Discussion: Topography of the Central Retinal Artery Relevant to Retrobulbar Reperfusion in Filler Complications.

Abstract

www.PRSJournal.com 1301 T present article concerns the detailed analysis of the three-dimensional course of the central retinal artery and its topographic relations to the optic nerve as it passes from its origin (ophthalmic artery) to its final destination in the retina.1 The central retinal artery is a terminal artery that supplies the inner retina, which has no other blood supply (except for some individuals who have cilioretinal artery collateral vessels).2 This is relevant because the pathophysiology of fillerassociated blindness seems to be experimentally attributable to retrograde flow of filler within branches of the ophthalmic artery (from the facial region) and into the central retinal artery.3 The authors wanted to determine the best retrobulbar injection pathway for approaching the central retinal artery safely. The ultimate purpose of this cadaveric study was to determine the precise course of this important vascular structure within the retrobulbar space so that clinicians can better place hyaluronidase close to the central retinal artery in the event of filler-related blindness. This is a beautifully done anatomical study with stunning visualization of the central retinal artery, and the authors are to be congratulated for their excellent work. There is no argument about their findings, nor with their recommendations on how to best approach retrobulbar injection technique. The ultimate consideration, however, is whether or not retrobulbar hyaluronidase should be undertaken in the first place. In a recent animal model, retrobulbar hyaluronidase did not improve outcomes.4 To date, the evidence has been sparse to nonexistent that retrobulbar hyaluronidase has any benefit whatsoever (e.g., Zhu et al.5), apart from a case report that might also be consistent with vasospasm or other causes of visual impairment.6 There are two interrelated issues to consider: location and time. Let us consider time first. The retina is extraordinarily sensitive to hypoxia (it is really an extension of the brain, embryonically from the same neural tissues), and injury is irreversible within minutes of onset7 (again, very similar to the brain). (In contrast, barbiturateanesthetized primates show full recovery following approximately 90 minutes of retinal ischemia.8) There is not very much time allowance to break down the filler embolus before blindness is permanent. Dermal fillers are formulated to be hyaluronidase resistant, so that they will last when injected, and there are differences in sensitivity also (some are easier to dissolve than others).9–14 Although I am referring to hyaluronidase as a generic product, there may be some differences in effectiveness between different sources (bovine, ovine, or human recombinant hyaluronidase) even though they are supposed to be normalized to the same standard international unit (such that one unit of one should be equally effective as one unit of another hyaluronidase).15 Consider also the location of the embolus. We know that, clinically, hyaluronidase seems more effective when administered subcutaneously rather than intraarterially, as confirmed in an animal model.16 Our objective then is to inject hyaluronidase as close as possible around the vessel segment containing the embolus. If the filler has entered the optic nerve and the retina (it seems that hyaluronidase cannot passively diffuse through the dura17), the only pathway for externally administered hyaluronidase is by diffusion through the retrobulbar space, then through the vessel wall of the exposed portion of the central retinal artery (before it enters the optic nerve), and finally passively diffuse along a stagnant column of blood within the vessel to begin the hydrolysis of the filler embolus. Even after reaching the filler embolus within the optic nerve or retina, hyaluronidase can only start