Macular infarction after intravitreal amikacin
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《英国眼科学杂志》
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2 Carney Hospital, 2100 Dorchester Avenue, Boston, MA 02124, USA
Correspondence to:
Dr Bernard H Doft
Accepted for publication 20 November 2003
Keywords: macular infarction; intravitreal amikacin
We write in reference to the letter by Galloway et al.1
The authors report a single case of macular infarction in a patient who had been given intravitreal amikacin for endophthalmitis. They cite that single case plus some previous literature as a reason to support a change in the choice of antibiotic for intravitreal injection from the treatment guidelines based on the results of the Endophthalmitis Vitrectomy Study (EVS).
While aminoglycoside induced retinal toxicity certainly can occur, we disagree with their statement that there is good evidence that aminoglycosides should not be primary drugs of choice in this disease. There are several theoretical and practical advantages of aminoglycosides over ceftazidime. Amikacin provides concentration dependent killing (so that the higher concentration of drug the more rapid the kill) which is not true for ceftazidime. This is an important issue since high concentrations of drug are administered by intravitreal injection, thus possibly allowing for more rapid kill with amikacin.
Amikacin is considered to be synergistic with vancomycin for certain Gram positive species, so its use provides benefit against Gram positive organisms, not just for Gram negative organisms. Gram positive organisms make up the overwhelming majority of cases of endophthalmitis. In addition, there has been a recent report that ceftazidime may precipitate in the vitreous at normal body temperature,2 possibly making it less available than one might wish in the vitreous cavity.
Finally, and very importantly, is the fact that amikacin has been found to be effective in a clinical trial but there is no such evidence yet available on ceftazidime. The only apparent advantage of ceftazidime is that it may be a somewhat safer drug in the sense that macular toxicity has not been reported. Even so, the incidence of macular toxicity is extremely rare (only one in 420 eyes in the EVS suffered macular toxicity possibly from the drug). In a very severe disease such as endophthalmitis a risk this low is worth tolerating when there may be substantial potential advantages.
References
Galloway G, Ramsay A, Jordan K, Macular infarction after intravitreal amikacin: mounting evidence against amikacin, et al. Br J Ophthalmol 2002;86:359–60.
Kwok AK, Hui M, et al. An in vitro study of ceftazidime and vancomycin concentrations in various fluid media: implications for use in treating endophthalmitis. Invest Ophthalmol Vis Sci 2002;43:1182–8.(B H Doft1 and M Barza2)
2 Carney Hospital, 2100 Dorchester Avenue, Boston, MA 02124, USA
Correspondence to:
Dr Bernard H Doft
Accepted for publication 20 November 2003
Keywords: macular infarction; intravitreal amikacin
We write in reference to the letter by Galloway et al.1
The authors report a single case of macular infarction in a patient who had been given intravitreal amikacin for endophthalmitis. They cite that single case plus some previous literature as a reason to support a change in the choice of antibiotic for intravitreal injection from the treatment guidelines based on the results of the Endophthalmitis Vitrectomy Study (EVS).
While aminoglycoside induced retinal toxicity certainly can occur, we disagree with their statement that there is good evidence that aminoglycosides should not be primary drugs of choice in this disease. There are several theoretical and practical advantages of aminoglycosides over ceftazidime. Amikacin provides concentration dependent killing (so that the higher concentration of drug the more rapid the kill) which is not true for ceftazidime. This is an important issue since high concentrations of drug are administered by intravitreal injection, thus possibly allowing for more rapid kill with amikacin.
Amikacin is considered to be synergistic with vancomycin for certain Gram positive species, so its use provides benefit against Gram positive organisms, not just for Gram negative organisms. Gram positive organisms make up the overwhelming majority of cases of endophthalmitis. In addition, there has been a recent report that ceftazidime may precipitate in the vitreous at normal body temperature,2 possibly making it less available than one might wish in the vitreous cavity.
Finally, and very importantly, is the fact that amikacin has been found to be effective in a clinical trial but there is no such evidence yet available on ceftazidime. The only apparent advantage of ceftazidime is that it may be a somewhat safer drug in the sense that macular toxicity has not been reported. Even so, the incidence of macular toxicity is extremely rare (only one in 420 eyes in the EVS suffered macular toxicity possibly from the drug). In a very severe disease such as endophthalmitis a risk this low is worth tolerating when there may be substantial potential advantages.
References
Galloway G, Ramsay A, Jordan K, Macular infarction after intravitreal amikacin: mounting evidence against amikacin, et al. Br J Ophthalmol 2002;86:359–60.
Kwok AK, Hui M, et al. An in vitro study of ceftazidime and vancomycin concentrations in various fluid media: implications for use in treating endophthalmitis. Invest Ophthalmol Vis Sci 2002;43:1182–8.(B H Doft1 and M Barza2)