98  OPHTHALMOLOGY SECRETS IN COLOR

15.What is the treatment for bacterial conjunctivitis?

Bacterial conjunctivitis is treated with erythromycin or gentamicin ointment applied four times/day for 2 weeks for gram-positive or gram-negative conjunctival swab results, respectively. The antibiotic

choice may be altered later once culture and sensitivity results are known. In cases of corneal involvement, as seen with virulent organisms such as Pseudomonas sp., fortified topical antibiotics are administered and are often supplemented with systemic treatment.

KEY POINTS: POTENTIAL OCULAR COMPLICATIONS

OF NEONATAL CONJUNCTIVITIS

1.Corneal scarring

2.Symblepharon

3.Corneal perforation

4.Endophthalmitis

16.What is the treatment for herpes simplex viral conjunctivitis?

Intravenous acyclovir, 10 mg/kg, is given every 8 hours for 10 days, along with vidarabine 3% ointment (Vira-A), five times/day, or trifluorothymidine 1% (Viroptic), every 2 hours, for 1 week.

17.How can the incidence of ophthalmia neonatorum be reduced in future generations?

The population most at risk for contracting neonatal conjunctivitis is infants born to mothers without adequate prenatal care or mothers involved with substance abuse. Because of its high association with serious systemic disease, neonatal conjunctivitis is still an important public health issue worldwide. Although not universally accepted, some countries (e.g., Sweden and England) have abandoned the use of routine prophylaxis after birth in favor of careful screening for sexually transmitted diseases and better prenatal care.

WEBSITE

www.emedicine.com/oph/topic/325.htm

Bibliography

Albert DM, Jakobiec FA: Principles and practice of ophthalmology, Philadelphia, 1994, W.B. Saunders. Chandler JW: Controversies in ocular prophylaxis of newborns, Arch Ophthalmol 107:814–815, 1989. Gerstenblith AT, Rabinowitz MP: The Wills eye manual, ed 6, Philadelphia, Lippincott, 2012, Williams & Wilkins.

Elnifro E, Storey C, Morris D, Rullo A: Polymerase chain reaction for detection of Chlmaydia trachomatis in conjunctival swabs, Br J Ophthalmol 81(6):497–500, 1997.

Hammerschlag M: Neonatal conjunctivitis, Pediatr Ann 22:346–351, 1993.

Laga M, Naamara W, Brunham R, et al.: Single-dose therapy of gonococcal ophthalmia neonatorum with ceftriaxone, N Engl J Med 315:1382–1385, 1986.

Matejcek A, Goldman R: Treatment and prevention of ophthalmia neonatorum, Can Fam Physician 59(11):1187–1190, 2013.

O’Hara M: Ophthalmia neonatorum, Pediatr Clin North Am 40:715–725, 1993.

Skuta G, Cantor L, Weiss J: Basic and clinical sciences course, Am Acad Ophthalmol 6(16):187–189, 2012. Weiss A: Chronic conjunctivitis in infants and children, Pediatr Ann 22:366–374, 1993.

1.You are an antibiotic or steroid eyedrop just placed in the conjunctival fornix.

Discuss the barriers to your journey into the eye.

Many eyedrop dispensers deliver a 50-μL eyedrop. However, only 20% of this volume is retained by the conjunctival cul-de-sac, and the excess immediately flows over the eyelids. Of the portion that remains, approximately 80% drains through the lacrimal system. In addition, because of the 15%/ min tear turnover rate, almost all of the topically applied medication disappears from the conjunctival cul-de-sac in about 5 minutes. Irritating drugs produce reflex tearing and may be cleared even more quickly.

During this critical 5 minutes, the topically applied drug faces numerous tissue obstacles. Absorption by the conjunctiva quickly disperses the medication systemically via the conjunctival vasculature. The small portion that penetrates the episclera faces the relative impermeability of the sclera and the tight junctions of the retinal pigment epithelium. The cornea poses three different barriers to entry. The corneal epithelium and the endothelium possess tight junctions that force the drugs to pass through the cellular membranes and limit passage of hydrophilic drugs. The corneal stroma is water-rich and limits movement of lipophilic drugs. Even after entry into the anterior chamber, the lens effectively limits most drug penetration, and very little enters the posterior segment of the eye through topical administration.

