficial effects. However, strong acids such as hydrofluoric acid can penetrate as quickly as alkali chemicals. The most common solutions implicated in acid corneal burns include sulfuric acid (used in car batteries and the manufacturing of fertilizer and detergents), sulfurous acid (used as a bleaching agent), acetic acid (a component of vinegar), hydrofluoric acid (used in glass polishing and silicone production), and hydrochloric acid (used in petroleum production and metal cleaning).

Thermal burns are less common than chemical burns. The cornea may be exposed to thermal burns from a variety of sources.The nature of the resultant injury is determined by the form and temperature of the causative agent. Open flame burns are the most common cause of severe thermal burns. Other causes of thermal burns include hot objects or liquid, such as molten metal or glass that continues to radiate heat while in contact with the eye; boiling fluids; firecracker particles; lit match heads; curling irons; and steam from boiling water or after the preparation of microwave popcorn.

Diagnosis

A patient with a chemical or thermal burn typically reports the source. The patient generally presents soon after the injury or seeks care if ocular irritation persists after a day or two. The degree of symptomatology tends to be consistent with the extent of the ocular burn. Symptoms range from mild irritation and focal redness to severe pain, burning, redness, tearing, and photophobia. Patients with chemical burns report that the offending solution or solid came in contact with one or both eyes or the face.The patient, a friend, or a family member can often identify the offending solution. Resources such as a poison control hot line or Grant’s Toxicology of the Eye are available to help determine the potential ocular effects of an identified chemical agent.

Because the tissue exposed in the palpebral fissure is most likely to be involved in an ocular burn, the clinical signs tend to be most prominent in that area. Bulbar conjunctival injection is most pronounced within the palpebral fissure. However, diffuse conjunctival injection may be present. In mild chemical burns, punctate epithelial erosions are noted at the areas of chemical contact with the cornea. NaFl staining of the bulbar conjunctiva and corresponding inferior palpebral conjunctiva may also be present. A thermal epithelial corneal burn appears as a focal, milky, gray-white coagulation of tissue that tends to slough (eschar), often within the palpebral fissure (Figure 26-34). Depending on the extent of the injury, the skin of the eyelids and face also may exhibit involvement, including lash and brow singeing or chemical burn, depending on the nature of the injury. A grading system has been described to determine the severity of ocular burns, which also impacts prognosis (Table 26-2).