Mind the Suction II – Focus on Scleral Lens Channel Technology
By Karen G. Carrasquillo, OD, PhD, FAAO, FSLS, FBCLA
In the November 2018 issue of Scleral Lens Monthly, Dr. Melissa Barnett wrote the original piece to this series, titled “Mind the Suction.”1 In that issue, she referenced how the topic and the notion of scleral lens suction was starting to finally gain traction among scleral lens practitioners. She also referenced an article that I wrote with Dr. Steve Byrnes in which we addressed how lens suction could also contribute to the clinical manifestations of microcystic epithelial corneal edema.2 I have kept this notion and topic at the top of my mind, given that this is one aspect of scleral lens fitting that is not “tangible and/or measurable”—at least until now—and because it is something that can continue to get lost in the troubleshooting armamentarium of practitioners.
As we transitioned from polymethyl methacrylate (PMMA) and GP fenestrated scleral lenses to fluid-ventilated scleral lenses in the late 1980s, one of the challenges when fitting non-fenestrated scleral lenses was preventing clinically significant lens suction. One of the concepts that was imparted upon me as I learned to master this craft in the early 2000s was that clinically significant suction can occur when micro quantities of fluid are squeezed out of the fluid reservoir as the lens lags during horizontal ductions and when it is compressed during blinking.
If this volume is not fully replaced when the eye returns to its primary position and during its decompression between blinks, negative hydrostatic pressure builds up in the lens reservoir. This can lead to limbal chemosis (Figure 1) and wearing discomfort. Under some circumstances, dangerous suction develops that can cause the paralimbal bulbar conjunctiva to be sucked against the back surface of the lens; lens seal-off; dull-ache, tenderness, and hyperemia after lens removal; neovascularization; microcystic epithelial edema; and limbal edema. Suction can result from tight-fitting lenses, use of spherical lens designs on an asymmetric sclera, circumferential limbal crowding/touch, distribution of high total sagittal depths over small lens surface areas (i.e., imbalance of weight distribution over haptic landing zones), and the effect of lens settling over time.
Figure 1. Clinical signs of limbal chemosis as a result of lens suction. Image courtesy of BostonSight
In addition to making sure that we monitor our fits and strive to ensure viable physiologically compatible fitting endpoints, a lens design feature that can help minimize and/or mitigate lens suction in fluid-ventilated designs are venting channels (Figure 2). Lathed or milled channels can be added to the back surface of a scleral lens to prevent it from becoming sealed. These channels also potentially serve to promote or enhance tear exchange.
Figure 2. Schematic and illustration of venting channels on the back-surface haptic area of a scleral lens. Image courtesy of BostonSight
Determining the Effects of Suction
We can’t truly talk about scleral lens channel technology without talking about spline curve technology; this allows a special degree of control over the scleral lens design. Just as the back surface of the lens can be manipulated to create virtually any desired seamless shape, the front surface of the haptic is also defined by a spline having a point-to-point relationship with the back surface of the haptic as its basis curve (Figure 3); this allows precise control over the thickness profile and contour of the haptic to ensure its structural integrity, especially when it incorporates lathed or milled channels.
Figure 3. Front-surface and back-surface curve point-to-point relationship, as powered by spline functions, to precisely control the thickness profile of a lens haptic and to properly accommodate lathed or milled channels. Image courtesy of BostonSight.
When incorporating these venting channels on a haptic’s back surface, not only are we helping to prevent lens seal-off and helping to promote tear exchange, we also are helping to prevent adverse sequelae that can occur as a result of suction; this results in the elimination of limbal and microcystic epithelial edema as well as neovascularization regression, ease of lens removal, and reduction of lens hyperemia upon lens removal (Figures 4 and 5).
Figure 4. Resolution of edema and neovascularization in a grafted cornea secondary to Fuchs’ dystrophy after adding two channels under the haptic surface at 3 o’clock and 9 o’clock.
Figure 5. (A) Microcystic epithelial edema (yellow box) and neovascularization (red box). (B) Resolution of microcystic edema (yellow box) and neovascularization regression (red boxes – ghosted vessels) in a neurotrophic keratopathy case after the addition of two channels under the haptic surface at 3 o’clock and 9 o’clock.
Our clinic is engaged in a prospective study setup, with the goal to research, quantitate, and share the effects of scleral lens suction on the physiological outcome of a scleral lens fit as well as the role of scleral lens channels to mitigate effects of suction. The more we learn and understand, the better we will serve our patient populations. Stay tuned. Until then, let’s all continue to “mind the suction."