David L. Epstein, MD, MMM
Cyclodialysis1 performed in an eye rendered previously aphakic or as part of a combined intracapsular cataract operation2 used to be a frequently performed glaucoma procedure. Although the success was only in the 30% to 40% range, it was a fairly quick procedure with a rapid postoperative recovery. It has fallen into disuse with the advancement in techniques of combined cataract/filtration surgery (see Chapter 62), but perhaps it deserves further evaluation in pseudophakic eyes with good central visual acuity that are not suitable for filtration surgery, prior to consideration of a laser ciliodestructive procedure (which has some risk of inducing cystoid macular edema and decreased central acuity). Some have proposed combination surgery of cyclodialysis with extracapsular cataract surgery.3
The mechanism of intraocular pressure (IOP) lowering with cyclodialysis is likely due to increased out flow into the nonconventional outflow pathway4,5 via the surgically created cleft as has previously been de scribed (see Chapters 2 and 3), although some have thought that the procedure also acts to decrease the rate of aqueous humor formation.6 The technique of the surgical procedure will be described in this chapter.
SYNDROME OF SUDDEN CLOSURE OF A CYCLODIALYSIS CLEFT
One of the unfortunate complications that sometimes occurred in some of the “successes” with the cyclodialysis surgical procedure was ocular hypotony.7 But, in addition, what was occasionally also observed was a syndrome of a sudden high IOP if the cyclodialysis cleft was suddenly closed. Often, the IOP observed in this syndrome would far exceed the preoperative IOP levels for a day or so. The mechanism for this phenomenon was believed to involve the fact that when the cyclodialysis cleft was functioning, aqueous humor was flowing not into the trabecular meshwork (TM) but into the cleft. When the cleft closed, the TM, having been previously underperfused and underutilized, temporarily offered substantially more resistance to aqueous outflow than prior to surgery. It is noteworthy that an early explanation of this phenomenon was made by Goldmann.8 There have been histological studies of experimentally produced hypoperfusion of the TM, which demonstrated increased proteinaceous material extracellularly in the outflow pathway, as well as other structural changes.9 Such an acute underperfusion syndrome of the TM theoretically might also occur after filtration surgery if the fistula were to suddenly close due to iris incarceration or blood, for example. Clinically, this sudden cleft closure syndrome lasted only 1 to 2 days, after which there was return to baseline glaucoma status (likely continued poor control).
Patients who were postoperative from cyclodialysis procedures would routinely be maintained on miotics indefinitely in order to cause ciliary muscle contraction, and therefore both to pull the ciliary body further away from the separated scleral spur and to narrow the ciliary body ring (see Chapter 30) and thus expand the potential fluid space beneath the sclera. Sometimes, sympathomimetic drugs such as phenylephrine were used in addition to miotics to contract the iris dilator muscle because it was felt that this action might, by increasing iris tone, act with coexisting cholinergic miotics to move the iris away from the cleft. Also, sympathomimetic drugs may cause weak contraction of the ciliary muscle.10
David L. Epstein, MD, MMM
I was once presented with the following case: A patient had just undergone trabeculectomy, per formed elsewhere, for uncontrolled IOP in the 20s. On the first postoperative day, the IOP was 6 mm Hg, but there was no obvious bleb. On day 2, the IOP had suddenly increased to 60 mm Hg, which was much higher than it ever had been before. The angle was described as being open. One drop of 1% pilocarpine was placed in the eye and the IOP decreased to 9 mm Hg.
This patient proved to have an inadvertent cyclodialysis cleft as a result of the trabeculectomy, but it is important for the reader to realize that when trabeculectomy was first introduced as a surgical technique, it was common to extend the sclerectomy posteriorly and excise the scleral spur.1 If one reads the early literature after the develop ment of the procedure of trabeculectomy, there is often much confusion about the absence of blebs despite good IOP results in many patients. (We believe now that this was likely due to having produced a cyclodialysis rather than a filter in such patients; maybe cyclodialysis is not such a bad operation after all!) Trabeculectomy originally was conceptualized to remove diseased TM and allow aqueous humor to flow into the cut ends of Schlemm’s canal.2 This does not, in fact, happen as the cut ends of the canal collapse.3 Regardless, there would be little potential anyway for resulting circumferential flow of aqueous humor in Schlemm’s canal as the out flow pathway functions in a segmental manner4,5 (see Chapter 3). Thus, this was not the first time, nor likely the last, that a procedure designed to work by one mechanism actually worked by another. Trabeculectomy functions really as a guarded filtering procedure in which, under a scleral flap, a fistula is created to the subconjunctival space.6
The key to the mystery diagnosis in this case was the sudden occurrence of a high IOP far above baseline postoperatively despite an open angle and the super-response to pilocarpine that actually resulted in the re opening of the cleft rather than a mechanical tension on the TM. (The first suspicion from the history, of course, was that with such a pilocarpine effect, the patient might have developed angle closure that was relieved with this weak miotic therapy or perhaps suffered a miotic-related retinal detachment, but this proved not to be the case.) Likely, in this case (and others), the routine use of a cycloplegic drug post-trabeculectomy may have precipitated the sudden cleft closure syndrome.
