BLOG: How to leverage the distal outflow pathway with novel glaucoma therapeutics
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In my ophthalmology residency and also my fellowship, I learned to think about the modification of aqueous dynamics for treatment of glaucoma with respect to inflow (aqueous production) and outflow (aqueous drainage).
At that time, we thought about conventional (trabecular) and uveoscleral outflow pathways, but not much consideration was given to the distal outflow pathway. The distal outflow pathway refers to aqueous flow beyond the trabecular meshwork and Schlemm’s canal. The average individual has 24 to 35 collector channels that drain circumferentially from Schlemm’s canal. From the collector channels, aqueous drains into the episcleral vasculature. The episcleral vasculature resists aqueous flow and is responsible for approximately 7 mm Hg to 11 mm Hg of pressure. This episcleral vasculature often represents a “floor” beyond which IOP cannot be lowered without surgical intervention that bypasses Schlemm’s canal — until now.
We now have highly effective and low-risk methods for treatment and modification of the distal aqueous outflow pathways in order to manage IOP in our patients with glaucoma and ocular hypertension. From a medical standpoint, the availability of netarsudil has allowed us to decrease episcleral venous pressure and thereby decrease the “floor” of IOP. Netarsudil belongs to the medication class of Rho kinase inhibitors. By inhibiting the Rho kinase enzyme, vascular smooth muscle walls are relaxed, and this is what leads to a decrease in episcleral venous pressure. This mechanism complements the effects of the medication on the conventional outflow pathway, where outflow resistance is also reduced.
From a surgical standpoint, microinvasive glaucoma surgery has revolutionized the field. Our first MIGS platforms were designed to target the proximal outflow pathway. More recent devices and techniques target the distal outflow pathway as well. Canaloplasty is a long-standing technique that involves inflation of the collector channel system to enhance aqueous drainage and flow. Until relatively recently, this technique was performed ab externo, necessitating a conjunctival peritomy, scleral flap dissection, a cutdown to externally identify Schlemm’s canal and then threading of a microcatheter capable of infusing viscoelastic to inflate the collector channel system. Nowadays, we can perform canaloplasty in an ab interno fashion via a clear corneal incision. Three devices, the iTrack microcatheter (Nova Eye Medical), the Omni surgical system (Sight Sciences) and the Streamline surgical system (New World Medical, Figure 1), have enhanced our ability to perform ab interno canaloplasty. Ab interno canaloplasty first involves creation of a clear corneal incision followed by a localized goniotomy to gain entrance into Schlemm’s canal. Schlemm’s canal is then catheterized with one of the aforementioned surgical systems and then inflated with viscoelastic. Pressurized viscodilation allows for expansion of the distal collector channels as well. Often, one can visualize the effects of pressurized viscodilation intraoperatively as the episcleral vasculature is blanched (Figure 2). The reestablishment of aqueous flow distally leads to decreased IOP, which has been well supported in the ophthalmic literature.
Much remains to be learned with regards to the distal outflow pathway. There are sure to be innovations within the next decade to augment our surgical techniques and enhance our ability to offer sustained and safe outcomes for our patients.
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