Various nonpenetrating glaucoma procedures have been developed recently to improve the safety of conventional filtering procedures by avoiding postoperative complications such as hypotony, flat anterior chamber with iridocorneal contact, and choroidal effusions.1
Canaloplasty is a nonpenetrating surgical procedure that involves circumferential catheterization and viscodilation of canal of Schlemm with placement of a tensioning suture.2,3 The tension suture is believed to increase the natural aqueous outflow by restoring the trabeculocanalicular outflow that is believed to malfunction in patients with open-angle glaucoma.2,3 Despite canaloplasty's increased safety profile, postoperative complications such as microhyphema (7.9%), early and late intraocular pressure (IOP) elevations (7.9% and 2.4%, respectively), wound hemorrhage (2.4%), suture extrusion (1.6%), Descemet membrane detachment (DMD) (1.6%), and hypotony (0.8%) have been reported.2
Descemet membrane detachment is a potentially vision-threatening complication that can occur following diverse ocular surgeries, including cataract, glaucoma, and corneal surgery.4–9 Few DMD cases occur weeks after surgery (delayed-onset DMD); most reported cases occur in the early postoperative period. All cases of DMD after canaloplasty have been reported in the early postoperative period; all are unilateral. The reported incidence of DMD following canaloplasty is 1.6%.2 We report a case of bilateral DMD following consecutive canaloplasty surgeries in a patient with open-angle glaucoma and uncontrolled IOP.
A 70-year-old Portuguese man presented to our service with medically uncontrolled primary open-angle glaucoma. Nonpenetrating glaucoma surgery was recommended, and the patient had 2 consecutive canaloplasty procedures (1 week apart) in both eyes. Preoperatively, the corrected distance visual acuity (CDVA) was 20/60 in the right eye and 20/50 in the left eye (refraction −3.50 −2.75 × 90 and −3.75 −2.00 × 100, respectively). The IOP under maximum topical antiglaucoma medications was 24 mm Hg in the right eye and 23 mm Hg in the left eye.
A standard canaloplasty surgical technique was used in both eyes: A 5.0 mm × 5.0 mm superficial parabolic scleral flap followed by a deeper 4.0 mm × 4.0 mm scleral flap was created and dissected anteriorly until canal of Schlemm was identified. A viscoadaptive ophthalmic viscosurgical device (OVD) (Healon5) was injected through the opening of canal of Schlemm on either side. As the illuminated microcatheter was removed, viscodilation of the canal was performed simultaneously and continuously except for a short pause to regrasp the microcatheter at the 6 o'clock position in both eyes. A one-eighth turn of the OVD dispenser was performed every 2 clock hours by the assistant. A 10-0 polypropylene suture was then inserted 360 degrees and tied to dilate the canal and distend the trabecular meshwork inwardly. The deeper scleral flap was excised, and the superficial scleral flap was closed with a 10-0 nylon suture.
Canaloplasty was initially performed in the patient's right eye. On postoperative day 1, the visual acuity (with the preoperative refraction correction) and IOP were 20/70 and 12 mm Hg, respectively. A week later, canaloplasty was performed in the left eye and postoperatively (day 1), the CDVA and IOP were 20/50 and 11 mm Hg, respectively. On postoperative day 1, slitlamp examinatinn of both eyes revealed an unscrolled DMD inferonasally in both eyes (right eye>left eye) with a deep and quiet anterior chamber. The corneas were clear and had no striae (Figure 1). On gonioscopy, an intact, lightly pigmented, and distended trabecular meshwork was noted, with no evidence of suture extrusion or Descemet tear (Figure 1).
Fourier-domain optical coherence tomography (FD-OCT) was obtained and revealed a widely dilated canal of Schlemm with extensive trabecular distention and an inferior retrocorneal hyperreflective membrane corresponding to the DMD (right eye>left eye) (Figure 2). The patient was followed conservatively for 3 months at which time the DMD resolved spontaneously and the IOP was well controlled (18 mm Hg in both eyes) using 1 antiglaucoma medication.
Early diagnosis of DMD after canaloplasty is crucial to avoid irreversible visual loss. Predisposing factors that could lead to postoperative DMD include a preoperative diagnosis of glaucoma, a recent episode of corneal edema, hypotony, previous ocular surgery, corneal scarring, and anatomical predisposition.4 The incidence of post-canaloplasty DMD is reported to be 1.1% to 1.6%.2,3 In their 2-year clinical study, Lewis et al.2 report that DMD was encountered in only 2 of 127 eyes of patients who had unilateral canaloplasty. Post-canaloplasty DMD is not a rare event; however, surgical intervention is usually not needed and no irreversible visual loss has been reported.
To our knowledge, this is the first reported case of bilateral DMD following canaloplasty. In our patient, bilateral DMD was noted on the first postoperative day and was located inferonasally. Despite the presence of a DMD in the right eye, we decided to perform canaloplasty in the fellow eye (left eye) because of uncontrolled IOP using maximum antiglaucoma medications and postoperative IOP improvement in the right eye. Documented progression of the DMD in the right eye over the first week and/or the presence of corneal edema would have obliged us to defer surgery in the left eye. The final surgical outcome was successful as the DMD did not progress bilaterally and resolved spontaneously, while the IOP was well controlled postoperatively with less antiglaucoma medication.
To date, the exact mechanism of DMD after canaloplasty is not understood. Yalvac et al.9 reported a hemorrhagic DMD after viscocanalostomy (a similar nonpenetrating surgery) and believed that the DMD might have occurred while pressure was applied at the level of Schwalbe line during deroofing or injecting OVD over the pre-Descemet window. In our patient, an anatomical predisposition should be considered as a potential predisposing factor since other reported predisposing factors (except prior diagnosis of glaucoma) were not present. In this case, the bilateral and symmetrical location of DMD supports the presence of intrinsic factors. We believe that initially a focal DMD occurred intraoperatively during viscodilation of the canal. During careful intraoperative observation of the fellow eye (left eye), we visualized a localized, small DMD occurring directly after withdrawal of the microcatheter was interrupted at the 6 o'clock position while viscodilation of the canal continued. Postoperatively, there was no evidence of a Descemet tear and/or surgical trauma to the cornea. Therefore, we hypothesize the noncontinuous withdrawal of the microcatheter with continuous canal viscodilation along with the presence of a possible anatomic predisposition led to this complication. Injecting an excessive amount of OVD in a localized area of the canal can induce a shearing force to an already weakened Descemet–stromal complex, leading to a DMD.
Multiple studies have described a delayed-onset DMD following cataract surgery.7,8,10 The authors conclude that an underlying predisposition such as a preexisting intrinsic abnormality in stromal adherence to the Descemet membrane might have contributed to the detachment.
We would like to stress the importance of imaging in diagnosing and monitoring complications after canaloplasty. Ultrasound biomicroscopy and OCT have been used to evaluate canal of Schlemm and the degree of trabecular meshwork distention following canaloplasty.3,11–13 Fourier-domain-OCT is a noncontact technology providing high-resolution images that can be used to evaluate signs of morphological changes after surgery such as canal dilation and trabecular distension, which are believed to be associated with functional success.3 In our case, FD-OCT was useful in assessing the postoperative dilation of the canal, as well as confirming the presence of a DMD. Further studies are needed to understand the exact mechanism of DMD after canaloplasty.
In conclusion, bilateral DMD should be considered one of the potentially vision-threatening complications following canaloplasty. Although predisposing factors such as an anatomic predisposition may be present, uninterrupted microcatheter withdrawal and cautious viscodilation of the canal may prevent such a complication.
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