Ciliochoroidal effusion with persistent hypotony after trabectome surgery

Abstract

The trabectome is a novel form of ab interno trabeculectomy that ablates and remove the trabecular meshwork and the inner wall of Schlemm's canal and subsequently expose the natural drainage pathway (the collector channels) to aqueous humor. Complications associated with the trabectome are few and among them is transient hypotony. We report a case of a prolonged ciliochoroidal effusion with hypotony after ab interno trabeculectomy using the trabectome with cyclodialysis cleft detected by 80 MHz ultrasound biomicroscopy in a previously neither nonoperated nor traumatized eye. Transient hypotony has been reported after the trabectome surgery. Very few cases were associated with inadvertent intraoperative cyclodialysis, but there are no cases of prolonged hypotony with ciliochoroidal effusion with cyclodialysis. In our case, associated transient intraoperative and postoperative hypotony with a history of chronically high pressure along with the possible contribution of low-grade postoperative inflammation may have precipitated the ciliochoroidal effusion with prolonged hypotony associated with cyclodialysis.

The trabectome, a novel form of ab interno trabeculectomy, has safe ablation, removal of the trabecular meshwork, and inner wall of Schlemm's canal. The handpiece includes an infusion sleeve away from the surgical site and a longer coaxial adjustable aspira on the port which is 0.3 mm away from the spark site.[1,2] The continuous infusion helps to avoid heat-related damage, maintain the anterior chamber and removes tissue debris and thereby reducing inflammatory stimuli and the opportunity for scarring.[3] The foot pedal controls the irrigation, aspiration and electrocautery ablation,[4,5] less surgical time, neither bleb formation nor late infection risk.

Case Report

A 33-year-old gentleman with a 12 years history of unilateral juvenile open-angle glaucoma in the left eye was referred to our clinic because of long standing uncontrolled intraocular pressure (IOP) despite anti-glaucoma medications. He was on three topical anti-glaucoma medications with uncontrolled IOP with end-stage glaucomatous optic nerve cupping. His vision was the light perception, and the IOP was 24 mmHg. Anterior segment examination on was unremarkable, and the angle was open and there was total cupping with the flat retina. He was not using any systemic medications nor having the systemic illness. There was no prior history of surgery or trauma. The right eye had 20/20 vision with IOP of 16 mmHg and normal disc.

Treatment modalities were discussed with the patient, and both advantages and disadvantages were explained and the decision was to go for ab interno trabeculectomy by the trabectome. Under local anesthesia, a good view was obtained using modified Swan-Jacobs lens (Ocular Instruments, Bellingham, Washington, USA). Then the goniolens was temporarily put aside, and a 1.7 mm temporal clear corneal incision was made with internal enlargement. Viscoelastic was injected to the anterior chamber followed by the insertion of the trabectome tip just beyond the infusion port, and then the goniolens was applied again. The trabectome tip was inserted through the trabecular meshwork into the Schlemm's canal, and arcs of tissue ablated nasally totaling 90°. Irrigation/aspiration by Simco was performed to aspirated minimal back bleeding from Schlemm's canal and the viscoelastic. Single 10.0 nylon suture was placed followed by subconjunctival injection of gentamicin and dexamethasone. Postoperative medications were pilocarpine 2% drops, predforte 1% drops, and oflox drops all 4 times daily for 2 weeks. The first day after surgery, the IOP was 6 mmHg, and the chamber was deep with microscopic hyphema. The wound was secured with open Schlemm's canal wall by gonioscopy and no choroidals. One month later, the vision was the light perception, and the IOP was 5 mmHg with shallow chamber mostly at the periphery [Fig. 1]. 35 MHz ultrasound biomicroscopy (UBM) was done and showed 360° peripheral ciliochoroidal effusion but no evidence of cyclodialysis cleft [Fig. 2]. Atropine 1% drops were started. Two months postoperatively, the patient presented with the shallower chamber and unrecordable pressure but still no clinically detectable choroidals [Fig. 3]. 80 MHz UBM was done and confirmed the presence of cyclodialysis cleft [Videos 1 and 2] with increased effusion nasally, the cyclodialysis cleft was in nasal quadrant and correspond to site of trabectome around 2 h between 8 and 10 o’clock and optical coherence tomography macula did not show macular folds [Fig. 4]. Four months after the trabectome surgery, the patient presented with a deep chamber-4 mm-and the IOP was 2 mmHg with no choroidals. UBM was done and showed the regressing ciliochoroidal effusion and visual acuity was LP, and the cleft was still the same size in the nasal quadrant.

Figure 1.

One month after trabectome surgery

Figure 2.

Ultrasound biomicroscopy showing ciliochoroidal effusion

Figure 3.

Two months after trabectome surgery

Figure 4.

Optical coherence tomography showed no macular folds

Discussion

Ciliochoroidal effusion is an abnormal accumulation of fluids in the supraciliary and the 30 μm suprachoroidal space. Ocular disorders such as inflammation following intraocular surgery or laser treatment, vascular causes, trauma, tumors, medications, primary sclera abnormality, and arteriovenous fistula are associated with ciliochoroidal effusion. In the early stages, ciliary effusion without obvious choroidal effusion can be best-detected by UBM. The relation between hypotony and ciliochoroidal effusion is not clearly understood. Ciliochoroidal effusion causes hyposecretion of the ciliary body and in the same time enhance uveoscleral outflow and precipitates hypotony. During hypotony, the low IOP will fail to tamponade the potential supraciliary and suprachoroidal space and will cause transudation from choroidal capillary wall to the potential space and subsequently will increase the uveoscleral outflow.[6] Furthermore, inflammatory mediators play an important role in relaxing the ciliary body and remodeling the extracellular matrix with subsequent hyposecretion and increased uveoscleral outflow.[7]

Transient hypotony has been reported after trabectome surgery where very few were secondary to inadvertent intraoperative cyclodialysis.[8] The unique about our case that there was a persistent ciliochproidal effusion and hypotony with evidence of cyclodialysis cleft detected only by 80 MHz UMB and without a prior history of trauma. We believe that important precipitating factors were the transient intraoperative and postoperative hypotony in a patient with a long-standing high IOP as well as the contribution of the pressure lowering effect of the trabectome by exposing the collector channels to aqueous caused a ciliochoroidal effusion which was aggravated by the low grade postoperative inflammation. In an extended follow-up of 1127 trabectome surgeries, Minckler et al. reported transient hypotont in only 17 cases with no single case of sustained hypotony nor choroidal effusion.[1]

Potential vision threatening complications of prolonged hypotony include: Hypotony maculopathy, band keratopathy, cataract formation, optic nerve edema, ciliary body membrane formation, and even phthisis bulbi.[9]

Treatment of hypotony with ciliochoroidal effusion is usually directed toward the underlying cause. In general, inflammatory conditions are treated with steroidal and nonsteroidal anti-inflammatory medications. Cycloplegic and mydriatic agents are used to normalize the iris-lens diaphragm and ciliary body position and to prevent synechia in miotic position. Surgically precipitating factors such as wound leak, overfiltration, and cyclodialysis are treated accordingly. Usually, surgical intervention is recommended whenever there is a risk for visually threatening complication. In our case, an end-stage disease with the gradually regressing effusion did not encourage us for an invasive intervention. Cyclodialysis cleft with persistent hypotony with ciliochoroidal effusion can happen after trabectome surgery. 80 MHz UBM is a useful diagnostic utility to detect such clefts in the shallow chamber.