Such formidable barriers seem insurmountable, but inflammation and infection render these barriers less effective, and modifications of the drug and/or its vehicle can facilitate entry into the eye. In addition, the desired site of action may be the ocular surface and not inside the eye.

2.Given the above barriers, how would you increase delivery of topical antibiotics or steroids to the desired site of action?

The patient can perform punctal occlusion to decrease the amount of drainage through the lacrimal system by 65% and leave more drug for intraocular absorption. Of course, frequent instillation also increases drug absorption, but the practical limit is probably every 5 minutes because the subsequent eyedrop can wash out the previous eyedrop before intraocular absorption.

Changing the characteristics of the drug and/or its vehicle can also improve delivery. Increasing the concentration of the drug may be limited by the solubility of the drug in the vehicle, and the high tonicity of higher concentrations triggers reflex tearing that quickly clears the drug from the ocular surface. Also, increasing lipid solubility of the drug appears to promote corneal passage despite

the dual barrier characteristic of the cornea. In addition, adding surfactants that disturb the corneal epithelium dramatically increases drug entry.

3.Name the four different formulations of topical medications and the advantages and the disadvantages of each.

•Solutions are easily instilled, but contact time is minimal, requiring frequent administration. In addition, the “pulse” nature of absorption invites transient overdose and toxicity.

•Suspensions allow longer contact time, but the particulate nature of the preparation may be irritating and trigger reflex tearing. Suspensions settle to the bottom of the bottle and need to be shaken before the eyedrops are instilled. Patients also may complain of accumulation of the precipitates or forget to shake the bottle before administering the eyedrops.

•Gels are more viscous than solutions and suspensions and they are retained on the eye longer, allowing for better penetration of the active ingredients. In contrast to the suspensions, in which the active ingredient may precipitate, the gels allow for a more uniform distribution.

•Ointments increase the contact time further, requiring the least frequent instillation, but leave a film over the eye that blurs vision. In addition, water-soluble drugs do not dissolve in the ointment vehicle and are present as crystals. Crystals are trapped in the ointment vehicle until the crystals on the

99

100  OPHTHALMOLOGY SECRETS IN COLOR

surface of the ointment contact the ocular surface after the ointment vehicle melts with exposure to body temperature. This type of absorption allows entry of constant but low amounts of the drug.

Other methods of delivery include soft contact lenses, soluble ocular inserts, or implantable devices. Medications inserted into punctal plugs are also being studied.

KEY POINTS: STRATEGIES TO INCREASE THE PENETRATION OF TOPICAL MEDICATIONS

1.Punctal occlusion.

2.Increase the frequency.

3. Increase the concentration of drug in the drop. 4. Increase the lipid solubility of the drug.

5. Use surfactants to disturb the corneal epithelium.

4.What are some of the indications for using topical antibiotics?

Topical antibiotics are used to treat conjunctivitis, conjunctival ulceration, corneal ulceration, and canaliculitis. They are also used as prophylaxes against infection before and after ocular surgeries such as cataract, glaucoma, retina, corneal transplant, refractive surgery, and ocular surface surgeries. Topical antibiotics are also used as prophylaxes in patients with corneal epithelial defects and in some cases patients who wear therapeutic contact lenses. Prophylaxis with antibiotics is becoming more controversial as it may select for more resistant bacteria should an infection occur.

5.A 60-year-old man complains of crusting of the eyelids in the morning and chronic foreign-body sensation. Examination reveals moderate blepharitis with numerous collarettes around the eyelashes. What would you recommend?

Blepharitis often responds well to just warm compresses and eyelid scrubs, but supplemental antibiotic gels or ointments applied to the eyelash base or conjunctiva may be helpful, especially when numerous collarettes are seen around the eyelashes. Frequently used antibiotic ointments include erythromycin, bacitracin, and Polysporin. Azithromycin comes as an ophthalmic gel drop. Erythromycin and azithromycin are macrolide antibiotics that inhibit bacterial protein synthesis by binding to the 50S ribosomal unit. They have a broad spectrum of coverage but suffer from relatively poor intraocular absorption. They are most appropriate for blepharitis and conjunctivitis. Bacitracin is composed of numerous polypeptides that inhibit bacterial cell wall synthesis. Polysporin combines bacitracin and polymyxin B, which are peptides that act like detergents to lyse bacterial cell membranes, and offers better coverage of gram-negative bacteria.

