Signs and Symptoms
Mucopurulent discharge may emanate from the lesion. The cornea may be edematous. The conjunctival and episcleral vessels will be deeply engorged and inflamed, often greatly out of proportion to the size of the corneal defect. In bacterial keratitis, injection is typically 360 degrees rather than sectoral as seen in non-infectious keratitis. A pronounced anterior chamber reaction, often with hypopyon, is present in severe cases. Intraocular pressure may be reduced due to secretory hypotony of the ciliary body, but may be elevated due to blockage of the trabecular meshwork by the inflammatory cells. Often, the eyelids will also be edematous.
Once the corneal defenses are breached, the cornea is prone to colonization and infection by pathogenic bacteria. Factors known to compromise corneal defenses include direct corneal trauma, chronic eyelid disease, systemic immune disease, tear film abnormalities affecting the ocular surface and hypoxic trauma from contact lens wear.2
Pathogenic bacteria colonize the corneal stroma and immediately become antigenic, both directly and indirectly, by releasing enzymes and toxins. This sets up an antigen-antibody immune reaction with chemotactic factors inducing an inflammatory reaction. The body mobilizes polymorphonuclear leukocytes (PMN), which aggregate at the area of infection, creating an infiltrate. The PMNs phagocytize and digest the bacteria and damage stromal tissue by releasing numerous enzymes that directly affect and damage stromal tissue.
The collagen of the corneal stroma is poorly tolerant of the bacterial and leukocytic enzymes, and undergoes degradation, necrosis and thinning. This leads to scarring of the cornea. As thinning advances, the cornea may perforate, thus introducing bacteria into the eye with ensuing endophthalmitis.
The most commonly occurring organisms in bacterial keratitis vary depending on the precipitating factors of the ulcer and the geographic location of the patient. In cases involving contact lens wear and cosmetic mascara, the most common infective organism is Pseudo-monas aeruginosa. Throughout North America, the most common infective organism in bacterial keratitis is Staphylococcus aureus, and it appears that there is an increased incidence of Gram-positive recovery in infectious keratitis.3
Proper diagnosis and prompt therapy are essential to preserve vision in bacterial keratitis. The first step in management should be to obtain corneal scrapings for microbiologic studies. The standard of care describes the use of a platinum spatula with plating directly onto blood and chocolate agar medium. However, the effectiveness of the fluoroquinolones has led many practitioners away from this standard. Identification, as well as sensitivity studies, will aid in management. An alternative for treatment of less severe keratitis is a mini-tip calcium alginate culturette and transport-media-containing carrier. The results of this technique compared to platinum spatula collection and plating was 83.3% sensitivity and 100% specificity. The conservative approach supports culturing most, if not all, suspected infectious ulcers. We advocate obtaining cultures for central lesions that threaten vision, are at risk of perforation, and in institutionalized patients in nursing homes and hospitals where methicillin-resistant Staph. aureus infections are possible.4
If the patient has been cultured, initiate broad-spectrum, empirical antibiotic therapy prior to receiving the results. Monotherapy with fluoroquinolone eye drops has been shown to result in shorter duration of intensive therapy and shorter hospital stay when compared with combined fortified therapy (tobramycin-cefazolin). This finding may have resulted from quicker clinical response of healing as a result of less toxicity found in the patients treated with fluoroquinolones. However, as some serious complications were encountered more commonly in the fluoroquinolone group, caution should be exercised in using fluoroquinolones in large, deep ulcers in the elderly.5
Despite clear efficacy of fluoroquinolones in the management of bacterial keratitis,2,6-8 consideration must be given to the increasing resistance to these drugs. Since their inception, there has been a rise in the incidence of bacterial isolates in keratitis that exhibit resistance to the early generation fluoroquinolones.2,3,9 One method of combating the increasing problem of fluoroquinolone resistance and rising level of Gram-positive infections is to use the new fourth-generation topical fluoroquinolones.
Traditional initial monotherapy has utilized the fluoroquinolone Ciloxan (ciprofloxacin, Alcon), two drops every 15 minutes for six hours, followed by two drops every 30 minutes for 18 hours, and then tapered depending on patient response. Another second-generation fluoroquinolone, Ocuflox (ofloxacin, Allergan), is also an effective treatment for bacterial keratitis.7 Both fluoroquinolones have been proven to be as effective for managing bacterial keratitis as the previously used fortified antibiotics, but with significantly fewer side effects. Unfortunately, bacterial resistance to the second-generation fluoroquinolones has been increasing, especially among the Gram-positive organisms. The two most recently available fourth-generation fluoroquinolones, moxifloxacin (Vigamox, Alcon) and gatifloxacin (Zymar, Allergan), have a greatly lowered resistance rate while providing much greater Gram-positive activity than previous generation fluoroquinolones.10 In the future, Zymar or Vigamox dosed on an hourly basis may become the mainstay therapy for bacterial keratitis.
Strong cycloplegia is also mandatory in order to increase patient comfort and minimize inflammation. The weakest cycloplegic that should be employed is scopolamine 0.25% tid. If this is insufficient, then atropine 1% bid is indicated. Adjunctive use of cold compresses will also help to reduce inflammation.
The patient should be followed daily until the infection is well controlled. If the results of cultures and sensitivities show that the initially prescribed antibiotic is appropriate for the infective organism, or if the patient shows signs of clinical improvement (the ulcer does not worsen, and pain and photophobia are reduced) at the 24 to 48 hour follow-up visit, a topical corticosteroid such as prednisolone acetate 1% or loteprednol etabonate 0.5% q2h can be added to speed resolution and decrease corneal scarring.
While steroids have historically been avoided in the management of infectious keratitis, judicious use can be beneficial. Antibiotics can suppress the infective organism, while corticosteroids can inhibit the corneotoxic inflammatory response. It has been feared that the immunosuppressive effects of steroids could enhance bacterial replication and worsen infection. However, if the chosen antibiotic is effective against the organism, then the concurrent use of steroids will not inhibit the bactericidal effect of the antibiotic.1117 But note that steroids should not be employed until the antibiotic has been given enough time to sterilize the ulcer, minimally 24 hours. One also must be certain that there is not a simplex viral, fungal, or protozoan infection prior to the initiation of topical steroids. Also, steroids should only be used in conjunction with true bactericidal antibiotics such as fluoroquinolones.
Other reports in this section
Eyelids & Eyelashes | Conjunctiva & Sclera | Cornea
Uvea | Vitreous & Retina | Neuro-Ophthalmic Disease | Oculosystemic Disease
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