Malignant glaucoma after phacoemulsification ...

J CATARACT REFRACT SURG - VOL 33, JANUARY 2007

CASE REPORTS

Malignant glaucoma after phacoemulsification: Treatment with diode laser cyclophotocoagulation Mahiul M.K. Muqit, MD, MRCOphth, Mitchel J. Menage, MD, FRCS, FRCOphth

Phacoemulsification was performed in an 84-year-old woman with ocular hypertension and narrow drainage angles, previously treated by neodymium:YAG (Nd:YAG) laser peripheral iridotomy. Despite temporal zonular weakness, the surgery was uneventful. An intraocular lens (IOL) was placed and centered in the capsular bag. Two months later, the patient presented with malignant glaucoma. The IOL optic was anteriorly displaced in the capsular bag, and the IOL shift correlated with a 4.0 diopter myopic refractive error. There was no response after medical treatment or Nd:YAG hyaloidotomy. One week later, a single treatment with transscleral diode laser cyclophotocoagulation was performed. The intraocular pressure normalized and the anterior chamber deepened within 48 hours. The patient’s condition has remained stable for 3 months with no further treatment; the Snellen visual acuity is 6/9. If medical therapy fails to control malignant glaucoma, cyclodiode laser treatment may be more effective and have fewer risks than current laser and surgical interventions. J Cataract Refract Surg 2007; 33:130–132 Q 2007 ASCRS and ESCRS

Malignant glaucoma was initially described by von Graefe1 and is defined by normal or elevated intraocular pressure (IOP) associated with axial shallowing of the entire anterior chamber in the presence of a patent peripheral iridotomy (PI). The condition develops in 2% to 4% of patients with a history of acute or chronic angle-closure glaucoma who have drainage surgery.2 The condition may be induced by miotics3 or laser iridotomy4 or may occur after extracapsular cataract surgery.5 The prognosis is often poor despite vitreous surgery, so the term malignant glaucoma is used. New

Accepted for publication July 5, 2006. From the Glaucoma Service, Department of Ophthalmology, Leeds General Infirmary, Great George Street, Leeds, United Kingdom. No author has a proprietary or financial interest in any material or method mentioned. Corresponding author: Mr. Mitchel J. Menage, MD, FRCS, FRCOphth, Glaucoma Service, Department of Ophthalmology, Leeds General Infirmary, Great George Street, Leeds, United Kingdom. Q 2007 ASCRS and ESCRS Published by Elsevier Inc.

techniques have been developed to manage this challenging condition.6,7 We describe our successful use of diode laser cyclophotocoagulation (cyclodiode) in a patient who developed malignant glaucoma after phacoemulsification. CASE REPORT An 84-year-old woman with ocular hypertension attended the glaucoma clinic because of visual deterioration in the left eye. Two years earlier, she had bilateral neodymium:YAG (Nd:YAG) PIs for narrow drainage angles and had persistently shallow anterior chambers. On initial examination, the PIs were patent, with Shaffer grade 1 angles and healthy optic nerve function. The refraction was 0.50 C2.25 140 in the right eye and C2.75 C1.25 50 in the left eye. The Snellen best corrected visual acuity (BCVA) was 6/9 and 6/12, respectively. The intraocular pressure (IOP) was 20 mm Hg in both eyes, and there was moderate nuclear cataract in the left eye. A-scan biometry demonstrated an axial length of 22.11 mm in the right eye and 21.04 mm in the left eye. The patient had phacoemulsification under sub-Tenon’s anesthesia in the left eye in September 2005. The preoperative anterior chamber depth (ACD) was 1.54 mm, and sodium hyaluronate 2.3% (Healon5) was used during surgery. During the capsulorhexis stage, zonular weakness was noted temporally, but 0886-3350/07/$-see front matter doi:10.1016/j.jcrs.2006.07.041

