Are You Still Withholding the "Trabeculectomy Cure"?
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(Note that this was commentary originally authored in 2011-2012)
When I was a resident, glaucoma fellow, and then junior faculty at Massachusetts Eye and Ear Infirmary (MEEI), we had a glaucoma surgical conference in which the residents would have to present their cases for filtration surgery to a large group of seasoned glaucoma experts, and they were expected to justify the need for surgical intervention. This evolved from the era of full-thickness filtration surgery, which actually was remarkably successful in achieving low intraocular pressures (IOPs) but had a significant complication rate, mostly due to postoperative flat chambers, choroidal detachments, inevitable cataract formation, etc; it took only one expulsive hemorrhage to give one a new perspective.
As I continued to advance in time on the faculty at MEEI, the more modern operation of trabeculectomy came into fashion, and I remember several of my own fellows questioning me why I was hesitant to offer the “trabeculectomy cure” more aggressively to my patients at earlier stages of their primary open-angle glaucoma (POAG) disease (without the need to document progression of their glaucoma). This was especially true after the introduction of antiproliferative eye therapy,[1] first by Richard Parrish, MD, from the Bascom Palmer Eye Institute, where we seemed to enter a some-what naïve “golden period” of 5 to 10 years of believing in a surgical cure for glaucoma. So, indeed, how could we withhold this cure?
Of course, “glaucoma is the curse of long-term follow-up,” and with further time and observation we noted some serious complications from trabeculectomy, and many glaucoma doctors became joyless “bleb doctors,” dealing with thin, leaking, and occasionally infected blebs, and we soon accumulated a cadre of unhappy bleb patients despite good IOP control. Plus, sometimes the “cure” failed with time, and glaucoma control was lost. Such was the long-term cure of POAG.
To me, it is amazing that now, with the further passage of time, some glaucoma experts have almost given up on trabeculectomy for POAG. I think this is an overreaction, as many patients still achieve good IOP control, but we apparently have now entered a new “curative” era of tubes and valves and external hardware that basically still just shunts fluid from the inside of the eye to the outside. Thus, “tube cures” are now replacing “trabeculectomy cures” for POAG in many places, although others are observing longer-term failures of certain tubes with their own complications, etc.
And so to me, it really is important to take a more comprehensive long-term view of our “surgical cures” for POAG. One should start at the beginning of the 20th century (that is, around 1900), when glaucoma was actually the most advanced of ophthalmology disciplines. At a time when cataracts were being couched, retinal detachments were inoperable, and corneal transplants were unknown, ophthalmologists knew that if the eye was firm, one applied the “herb” pilocarpine, and if the eye remained somewhat firm (they did not understand the difference between open-angle and angle-closure glaucoma), then one put a “hole” in the eye and externalized the anterior chamber to the subconjunctival space. Hence, this was the birth of full-thickness filtration surgery. The great advance of trabeculectomy perhaps 70 years later really consisted of still just “putting a hole in the eye,” but now under a guarded scleral flap. (It is also noteworthy that trabeculectomy was not designed to produce filtration; rather to “-ectomize” the site of Grant’s outflow resistance.[2]) Likewise, with modern- era “tubes,” we now are once again simply externalizing the inside of the eye (through a tube) to the outside of the eye (and its accompanying hardware). How far, then, has glaucoma surgery come compared with the other advances in ophthalmology? Glaucoma physicians are still surgically “curing” POAG with some type of smaller hole into the eye.
I also continue to be amazed that, although the IOP rises in glaucoma due to abnormalities in the outflow pathway tissue, we have no targeted drugs for this tissue (which is a subject for another day and has been my life-long quest). I still think the future of surgical “cures” for POAG will some-day involve an “intra-outflow pathway” surgical procedure. There seems to be beginning efforts for this today with various Schlemm’s canal surgical procedures, and I am growing optimistic, although I think we are not yet there. I think we are missing something that we do not understand, and I hope that inquisitive and observant clinicians and surgeons in the future may discover the clue to a successful Schlemm’s canal surgical procedure. But I am also disappointed that many surgeons do not understand the fundamental observations of Morton Grant, MD,[2] which are the sine qua non to develop such a successful intra- outflow pathway surgical procedure. Grant clearly showed that the outflow pathway functions segmentally, there is no circumferential flow in Schlemm’s canal, and there is some distal scleral resistance from the outer wall of Schlemm’s canal outward[2][3] that results in postoperative IOPs not being as low as when one places a true “hole” that bypasses the full outflow pathway.
Grant eliminated 75% of the resistance to aqueous outflow only by cutting into the inner wall of Schlemm’s canal throughout the entire 360-degree circumference.[2][3] Therefore, segmental surgical procedures involving only 1 or even 2 hours of the circumference will eliminate only the resistance in that segment, and hence the typically resulting postoperative IOPs are in the mid- to upper-teens. Further, although we have moved along towards more circumferential surgical procedures with various suture techniques for treatments of 360 degrees of Schlemm’s canal, the potential flaw here is that it has not been believed that collapse of Schlemm’s canal is responsible primarily for the increased resistance to outflow (at least initially) in many glaucomas. How then is the suture technique addressing the fundamental cause of the glaucoma (except perhaps by disrupting the inner wall of Schlemm’s canal)? What is the exact rationale? Further, there is a biological wound healing process inherent in trabecular meshwork outflow pathway cellular processes that can provide benefit (eg, in various laser procedures[4]) or can cause healing and scarring of the intended outcome.
So, I don’t think we are quite there yet, and it is poignant to me that with the passage of time, my former fellows have themselves become seasoned glaucoma experts, and it is now their fellows who are puzzled about their hesitancy to vigorously offer a “surgical cure” for POAG.
Someday, hopefully, this will all change, but so far to me it is remarkable and disappointing how little things, in truth, are different. I worry what Drs. Chandler and Grant would say about our progress. We will all continue to carry the burdens of our glaucoma patients home with us each night until there really are both therapeutic and surgical true cures for the various glaucomas. Hopefully, the breadth of wisdom of sometimes reflective, if wizened, senior glaucoma surgeons can be combined with the inquisitive spirit of the new glaucoma generation to discover the clues necessary to accomplish this. We desperately do need new surgical “cures.”
References
- ↑ The Fluorouracil Filtering Surgery Study Group. Three-year follow-up of the Fluorouracil Filtering Surgery Study. Am J Ophthalmol. 1993;115(1):82-92.
- ↑ 2.0 2.1 2.2 2.3 Grant WM. Experimental aqueous perfusion in enucleated human eyes. Arch Ophthalmol. 1963;69:783-801.
- ↑ 3.0 3.1 Rosenquist RC, Epstein DL, Melamed S, Johnson M, Grant WM. Outflow resistance of enucleated human eyes with two different perfusion pressures and different extents of trabeculotomy. Curr Eye Res. 1989;8(12):1233-1240.
- ↑ Melamed S, Epstein DL. Alterations of aqueous humor outflow following argon laser trabeculoplasty in monkeys. Br J Ophthalmol. 1987;71(10):776-781.