6.A 30-year-old woman with “cold” symptoms presents with redness and mucus discharge in both eyes. The ocular symptoms began in the right eye 1 week ago but now involve both eyes despite treatment of the right eye with sulfacetamide four times/day, as prescribed by her family physician. Examination reveals bilateral follicular conjunctivitis with preauricular adenopathy. What would you recommend?

History and examination are consistent with viral conjunctivitis. Artificial tears and cool compresses may provide comfort. Follow-up in 1 to 2 weeks is advisable to look for potential membranous conjunctivitis which may require topical steroids. Sulfacetamide is a bacteriostatic structural analog of p-aminoben- zoic acid and inhibits synthesis of folic acid. It has a broad spectrum of coverage and good corneal penetration and becomes more effective when combined with trimethoprim, which blocks a successive step in bacterial folate metabolism. It appears to be used often by nonophthalmologists for initial treatment of red eyes; it is fine for mild bacterial conjunctivitis but is not helpful for viral conjunctivitis.

7.A 55-year-old woman complains of discharge and redness of her right eye for 4 weeks. Her family physician told her that she had “pink eye” and prescribed erythromycin ointment, then sulfacetamide, and then ciprofloxacin, but the symptoms have not improved. Examination reveals diffuse papillary conjunctivitis with purulent discharge. There is no preauricular adenopathy or previous history of “cold” symptoms. What should you do?

The patient has chronic conjunctivitis, possibly bacterial. Topical therapy usually brings prompt relief, and you should make sure that she uses the medications properly. Assuming that she is getting

http://ophthalmologyebooks.com

102  OPHTHALMOLOGY SECRETS IN COLOR

produce a white precipitate over the ulcer, but this precipitate does not appear to impede the bactericidal activity and usually resolves when the dose is tapered.

Ofloxacin is also used but has different manufacturer’s recommendations:

•Days 1 and 2: One to two drops every 30 minutes while awake

•Awaken at 4 and 6 hours after retiring: Give one to two drops

•Days 3 to 7 or 9: One to two drops hourly while awake

•Days 7–9 to completion: One to two drops four times/day

Fourth-generation fluoroquinolones, gatifloxacin, moxifloxacin, and besifloxacin, are also available with better gram-positive coverage and comparable gram-negative coverage. These medications have not been FDA approved for the treatment of corneal ulcers but they are frequently used off-label for this condition.

11.The patient now prefers a “proven” treatment regimen with a long history and requests topical fortified antibiotics. However, he recalls that minimal bactericidal concentration for most pathogenic bacteria is far below that provided by the fortified antibiotics and accuses you of wasting money and drugs. Is he right?

No. In vitro and in vivo results in other sites of the body may not be applicable to the eye. Indeed, in the vitreous, the dose–response relationship has been demonstrated up to 100 times the in vitro minimal bactericidal concentration.

12.The patient reminds you that he is penicillin-allergic and does not enjoy anaphylaxis. What antibiotics should you choose? How do you begin therapy?

Penicillin is not often used in ophthalmology because of poor penetration into the eye and active transport out of the eye by the organic acid transport system of the ciliary body. However, inflammation improves ocular penetration. Penicillin inhibits bacterial transpeptidase and prevents bacterial cell-wall synthesis. Varieties of modification of the original compound have produced varying spectra of activity. Penicillin G and V are still highly effective for many gram-positive and gram-negative bacteria, but many strains of S. aureus and S. epidermidis are now resistant. Penicillinase-resistant penicillins such as methicillin are useful for penicillinase-producing staphylococci. Broad-spectrum penicillins, ampicillin and amoxicillin, have better gram-negative coverage, and semisynthetic penicillins such as carbenicillin, piperacillin, and ticarcillin extend coverage to Pseudomonas, Enterobacter, and Proteus spp.

Immediate allergic response to penicillin, such as hives or anaphylaxis, is a strong contraindication for its use, and there is 10% cross-reactivity with cephalosporins. Therefore, for patients with penicillin allergy, cefazolin should be replaced with vancomycin. Vancomycin is a complex glycopeptide that inhibits bacterial cell-wall synthesis with principally gram-positive coverage, including methicillin-resistant

S. aureus and Streptococcus faecalis, which is a frequent bacterial pathogen in infections of filtering blebs.

As mentioned above, an aminoglycoside is synergistic with cell-wall–inhibiting antibiotics, and the patient should be started on fortified vancomycin and tobramycin. Give the patient four doses—an alternating dose every 5 minutes—followed by alternation every half-hour to 1 hour. Actual dosing may vary in different institutions.