REFERENCES
1. Watson PG. Surgery of the glaucomas. Br J Ophthalmol. 1972;56:299-306.
2. Cairns JE. Trabeculectomy. Preliminary report of a new method. Am J Ophthalmol. 1968;66:673-679.
3. Spencer WH. Histologic evaluation of microsurgical glaucoma techniques. Trans Am Acad Ophthal Otol. 1972;76:389-397.
4. Van Buskirk EM, Grant WM. Lens depression and aqueous outflow in enucleated primate eyes. Am J Ophthalmol. 1973;76:632-640.
5. 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;8:1233-1240.
6. Grant WM. Symposium: microsurgery of the outflow channels. Trans Am Acad Ophthalmol Otolaryngol. 1972;76(2):398-404.
A common situation that precipitated the sudden cleft closure syndrome was when the patient was dilated for funduscopy with a cycloplegic drug. Presumably, the cycloplegic drug caused relaxation of ciliary muscle tone and dilation of the ciliary body ring (see Chapter 30), and this outward movement of the ciliary body could close the space between the ciliary body and sclera, which represented the cleft.
INADVERTENT CYCLODIALYSIS CLEFTS
Nowadays, one encounters cyclodialysis clefts mostly as in advertent complications resulting from trauma (see Chapter 44) or after anterior segment surgery.11–16 Sometimes, some of the newer scleral tunneling techniques16 in cataract surgery may inadvertently cause this separation of the ciliary body from the scleral wall.
How should such inadvertent cyclodialyses be treated? Building upon what we have learned from the above, a trial of cycloplegics, initially short-acting agents but later daily atropine or scopolamine, should be attempted first. This failing (the cleft), if small, may be therapeutically closed sometimes by applying argon laser gonioplasty–type applications to the visible scleral wall of the cleft, with perhaps a few applications to the peripheral iris in the same area.17–20 What one is really trying to do is cause inflammation to potentially encourage adhesion of the ciliary body back to the sclera. There fore, minimal to no steroids should be used and cycloplegics should be maintained after argon laser treatment. Because the sclera is white and does not absorb the energy well (which is why the peripheral iris is sometimes also treated nonspecifically to encourage inflammation), and because there are likely nerves in the sclera, this is an uncomfortable procedure for the patient, and likely it should be per formed in multiple smaller sessions. This argon laser procedure is not ideal and often fails. It probably is fruitless to attempt this procedure in the presence of a large cleft.
It is noteworthy in contemplating the limited efficacy of laser applications in closing clefts to realize that neodymium:yttrium-aluminum-garnet laser applications have been reported to reopen a cleft!21
The next alternative that I have had good success with is to treat the sclera external to the cleft with 2 rows of cyclocryotherapy (CCT; full freeze applications for 30 to 60 seconds each). One’s goal is to totally overlap the circumferential extent of the cleft (eg, 1 to 3 hours of the limbus). The efficacy of this modality is felt to be by the induced inflammation that the procedure causes. Retrobulbar anesthesia is necessary, but the postoperative morbidity is much less than after the standard 6 clock hour CCT for antiglaucoma therapy. However, one must also be prepared to deal with the high IOP of the sudden cleft closure syndrome should this procedure be successful.
Figure 64-1. (A) Large cyclodialysis cleft visible gonioscopically that occurred following blunt trauma from a handball. The patient developed an IOP of 0 to 2 mm Hg and hypotonous maculopathy. (B) After cycloplegics and laser failed to close the cleft, the ciliary body was resutured to the sclera. IOP was maintained in the mid-teens following 1 to 2 days of IOPs in the 40s in the immediate postoperative period. Visual acuity was restored to a level of 20/25.
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