SIGNS AND SYMPTOMS
The patient will 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. There is likely to be thick, ropy, mucopurulent discharge.
The cornea will be very 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 severe cases, there will be a pronounced anterior chamber reaction, often with hypopyon. Intraocular pressure may be low due to secretory hypotony of the ciliary body, but most often will be elevated due to blockage of the trabecular meshwork by inflammatory cells. Often, the eyelids will also be edematous.
Once the corneal defenses are breached, specifically the epithelial glycocalyx, the cornea is prone to infection. Possible causes 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 which leads to an inflammatory reaction. The body releases polymorphonuclear leukocytes (PMNs) which aggregate at the area of infection, creating an infiltrate. The PMNs phagocytize and digest the bacteria. 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, creating the possibility for endophthalmitis.
Throughout North America, the most common infective organism in bacterial keratitis is Staphylococcus aureus. However, in cases involving contact lens wear and cosmetics, the most common infective organism is Pseudomonas aeruginosa.
As with bacterial conjunctivitis, culturing the infection is the ideal way to determine the infecting organism but is often difficult or impractical. First and foremost, you must halt bacterial proliferation; do not delay treatment while waiting for the culture results. If you have the materials available, scrape the ulcer using a platinum spatula and plate the specimen onto blood and chocolate agar culture media. A simpler but less effective method is to use a culturette.
Regardless, immediately begin therapy with a broad spectrum antibiotic. A popular initial therapy is the fluoroquinolone ciprofloxacin 0.3% (Ciloxan) 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, ofloxacin 0.3% (Ocuflox) is also an effective treatment for bacterial keratitis. Both fluoroquinolones are as effective at managing bacterial keratitis as fortified antibiotics, but with significantly fewer side effects.
To increase patient comfort and minimize inflammation, strong cycloplegia is mandatory. Begin with a cycloplegic such as scopolamine 0.25% TID. If this is insufficient, switch to atropine 1% BID. Adjunctive use of cold compresses will also help to reduce inflammation. If there is evidence of secondary inflammatory glaucoma, Rx a topical beta-blocker BID.
Have the patient return daily for follow-up visits. Once the infection is controlled, add a topical steroid Q2H to the regimen. Continue the daily follow-up and begin to taper all medications as you see improvement.
If a patient presents with a corneal infiltrate but no overlying epithelial staining, the condition is not bacterial keratitis. If there is epithelial breakdown but only minor inflammation and anterior chamber reaction, then it most likely is not infectious bacterial keratitis.
The inflammatory reaction is as damaging to the cornea as the infective organism. Once you've halted bacterial proliferation, be sure to prescribe a steroid to speed healing and reduce corneal scarring. For steroids to be beneficial, they must be used while the ulcer bed is still open, usually within the first 24 to 48 hours. If you wait until the ulcer re-epithelializes before adding a steroid, the beneficial effects will be lost.