13.The next morning the ulcer looks worse with 4-mm corneal infiltrate and purulent material overlying the ulcer. The corneal culture confirms Pseudomonas aeruginosa. Why did the patient not improve?

Pseudomonas corneal ulcers sometimes require double coverage. Fortified piperacillin or ticarcillin could be added in a non-penicillin-allergic patient. Frequent ciprofloxacin (or another fluoroquinolone) could also be resumed, especially in this case.

14.The next day, the ulcer looks stable, but the patient complains of persistent and perhaps worsening pain. Examination reveals diffuse punctate corneal epithelial defects, inferior conjunctival erythema, and swollen lower eyelids. What should you do?

Toxicity is often less severe with topical administration; indeed, some common topical antibiotics such as neomycin and polymyxin cannot be given intravenously because of systemic toxicity. However, intensive regimens of potent antibiotics often produce surface toxicity with prominent involvement of lower more than upper conjunctiva. The toxicity is related to several factors, including the pH of the antibiotic drop and the presence of preservative in the solution. Fortified antibiotic drops, which are prepared

by diluting intravenous antibiotics with preservative-free artificial tears and topical moxifloxacin, are preservative free. Occasionally, only analgesics and cool compresses can be offered if the infection is not under control. Fortified vancomycin should be decreased or discontinued because tobramycin and ciprofloxacin are more important for Pseudomonas ulcer, and the ulcer appears to be stabilizing.

CHAPTER 10  TOPICAL ANTIBIOTICS AND STEROIDS  103

Figure 10-1.  Anterior segment of right eye demonstrates refractile superficial crystalline deposits overlying an area of epithelial defect in a patient who was treated with a prolonged course of topical ciprofloxacin.

15.One week later the patient presents to you complaining of a dense white infiltrate in his cornea. Examination reveals superficial dense white material with gritty appearance in the area of the healing ulcer (Fig. 10-1). What is going on?

Prolonged use of ciprofloxacin drops/ointments causes characteristic macroscopic deposits in up to 20% of patients through a compromised corneal epithelium. These eventually disappear after discontinuation of the ciprofloxacin eye medication.

16.The patient slowly improves, but significant corneal opacity remains. He would like binocular vision for his surgical career and asks you to get rid of his corneal haze. How do you respond?

Read on to learn about topical steroids. Often, inflammatory opacities fade well with topical steroids. When, how much, and how long to use topical steroids are controversial, but a trial of topical steroids is often warranted before considering surgical options. The infection should be under control first before applying any topical steroids.

KEY POINTS: CORNEAL ULCERS

1. Small, noncentral ulcers can be managed without cultures.

2. Fluoroquinolones every half-hour to 1 hour initially may offer similar efficacy with less toxicity than fortified topical antibiotics.

3. Pseudomonas ulcers may require double coverage.

4. The use of topical steroids after the infection is under control can decrease the size and density of the scar.

17.Review the currently available topical antibiotics in generic and brand names.

See Table 10-1.

18.How do topical steroids work?

The specific mechanisms of action of steroids are not completely understood. At a molecular level, inhibition of arachidonic acid release from phospholipids may be the most important effect. Arachidonic acid is converted to prostaglandins and related compounds that are potent mediators of inflammation. At a cellular level, steroids must be carried to the cytoplasm, where they bind to soluble receptors and then enter the nucleus to alter transcription of various proteins involved in immune regulation and inflammation. At the tissue level, steroids suppress the cardinal signs of inflammation such as edema, heat, pain, and redness through a variety of mechanisms. They cause vasoconstriction and decrease vascular permeability to inflammatory cells. Cellular and intracellular membranes are stabilized to inhibit release of inflammatory mediators such as histamine. Neutrophilic leukocytosis is inhibited, and macrophage recruitment and migration are

also decreased. Overall, steroids are potent anti-inflammatory and immunosuppressive agents with wide-ranging ophthalmic applications, but their adverse effects as well as their benefits should be understood before use.

104  OPHTHALMOLOGY SECRETS IN COLOR

Table 10-1.  Currently Available Topical Antibiotics

19.Because steroids are not cures, what general categories of disorders warrant ophthalmic use of topical steroids?

