Signs and Symptoms: The patient with bacterial keratitis will generally present with a unilateral, acutely painful, photophobic, intensely injected eye. Visual acuity is usually reduced, and profuse tearing is common. There will be a focal stromal infiltrate with an overlying area of epithelial excavation.
Mucopurulent discharge may emanate from the lesion. The cornea may be edematous. The conjunc tival and episcleral vessels will be deeply engorged and inflamed, often greatly out of proportion to the size of the corneal defect. A pronounced anterior chamber reaction, often with hypopyon, is present in severe cases. Intraocular pressure may be low due to secretory hypotony of the ciliary body, but often will be elevated due to blockage of the trabecular meshwork by the inflammatory cells. Often, the eyelids will also be edematous.
Pathophysiology: Once the corneal defenses are breached, specifically the corneal glycocalyx, the cornea is prone to infection by pathogenic bacteria. Precipitating factors to corneal defense breakdown include direct corneal trauma, chronic eyelid disease, tear film abnormalities affecting the ocular surface and hypoxic trauma from contact lens wear.
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 utilizing numerous enzymes that tend to leak from the PMN into the stroma.
The collagen stroma is poorly tolerant of the bacterial and leukocytic enzymes and undergoes degradation, necrosis and thinning. This results in scarring of the cornea. With severe thinning, 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 Pseudomonas aeruginosa. Overall throughout North America, the most common infective organism in bacterial keratitis is Staphylococcus aureus.
Management: Proper diagnosis and prompt therapy are essential to preserve vision in bacterial keratitis. Your first step in management should be to obtain corneal scrapings for microbiologic studies. The standard of care is to obtain a platinum spatula and plate onto blood-chocolate agar medium. However, the effectivity 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 Culturette. Scrape the lesion with the Culturette, then place it in the media-containing carrier. The sensitivity of this approach compared to platinum spatula collection and plating was 83.3% sensitivity and 100% specificity.
With the advent of fluoroquinolone antibiotics, many clinicians have dropped culturing as part of the diagnostic regimen. However, we recommend you still obtain cultures for central lesions that threaten vision, are at risk of perforation, and in patients in institutions such as nursing homes and hospitals where methicillin-resistant Staph. aureus infections are possible.
Even if the patient has been cultured, you must initiate broad-spectrum, empirical antibiotic therapy prior to receiving the results. A popular initial therapy is 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 fluoroquinolone, Ocuflox (ofloxacin, Allergan) is also an effective treatment for bacterial keratitis. Both fluoroquinolones have been proven to be as effective at managing bacterial keratitis as the previously used fortified antibiotics, but with significantly fewer side effects. Newer fourth-generation fluoroquinolones promise to have similar efficacy against gram-negative pathogens and broader activity against gram-positive species.
Strong cycloplegia is also mandatory in order to increase patient comfort and minimize inflammation. The weakest cycloplegic that you should use is scopolamine 0.25% tid. If this is insufficient, then prescribe atropine 1% bid. Adjunctive use of cold compresses will also help to reduce inflammation.
If there is evidence of secondary inflammatory glaucoma occurring, then a topical aqueous suppressant agent may be indicated. Follow the patient frequently until the infection is well controlled. If the results of cultures and sensitivities show that the antibiotic you chose initially was appropriate for the infective organism, or if the patient shows signs of clinical improvement (or the ulcer does not worsen and pain and photophobia are reduced) at the 24-48 hour follow up visit, then add a topical corticosteroid such as Pred Forte (prednisolone, Allergan) or Lotemax (loteprednol, Bausch & Lomb) q2h. Follow the patient every 24 hours, and taper the medications as the condition improves.
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