Topical antibiotic drops are preferred. Consider subconj-unctival antibiotics if compliance is a concern. Systemic therapy is useful in cases of systemic infection (e.g., gonorrhea) or if the sclera is infected. Reserve ointments for minor cases or adjunctive nighttime therapy.21
Start topical broad-spectrum antibiotics empirically. Use a loading dose for severe keratitis (Table 63-8). Single-drug therapy with a fluoroquinolone is as effective as combination therapy. Resistance is seen with some fluoroquinolones. Because of this, choose a newer fluoroquinolone such as moxifloxacin or gatifloxacin in severe kerat-itis cases.6,21 Fortified antibiotic therapy is an option for severe or unresponsive infec tions, but may increase toxicity to the cornea and surrounding tissues. Fortified antibiotics must be compounded.2 All compounded formulations must comply with governmental 797 regulations concerning compounding of drug preparations.
Table 63-8 Pharmacologic Therapies for Bacterial Keratitis Organism
Unknown or multiple types of organisms
Cefazolin 50 mg/mL and tobramycin/
gentamicin 9-14 mg/mL or Fluoroquinolones various strengths Cefazolin 50 mg/mL or Vancomycin1' 15-50 mg/mL or Bacitracin" 10,000 international unit or iVioxifloxacin or Gatifloxacin various strengths Tobramycin 9-14 mg/mL or Gentamicin 9-14 mg/mL or Ceftazidime 50 mg/mL or Fluoroquinolones various strengths Ceftriaxone 50 mg/mL or Ceftazidime 50 mg/mL or Fluoroquinolones various strengths Amikacin 20-40 mg/mL or Oral clarithromycin, adults: 500 mg every 12 hours
Fluoroquinolones various strengths Amikacin 20-40 mg/mL or Trimethoprim 16 mg/mL and sulfamethoxazole 80 mg/mL
Severe keratitis: loading dose every 5-15 minutes for the first hour, then every 15 minutes to 1 hour around the clock. Less severe keratitis may use less frequent dosing
"Use for resistant Enterococcus and Staphylococcus species and penicillin allergy. No gram-negative activity, do not use vancomycin or bacitracin for single agent empiric therapy in bacterial keratitis.
Topical corticosteroids are employed in some cases of bacterial keratitis. The suppression of inflammation may reduce corneal scarring. However, local immunosup-pression, increased ocular pressure, and reappearance of the infection are disadvantages to their use. There is no conclusive evidence that they alter clinical outcomes. If the patient is already on topical corticosteroids when the keratitis occurs, discontinue use until the infection is eliminated.
• Monitor patient symptoms for improvement to determine therapeutic efficacy
• Modify treatment regimen based on results of culture and sensitivity testing, if necessary
• Modify the treatment regimen if the patient does not show improvement within 48 hours
• Gram-negative keratitis will have increased inflammation in the first 24 to 48 hours, even on appropriate therapy
• Taper therapy based on clinical response
• Reculture or biopsy if negative clinical response; to improve culture results, discontinue antibiotics for 12 to 24 hours before culturing.
macular degeneration EPIDEMIOLOGY AND ETIOLOGY
Age-related macular degeneration (AMD) is the primary cause of severe, irreversible vision impairment in developed countries (Figs. 63-2 and 63-3). The prevalence in-22
creases with age. In the United States, 1.75 million people age 40 or older have ad-
vanced AMD, and another 7 million people may have intermediate AMD. Because of the rapid aging of the U.S. population, it is projected that almost 3 million people
will develop AMD by 2020. The causes of AMD are not completely known (Table 63-9).22
AMD is a deterioration of the macula, the central portion of the retina. The macula facilitates central vision and highresolution visual acuity because it has the highest concentration of photoreceptors in the retina. The loss of central vision leads to irreversible loss of the ability to drive, read, and perform other fine visual tasks like recognize
faces. Peripheral vision is preserved, allowing mobility. AMD is characterized by one or more of the following: drusen formation, retinal pigment abnormalities (e.g.,
hypo- or hyperpigmentation), geographic atrophy, and neovascular maculopathy.
Definite ftjsk Factors
Potential Risk Factors
l ight pigmentation
vitamins or zinc
Increased body mass Index
Higher dietary fat intake
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