Abelson and Butrus identify three broad categories of disorders that warrant steroid use: postsurgical, immune hyperreactivity, and combined immune and infectious processes. Remarkably, postoperative use of steroids has not been evaluated in a well-controlled, double-blinded study. Although their use in this setting is almost universal, some ophthalmologists report adequate control of postoperative inflammation with topical nonsteroidals for various ophthalmic procedures. The second category includes various uveitides, allergic and vernal conjunctivitis, corneal graft rejections, and other processes in which the immune system activity is harmful to the host tissue. The last category includes viral and bacterial corneal ulcers, especially herpes simplex and herpes zoster, in which control of infectious processes must be balanced with control of inflammation that may scar delicate ocular tissue.

20.The physician with the residual corneal opacity wants to minimize his corneal opacity but is concerned about potential side effects of topical steroids. How do you advise him?

Exacerbation of the existing infection with reactivation of dormant organisms or inhibition of wound healing is the most immediate concern. Other well-known adverse effects include glaucoma and

CHAPTER 10  TOPICAL ANTIBIOTICS AND STEROIDS  105

cataracts, but numerous other side effects have been observed, including blepharoptosis, eyelid skin or scleral atrophy, and mydriasis.

In a randomized, multicenter clinical trial, investigators compared the effects of topical prednisolone sodium phosphate 1% to placebo in culture-positive bacterial corneal ulcers that were treated with topical moxifloxacin for at least 48 hours prior to randomization. No improvement in the overall best spectacle-corrected visual acuity at 3 months was observed in the group treated with corticosteroids compared to placebo. In addition there were no differences in the scar/infiltrate size, time to reepithelialization, and rate of corneal perforation between the groups. However, subgroup analysis demonstrated that ulcers with central location and presenting

vision of counting fingers (CF) or worse did better in the steroid-treated group. At 1 year, a small amount of visual improvement (one line) was noted in eyes treated with steroids whose ulcer was not caused by Nocardia, especially if the steroids were begun 2–3 days after the antibiotics were started, as opposed to 4 days or longer.

Systemic absorption may be significant with frequent use, and in such cases punctal occlusion should be encouraged. A 6-week regimen of topical 0.1% dexamethasone sodium phosphate has been shown to suppress the adrenal cortex, and some patients with systemic hay fever improve with topical ocular steroids. Of course, all of these effects are more frequent with intensive and chronic use of steroids.

21.After a lengthy discussion, the patient agrees to try topical steroids. However, given his interest in pharmacology, he requests a brief discussion of the pharmacokinetics of a few of the available topical steroids

Topical steroids may be prepared as solutions, suspensions, or ointments. Phosphate preparations may be prepared as solutions because they are highly water-soluble in the aqueous vehicles but penetrate less well into intact corneal epithelium than acetate or alcohol suspensions, which

have biphasic solubility. Nevertheless, 1% prednisolone phosphate achieves a significant corneal level of 10 μg/g within 30 minutes of instillation, which improves to 235 μg/g when the corneal epithelium is removed. Dexamethasone phosphate enters the cornea and anterior chamber within 10 minutes, reaches a maximum in 30 to 60 minutes, and slowly disappears over the next few to 24 hours.

22.The patient also requests that the most potent steroid be used with rapid taper so that the overall course may be shortened. Which steroid do you choose?

Anti-inflammatory effects of topical steroids differ depending on the clinical setting and method of measurement. However, certain generalizations can be made:

•Higher concentrations and more frequent instillations, up to every 5 minutes, increase concentrations of steroids in the cornea and aqueous.

•With corneal epithelium intact, prednisolone acetate suspension > dexamethasone alcohol solution > prednisolone sodium phosphate solution > dexamethasone phosphate ointment.

•With corneal epithelial defects, prednisolone sodium phosphate solution > dexamethasone phosphate solution > prednisolone acetate suspension.

23.The patient is started on 1% prednisolone acetate four times/day. His opacity is beginning to recede, but he returns 2 days later with complaints of a white

precipitate that forms on his conjunctiva and insists on a change of medication to prevent this annoying buildup. Which steroid do you choose now?

Suspensions leave a milky precipitate that some patients find unpleasant. In addition, despite shaking the bottles before instillation, a variable amount of the suspension may be delivered if particles are not evenly distributed. Therefore, some ophthalmologists prefer phosphate solutions despite lower potency with intact epithelium. A change to 1% prednisolone phosphate is reasonable if patient compliance is improved.

