Assessing Retrobulbar Hyaluronidase as a Treatment for Filler-Induced Blindness in a Cadaver Model.

BACKGROUND

Retrobulbar injection of hyaluronidase is a proposed but unproven treatment for blindness induced by hyaluronic acid gel fillers. This study examines the viability of this treatment by determining whether hyaluronidase can diffuse through the dural sheath of the optic nerve to clear a filler-mediated occlusion of the central retinal artery.

METHODS

Six human cadaveric optic nerves were studied in vitro. One optic nerve was selected as a control and maintained at physiologic temperature, without any exposure to hyaluronic acid gel or hyaluronidase. Another optic nerve was randomly selected to simulate the filler-induced central retinal artery occlusion with subsequent retrobulbar hyaluronidase injection. To simulate a central retinal artery occlusion, this experimental nerve and additional controls were injected with hyaluronic acid gel. These hyaluronic acid gel-injected nerves were then either injected directly with hyaluronidase to establish a control for intraneural hyaluronidase exposure, or immersed in undiluted hyaluronidase to simulate retrobulbar hyaluronidase injection. To control for passive diffusion of hyaluronic acid gel from neural parenchyma, one nerve was immersed in saline. Following fixation, the nerves were grossly and microscopically assessed for the quantity and distribution of hyaluronic acid.

RESULTS

Intact hyaluronic acid gel was observed grossly and microscopically in the control optic nerves injected directly with filler and not with hyaluronidase. The control optic nerve injected with intraneural hyaluronidase exhibited partial digestion of the filler. Immersion in undiluted hyaluronidase led to no apparent gross or microscopic digestion of injected intraneural hyaluronic acid gel.

CONCLUSION

Hyaluronidase does not demonstrate the ability to cross the dural sheath of the optic nerve, suggesting that retrobulbar hyaluronidase injection is unlikely to alleviate hyaluronic acid gel-mediated central retinal artery occlusion and blindness.