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CASE REPORTS: TREATMENT OF MALIGNANT GLAUCOMA AFTER PHACOEMULSIFICATION

a continuous curvilinear capsulorhexis (CCC) was successfully performed and hydrodissection was uneventful. There was no phacodonesis or visible zonular dehiscence, and a stop-andchop technique was performed. There was no evidence of vitreous in the anterior or posterior chamber, and the pupil was round. The intraocular lens (IOL) (AcrySof MA30, Alcon; C26.50 diopters [D], 12.5 mm overall, 5.5 mm optic) was centered in the capsular bag, and the Healon5 was aspirated from behind the IOL. The patient missed an initial follow-up appointment and was subsequently seen at 1 month by a trainee ophthalmologist. She reported no problems and Snellen BCVA was 6/36 (6/12 with pinhole), with an unremarkable anterior chamber and IOP of 20 mm Hg. She was referred to her local optometrist for routine refraction per our cataract surgery care protocol. Two months postoperatively, she reported decreased vision and elevated IOP. The Snellen BCVA was 6/60, and the IOP was 38 mm Hg with air tonometry. The refraction was 5.00 C1.50 100, with a Snellen BCVA of 6/12 in the left eye. The preoperative surgical target refraction was C0.16 D, and the patient had developed a 4.41 D myopic refractive surprise. The patient returned to the hospital, and the IOP was found to be 30 mm Hg. The PI was patent with anterior chamber shallowing, and the ACD was 1.82 mm. The IOL was displaced anteriorly and tilted temporally in the capsular bag. On indentation gonioscopy, the angle was Shaffer grade 1 with peripheral anterior synechias (PAS). There were no signs of a choroidal detachment, and the retina was flat. A diagnosis of malignant glaucoma was made. Standard primary treatment of cycloplegia (atropine 1%) and oral acetazolamide 250 mg, each 3 times daily, were instituted. The patient remained on conventional therapy for 1 week. There was no clinical change, and an Nd:YAG laser hyaloidotomy was performed through the PI. The procedure was difficult in the presence of a small PI and poorly dilating pupil, and the aqueous misdirection did not resolve. The patient had described floaters after cataract surgery, and examination confirmed a posterior vitreous detachment (PVD). Contact transscleral cyclodiode (CTC) was performed under sub-Tenon’s anesthesia with lignocaine 2%. The OcuLight SLx 810 nm diode laser photocoagulator and the Iris G-probe (both from Iris Medical Instruments) were used. The location of the ciliary body was identified with transillumination, and the G-probe was placed 1.2 mm posterior to the limbus. Two rows of 5 laser spots, one at 1.2 mm and the other at 1.25 mm, both posterior to the limbus, were made inferotemporally. A single row of 4 spots superotemporally, and a single row of 3 spots in each of the remaining 2 nasal quadrants were made. The settings were 2 seconds at 2 W, with a total energy of 80 J. The ACD appeared to deepen during laser delivery. The procedure was otherwise uneventful. Postoperatively, prednisolone 1% was prescribed 4 times daily. The patient was reviewed at 48 hours, and the IOP was 12 mm Hg with an ACD of 2.66 mm. There was mild pigmentary anterior uveitis. After 3 weeks, the refraction had improved to 2.00 C1.25 115 and the ACD was stable. At 3 months, the refraction was stable and the median ACD was 2.94 mm. On indentation gonioscopy, the angle had deepened to Shaffer grade 2 with PAS. There was no significant uveitis, and Snellen BCVA was 6/9.