24.On day 10 of steroid therapy, the corneal opacity is receding rapidly, but the patient complains of foreign-body sensation. Examination reveals large corneal epithelial dendrites. What should you do?

Steroids do not cause herpetic keratitis but may promote herpetic keratitis when viral shedding is timed with the presence of steroids on the ocular surface. Often the dendrites are large and numerous in the presence of steroids, and steroids should be rapidly tapered or stopped. Of course, start full dosing of a topical antiviral (e.g., ganciclovir or trifluridine) or an oral antiviral (e.g., acyclovir, valacyclovir, or famciclovir).

http://ophthalmologyebooks.com

106  OPHTHALMOLOGY SECRETS IN COLOR

25.Fortunately, the dendrite heals rapidly and the previous corneal opacity has faded significantly with return to 20/20 vision in that eye. Four years have passed, and the patient is now seeking employment. Opportunities are scarce, and his only job offer is from a large organized health company that hopes to use him as a pharmacist as well as a physician as a cost-saving measure. Understandably, he is stressed. Now he notices extreme photophobia and redness of his eye. Examination reveals corneal stromal edema and focal keratic precipitates consistent with herpes simplex keratouveitis. What should you do?

Many stimuli, including stress, may promote recurrence of herpetic keratitis. Other stimuli include menses, sun exposure, and fever. If the inflammation is severe or central vision is threatened, steroids should be given with antiviral coverage to decrease corneal scarring and intraocular inflammation. One regimen may be acyclovir 400 mg two times/day and 1% prednisolone acetate four times/day. Other regimens may be acceptable. Antiviral coverage is probably unnecessary below one drop/day of 1% prednisolone acetate.

26.Two days later, only marginal improvement is noted, but intraocular pressure is 35 mmHg. What happened?

Significant steroid-induced rises in intraocular pressure have been demonstrated in up to 6% of patients after 6 weeks of topical dexamethasone, and patients with glaucoma or family history of glaucoma are particularly susceptible. The mechanism appears to be decreased aqueous outflow, perhaps as a result of deposition of mucopolysaccharides in the trabecular meshwork. The extent of intraocular pressure rise varies with type and dose of steroids. Usually, steroids with greater anti-inflammatory potency elicit greater elevation of intraocular pressure. For example, steroids with low intraocular bioavailability and potency, such as fluorometholone, cause lower rises in intraocular pressure after a greater duration of therapy than more potent steroids such as dexamethasone. Loteprednol appears to be an exception. It appears to have similar suppression of anterior chamber

cell and flare compared to 1% prednisolone acetate, with intraocular pressure elevation similar to that of fluorometholone. Regardless, the elevated intraocular pressure subsides, usually within 2 weeks, by decreasing or discontinuing steroid therapy, but topical aqueous suppressants may be needed in some patients.

However, steroid-induced rises in intraocular pressure rarely occur in less than 2 weeks and certainly not after 2 days of steroid therapy. Patients with intraocular inflammations, especially in herpetic keratouveitis, may have increased intraocular pressure as a result of intraocular inflammation. Therefore, in the present patient, the topical steroids should be increased and not decreased.

27.The frequency of prednisolone acetate administration was increased to every 3 hours while awake, and timolol, two times/day, was added. One week later the intraocular pressure is normal, and intraocular inflammation has subsided. Prednisolone acetate is tapered to two times/day. The patient returns 2 days later with recurrence of pain and photophobia and return of intraocular inflammation. What happened?

You tapered the steroids too quickly. A useful rule is to decrease steroids by no more than half of the previous dose every week to many weeks, especially in herpetic keratouveitis, in

which rebound inflammation is frequent. Make sure that the patient is still taking the eyedrops. Sometimes patients abruptly stop the eyedrops when they feel better and then suffer rebound inflammation.

28.Review the commonly available topical steroids and their generic and brand names.

See Table 10-2.

29.What are some of the topical antibiotic/steroid combinations and when is it appropriate to use them?

There are many antibiotic/steroid combination drops and ointments available on the market. See Table 10-3.

These medications are often used in eyes with mild superficial infections associated with some inflammation, such as staphylococcal marginal hypersensitivity. Combination medications should be used cautiously as steroids can cause a rapid progression and worsening of corneal ulcer. Also, longterm use of these medications can lead to formation of cataract and elevated intraocular pressure and/or glaucoma.