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My MIGS of Choice, with Kin Sheng Lim

Glaucoma is caused by inadequate drainage of aqueous humor, resulting in raised intraocular pressure, damage to the optic nerve, and vision loss. The majority of aqueous drainage – between 70 and 95 percent – occurs in the conventional pathway via the trabecular meshwork, Schlemm’s canal, collector channels, and episcleral veins (1, 2). The uveoscleral pathway contributes to the remaining aqueous outflow via the supraciliary and suprachoroidal space. Resistance to outflow in the conventional pathway plays a fundamental role in the development of primary open angle glaucoma (POAG); the uveoscleral pathway is not significantly different between glaucoma patients and healthy individuals (3).

The primary causes of outflow resistance occur in the trabecular meshwork, Schlemm’s canal, and collector channels of the conventional pathway. Endothelial cell loss results in the fusion of trabecular columns (4) and the accumulation of extracellular matrix and banded fibrillar elements embedded within different glycoproteins, creating “plaque material” that causes stiffness within the trabecular meshwork (5) (6) (7). Such herniations of the trabecular meshwork tissue frequently block collector channels within glaucomatous eyes (8) (9), likely resulting in elevated IOP when compared with healthy eyes (10). Glycosaminoglycans – whose levels are elevated in glaucoma – attract and retain water, reducing the space available for fluid outflow. Loss of vacuoles in the inner wall of Schlemm’s canal also contributes to increased outflow resistance (11). Additionally, Schlemm’s canal in POAG eyes is shorter, narrower, and often collapsed, reducing the effective outflow area and obstructing the flow of aqueous drainage from the anterior chamber into the bloodstream via the anterior ciliary veins (12).

A treatment modality addressing all these potential areas of resistance and providing effective reduction of IOP to preserve the optic nerve offers significant utility in clinical practice.

The science behind canaloplasty

Canaloplasty is an implant-free procedure that preserves the trabecular meshwork and can be deployed across the entire glaucoma disease spectrum. The surgical technique involves the insertion of a flexible microcatheter for 360˚ catheterization of Schlemm’s canal. Subsequent viscodilation of Schlemm’s canal occurs upon withdrawal of the microcatheter alongside simultaneous injection of high-molecular weight hyaluronic acid (HA)-based ophthalmic viscosurgical devices (OVD) along the length of Schlemm’s canal. This ensures complete dilation and improves aqueous outflow in both Schlemm’s canal and the collector channels.

Canaloplasty can be performed via one of two surgical techniques:

  • Ab externo approach – performed in eyes with severe glaucoma through a conjunctival incision. A suture is left in tension to facilitate aqueous outflow.
  • Ab interno approach – performed in cases of mild to moderate glaucoma via a clear, self-healing corneal-limbal incision.

Canaloplasty improves outflow facility through mechanical, hydrostatic, and biophysical mechanisms. The 360° catheterization of Schlemm’s canal mechanically breaks adhesions within the canal while pushing herniations of the trabecular meshwork out of the collector channel ostia to improve outflow. The hydrostatic pressure caused by OVD delivery stretches the trabecular meshwork, possibly creating microperforations within the anterior chamber, while also dilating Schlemm’s canal and the collector channels (6, 7, 8). Another hypothesis is that the pressurized injection of HA-based OVD into Schlemm’s canal may bind with sCD44, reversing cytotoxicity in POAG eyes and improving the cellular function, architecture, and outflow.

Going above and beyond the trabecular meshwork

Canaloplasty offers a number of advantages to both clinicians and patients. First, it permits surgical intervention earlier in the disease process, potentially eliminating the need for invasive and ablative filtering surgery such as trabeculectomy or valve implants. Some of my colleagues across Europe report that they have halted filtering surgeries altogether and adopted canaloplasty as the first-line treatment in patients with open angle glaucoma.

Second, canaloplasty is comprehensive. Resistance to aqueous outflow in glaucoma occurs at multiple levels; the canaloplasty procedure involves 360˚ catheterization and viscodilation, making it a more comprehensive treatment of the outflow pathway than most MIGS options, which consist of focal implants that bypass the trabecular meshwork. Although they are effective in reducing IOP and medication burden, stent-based MIGS procedures do not treat the entire outflow system. With canaloplasty, all points of potential outflow resistance are addressed, including the diseased trabecular tissue.

Third, canaloplasty aims to enhance both the proximal and distal outflow systems by reducing outflow resistance at all possible sites of obstruction. This improves the physiological flow of aqueous humor, making canaloplasty a restorative procedure that does not preclude further surgical options.

Fourth, canaloplasty is safe and effective. Its clinical utility is evident in peer-reviewed studies (13), (14). A recent study by Gallardo demonstrated the 36-month effectiveness of ab interno canaloplasty as a standalone procedure or combined with cataract surgery. Both IOP and medication burden were significantly reduced (by 33.9 percent and 60.7 percent, respectively) in all eyes at 12 months; the reduction remained stable at 24 and 36 months in both groups. No serious adverse events were recorded; early postoperative IOP spikes and hyphema were observed in some cases, but were readily managed or resolved spontaneously without late sequelae (14).

