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Editors Selection IGR 11-4

Retinal ganglion cells: Pressure spikes and RGC damage

Comment by George Lambrou on:

19331 Acute retinal ganglion cell injury caused by intraocular pressure spikes is mediated by endogenous extracellular ATP, Resta V; Novelli E; Vozzi G et al., European Journal of Neuroscience, 2007; 25: 2741-2754

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Have we unknowingly been harming some of our patients for decades, possibly precipitating retinal ganglion cell damage? In a well-written basic-science paper, Resta et al. (864) report that rapid (1-2 min) IOP spikes of high amplitude (50-90 mmHg) induce irreversible damage in a small but significant number of RGCs and probably increase the vulnerability of many more to subsequent pressure insults. They have collected corroborating evidence from a number of in-vivo and ex-vivo experiments, supporting the hypothesis that this effect is independent of any ischemic insult and is mediated through cytotoxic P2X receptors by endogenous extracellular ATP - known to be released by stimulation of retinal glia. Interestingly, this deleterious effect seems to be related to the abruptness of the IOP spike rather than to the pressure level or to the total duration of the pressure insult. Thus, a slow-onset, slow-offset 7-min exposure to 90 mmHg caused no RGC damage at all in isolated rat retinas, whereas seven 1-min abrupt 90 mmHg pressure spikes caused maximal damage with up to 80% of RGCs showing signs of injury in their somata or dendritic trees. So what is the relevance of these findings to human patients? With the exception of ocular trauma, the experimental conditions created by the authors do not occur naturally (even acute glaucoma is much closer to their 'slow 90 mm pulse' which was harmless).

If further evidence confirms that IOP spikes of 1-2 mins of 50-90 mmHg induced irreversible damage, we may need to amend LASIK protocols

We have, however, been abruptly increasing IOP during ophthalmodynamometry for decades, then - more recently - during experimental investigational procedures such as ocular plethysmography, oculo-oscillo-dynamography, pressure-compliance testing of the optic nerve, or Ocular Blood Flow measurements. We have used these procedures knowing that they cause temporary visual disturbances, but we attributed those to transient ischemia and presumed that they were totally reversible. And, whereas these techniques were seldom used - in specific investigational settings as a rule - the widespread use of laser refractive surgery (LASIK) has caused an exponential increase in the number of IOP spikes we apply to our patients' eyes each day. If further evidence comes to confirm the hypothesis of Resta et al., then we may need to amend LASIK protocols, e.g., by limiting the rate of IOP increase during eye immobilization.

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