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Evolution of morphologic changes after intravitreous injection of gentamicin
J Hines1, S A Vinores, P A Campochiaro
1Wilmer Ophthalmological Institute, Johns Hopkins Hospital, Baltimore, MD 21287.
Current Eye Research
|June 1, 1993
Summary
Gentamicin causes retinal damage, starting with hemorrhages and progressing to vascular issues. Inner retinal neurons and glia are primary targets, leading to secondary infarction, not solely pH-related.
Area of Science:
- Ophthalmology
- Toxicology
- Neuroscience
Background:
- Gentamicin is known to cause retinal toxicity in various species, including humans.
- The precise mechanism underlying gentamicin-induced retinal toxicity remains poorly understood.
Purpose of the Study:
- To elucidate the sequential changes in the retina following intravitreous gentamicin injection.
- To identify the primary cellular targets and the sequence of events leading to gentamicin retinal toxicity.
Main Methods:
- Intravitreous injection of gentamicin (3 mg) or vehicle into pig eyes.
- Ophthalmoscopy, fluorescein angiography, light, and electron microscopy were used for examination.
- Histological analysis was performed at time points from 3 to 72 hours post-injection.
Main Results:
- Early ophthalmoscopic signs included retinal hemorrhages at 3 hours.
- Retinal whitening, thickening, and vascular nonperfusion were observed by 48 hours via fluorescein angiography.
- Inner retinal vacuolization and perivascular swelling occurred by 6 hours, progressing deeper into the retina.
- Vascular congestion and leukocyte margination were noted in retinal vessels at 48-72 hours.
- Changes were independent of gentamicin pH adjustment to 7.2.
Conclusions:
- Gentamicin retinal toxicity is not solely a pH-dependent phenomenon.
- Neurons and glia of the inner retina are the primary targets of gentamicin toxicity.
- Secondary retinal infarction may result from leukocytic plugging in retinal vessels.