DISCUSSION

There are several theories about the sequential events leading to malignant glaucoma. Shaffer8 describes posterior misdirection and pooling of aqueous within the vitreous

and behind a PVD. The ciliolenticular theory is characterized by anterior rotation of the ciliary body, which has been confirmed by ultrasound biomicroscopy (UBM) studies.9 The common feature of aqueous misdirection is anterior displacement of the lens–iris and iris–hyaloid diaphragm, in association with aqueous impermeability of the anterior hyaloid face.2 Any intervention for malignant glaucoma aims at making a direct communication between the anterior chamber and the vitreous cavity or disrupting the blockage site at the ciliary–hyaloid interface. Fifty percent of patients may respond to medical therapy.2 Neodymium:YAG laser therapies and vitreous surgical interventions are well reported in the literature9; however, these procedures may be technically demanding and have additional potential risks. Contact transscleral cyclodiode has been described for malignant glaucoma following drainage surgery, acute angle closure, and extracapsular cataract extraction.10–12 Reports in the literature are not clear about the timing of CTC treatments, and the CTC regimen is not clearly reproducible. Carassa et al.10 outline results of CTC following Nd:YAG laser anterior hyaloidotomy. The laser technique and energy regimen are not fully described, and the authors propose that the patient have Nd:YAG hyaloidotomy before CTC. In a report by Sengupta et al.,11 one case subsequently required cataract extraction, which suggests poor IOP control following CTC. In neither report is there standard guidance for clinicians who may want to perform CTC as a therapeutic intervention for malignant glaucoma or for future management of the fellow eye. The causes of malignant glaucoma are multifactorial, and our case demonstrates several risk factors that explain the sequential development of malignant glaucoma. An Nd:YAG PI may be associated with zonular rupture,13 and this finding was observed in our case during the CCC stage of cataract surgery. The temporal zonular weakness may allow forward movement of the IOL–iris diaphragm, and a quantity of sodium hyaluronate (Healon5) may have passed through zonular defects into the vitreous cavity. Cataract surgery with underlying chronic angle closure may cause ciliary body spasm. In addition, the anterior chamber decompression during cataract surgery may have resulted in separation of the vitreous base from the pars plana. All these factors may contribute to anterior ciliary body rotation, with posterior misdirection of aqueous. The misdirected aqueous humor may accumulate with the Healon5 in the vitreous body. Contact transscleral cyclodiode has been shown to produce a characteristic injury to the pars plicata.14 The coagulative necrosis and shrinkage of the ciliary processes may disrupt the ciliary–hyaloid interface and subsequently allow normal aqueous flow and mechanical posterior rotation of the ciliary body.10 This effect occurs immediately and


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CASE REPORTS: TREATMENT OF MALIGNANT GLAUCOMA AFTER PHACOEMULSIFICATION

appears to remain stable, with satisfactory IOP reduction. In our case, the subjective refraction improved by 2.875 D, and this correlated with posterior movement of the IOL optic. In the absence of UBM technology, the condition may be monitored in clinic by refraction and ACD measurements. The method of CTC application required to disrupt the ciliary–hyaloid barrier remains unknown. It is not clear whether a localized application or a diffuse 360-degree application will effectively reverse the aqueous misdirection. We treated a single region (inferotemporal quadrant) with higher power and applied reduced energy to the remainder of the ciliary ring. This approach resulted in visible anterior chamber deepening intraoperatively. In our case, the patient will eventually require cataract extraction in the fellow eye. There is an increased risk for malignant glaucoma developing in the fellow eye postoperatively.2 It has been proposed that phacoemulsification in combination with a posterior capsulorhexis and anterior vitrectomy may be the procedure of choice.9 Zonulo-hyaloido-vitrectomy6 and videoendoscope-guided fluorescein-assisted vitrectomy7 are more technically challenging techniques, with the potential for serious complications. There is a choice of treatments available for our patient. Preoperative CTC laser ciliary ablation has been proposed before drainage surgery as a prophylactic measure.9 One approach would be to apply low-energy prophylactic CTC 3 weeks before phacoemulsification to prevent the onset of aqueous misdirection during phacoemulsification. The timing and reduced power output of CTC prophylaxis would minimize the degree of uveitis before cataract extraction. Standard atropine 1% at the end of surgery and a course of oral acetazolamide postoperatively would be mandatory. There may be a risk for worsening existing zonular weakness with this approach, and the surgeon should anticipate this complication. Another approach would be to perform phacoemulsification with IOL implantation initially. If malignant glaucoma develops, medical therapy is recommended.15 However, if there is no response within 1 week, we propose a single 360-degree CTC treatment. There is a risk for PAS formation and synechial angle closure, so cyclodiode therapy should not be delayed. Neodymium:YAG hyaloidotomy may be technically difficult through a small PI or IOL dialing hole. In essence, further experience is needed to determine the best approach to this challenging surgical situation. Our case provides guidance for refractive surgeons who may wish to perform this laser procedure for