What makes canaloplasty even more unique is that it avoids implantation of a device in the eye. The procedure induces little to no inflammation and endothelial cell count is seemingly unaffected (15), therefore maintaining the anterior chamber anatomy.

Canaloplasty and its challenges

Previously, canaloplasty involved a steep surgical learning curve. The procedure involved manual intubation of the microcatheter through Schlemm’s canal using forceps, guided by an illuminated fiber-optic tip. It required good understanding of the outflow pathway anatomy, along with excellent glaucoma surgical training, experience, and practice. There are currently two devices approved for canaloplasty on the market: the newly released iTrack Advance device, which leverages the features of its original canaloplasty microcatheter and incorporates a new handheld injector and purpose-designed cannula, and the OMNI Surgical System, which is indicated for canaloplasty followed by trabeculotomy to reduce intraocular pressure.

Canaloplasty effectively addresses all potential areas of blockage in the trabecular outflow pathway to optimize aqueous humor drainage. Glaucoma is a 360° disease, so it makes sense to treat it with a 360˚ procedure such as canaloplasty. Offering sustained long-term outcomes without the need to implant a device or remove or damage trabecular meshwork tissue, canaloplasty is a promising MIGS procedure for POAG patients.

Kin Lim has no financial conflict or disclosure with any procedure or product in this article.

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  1. CB Toris et al., “Aqueous humor dynamics in the aging human eye,” Am J Ophthalmol, 127, 407 (1999). PMID: 10218693.
  2. CB Toris et al., “Aqueous humor dynamics in ocular hypertensive patients,” J Glaucoma, 11, 253 (2002). PMID: 12140404.
  3. L Beltran-Agullo et al., “Comparative human aqueous dynamics study between black and white subjects with glaucoma,” Invest Ophthalmol Vis Sci, 52, 9425 (2011). PMID: 21980001.
  4. J Alvarado et al., “Trabecular meshwork cellularity in primary open-angle glaucoma and nonglaucomatous normals,” Ophthalmology, 91, 564 (1984). PMID: 6462622.
  5. JW Rohen et al., “Ultrastructure of the trabecular meshwork in untreated cases of primary open-angle glaucoma (POAG),” Exp Eye Res, 56, 683 (1993). PMID: 8595810.
  6. K Wang et al., “Trabecular meshwork stiffness in glaucoma,” Exp Eye Res, 158, 3 (2017). PMID: 27448987.
  7. DW Abu-Hassan et al., “The trabecular meshwork: A basic review of form and function,” 2 (2014). PMID: 25356439.
  8. H Gong et al., “Morphological changes in the distal outflow pathway of primary open angle glaucoma,” Invest Ophthalmol Vis Sci, 56, 3300 (2015).
  9. R Stegmann et al., “Viscocanalostomy for open-angle glaucoma in black African patients,” J Cataract Refract Surg, 25, 316 (1999). PMID: 10079435.
  10. SA Battista et al., “Reduction of the available area for aqueous humor outflow and increase in meshwork herniations into collector channels following acute IOP elevation in bovine eyes,” Invest Ophthalmol Vis Sci, 49, 5346 (2008). PMID: 18515571.
  11. RC Tripathi, “Aqueous outflow pathway in normal and glaucomatous eyes,” Br J Ophthalmol, 56, 157 (1972). PMID: 4113454.
  12. RR Allingham et al., “Schlemm’s canal and primary open angle glaucoma: correlation between Schlemm’s canal dimensions and outflow facility,” Exp Eye Res, 62, 101 (1996). PMID: 8674505.
  13. MA Khaimi, “Long-term medication reduction in controlled glaucoma with iTrack ab-interno canaloplasty as a standalone procedure and combined with cataract surgery,” Ther Adv Ophthalmol, 13, 25158414211045751 (2021). PMID: 34604698.
  14. MJ Gallardo, “36-month effectiveness of ab-interno canaloplasty standalone versus combined with cataract surgery for the treatment of open-angle glaucoma,” Ophthalmol Glaucoma, 5, 476 (2022). PMID: 35183815.
  15. D Lubeck, R Noecker, “Evaluation of Endothelial Cell Density Two Years following iTrackTM Ab-Interno Canal Based Surgery,” ASCRS (2022).
About the Author
Kin Sheng Lim

Kin Sheng Lim is a consultant ophthalmic surgeon at St Thomas’ Hospital and Professor of Glaucoma studies (Ophthalmology) at King’s College London. Lim is currently the glaucoma service’s clinical lead, the ophthalmology departmental lead for research and the director of KCL Frost Eye Research Department at St Thomas’.

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