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malignant glaucoma following phacoemulsification surgery. The energy delivery is lower than cyclodiode therapy for refractory glaucoma. This technique of cyclodiode treatment may not significantly compromise the scleral bed, allowing drainage surgery to be performed in the future. In summary, in patients with a history of narrow drainage angles having phacoemulsification, low-energy prophylactic CTC may be used preoperatively in high-risk cases. If malignant glaucoma develops, 360-degree CTC can be performed as a secondary treatment if medical therapy is not successful. The laser effect on IOP is immediate, with few uveitic complications, and the visual outcome is favorable. REFERENCES 1. von Graefe A. Beitra¨ge zur Pathologie und Therapie des Glaucomas. Albrecht von Graefes Arch Ophthalmol 1869; 15(3):108–252 2. Luntz MH, Rosenblatt M. Malignant glaucoma. Surv Ophthalmol 1987; 32:73–93 3. Merritt JC. Malignant glaucoma induced by miotics postoperatively in open-angle glaucoma. Arch Ophthalmol 1977; 95:1988–1989 4. Small KM, Maslin KF. Malignant glaucoma following laser iridotomy. Aust N Z J Ophthalmol 1995; 23:339–341 5. Duy TP, Wollensak J. Ciliary block (malignant) glaucoma following posterior chamber lens implantation. Ophthalmic Surg 1987; 18: 741–744 6. Lois N, Wong D, Groenewald C. New surgical approach in the management of pseudophakic malignant glaucoma. Ophthalmology 2001; 108:780–783 7. Chen SDM, Salmon JF, Patel CK. Videoendoscope-guided fluoresceinassisted vitrectomy for phakic malignant glaucoma. Arch Ophthalmol 2005; 123:1419–1421 8. Shaffer RN. The role of vitreous detachment in aphakic and malignant glaucoma. Trans Am Acad Ophthalmol Otolaryngol 1954; 58:217–231 9. Ruben S, Tsai J, Hitchings R. Malignant glaucoma and its management. Br J Ophthalmol 1997; 81:163–167 10. Carassa RG, Bettin P, Fiori M, Brancato R. Treatment of malignant glaucoma with contact transscleral cyclophotocoagulation. Arch Ophthalmol 1999; 117:688–690 11. Sengupta R, Austin M, Morgan J. Treatment of aqueous misdirection by trans-scleral diode laser photocoagulation [letter]. Eye 2000; 14:808–810 12. Reed JE, Thomas JV, Lytle RA, Simmons RJ. Malignant glaucoma induced by an intraocular lens. Ophthalmic Surg 1990; 21:177–180 13. Melamed S, Barraquer E, Epstein DL. Neodymium: YAG laser iridotomy as a possible contribution to lens dislocation. Ann Ophthalmol 1986; 18:281–282 14. McKelvie PA, Walland MJ. Pathology of cyclodiode laser: a series of nine enucleated eyes. Br J Ophthalmol 2002; 86:381–386 15. European Glaucoma Society. Secondary angle-closure glaucomas with posterior ‘‘pushing’’ mechanism without pupillary block. In: European Glaucoma Society. Terminology and Guidelines for Glaucoma, 2d ed. Savona, Italy, Dogma, 2003; 2.5.2


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