AQUEOUS MISDIRECTION SYNDROME AFTER PARS PLANA VITRECTOMY FOR RETINAL DETACHMENT Kamaljit S. Balaggan, BSC(HONS), MRCOPHTH, D. Alistair H. Laidlaw, MD, FRCOPHTH

Background: Aqueous misdirection syndrome (AMS) typically occurs after surgery for angle closure glaucoma, or surgery in hyperopic eyes with narrow angles. Pars plana vitrectomy (PPV) is often considered the definitive treatment for AMS. The authors describe a rare case of AMS developing de novo after PPV in an eye without any prior history of AMS, angle closure glaucoma, or narrow angles. Methods: Interventional case report. Results: A 72-year-old woman with vitreomacular traction syndrome developed an acute rhegmatogenous retinal detachment and underwent an uneventful PPV, posterior hyaloid peel, cryopexy, and C3F8 gas insertion. Initial postoperative raised intraocular pressure (IOP) was successfully managed medically. She returned 6 days postoperatively with a highly elevated IOP refractory to medical treatments, and signs of AMS. She therefore underwent emergency C3F8 removal, phacoemulsification, posterior chamber IOL insertion, anterior vitrectomy, peripheral irido-capsulo-hyaloidectomy, and retamponade with 30% SF6. In 2 years of follow-up, there has been no recurrence of AMS and her IOP has remained normal. Conclusion: This case demonstrates that AMS can develop in vitrectomized eyes without a pre-existing history of AMS, angle closure glaucoma, or narrow angles. AMS should therefore be considered as a potential cause of raised IOP in association with a shallow anterior chamber following vitrectomy. RETINAL CASES & BRIEF REPORTS 2:73–75, 2008

From the Department of Ophthalmology, St. Thomas’ Hospital, London, United Kingdom.

pars plana vitrectomy (PPV) is usually curative and is therefore often considered the definitive treatment of AMS. Recurrence has, however, been reported.1 We describe one of only five reported cases2– 4 of AMS developing de novo after PPV in an eye without any history of AMS, angle-closure glaucoma, or narrow angles.

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queous misdirection syndrome (AMS) was first recognized in 1869 by Albert von Graefe and typically occurs after surgery for angle-closure glaucoma or surgery on hyperopic eyes with narrow angles. Approximately 50% of patients with AMS respond to topical and/or systemic medical treatments alone, and the remainder may respond to various argon or Nd:YAG laser treatments. For patients who do not respond to these conservative therapies, single

Case Report A 72-year-old woman presented with a 1-week history of floaters, photopsia, and field loss in her left eye while awaiting surgery for vitreomacular traction syndrome. She also had mild bilateral cataracts but no additional pertinent ophthalmic history. Visual acuity was counting fingers in the left eye and 20/20 in the right eye with a prescription of ⫹3.25/-0.75 ⫻ 100 for the left eye and ⫹3.50/-0.75 ⫻ 100 for the right eye. Both anterior chambers (ACs) were deep and quiet, and intraocular pressure (IOP) was 20 mmHg in the right eye and 14 mmHg in the left eye. Left fundal examination revealed a localized macular tractional detachment with

The authors have no financial support or proprietary interests to report. Reprint requests: Kamaljit S. Balaggan, BSc(Hons), MRCOphth, Division of Molecular Therapy, Institute of Ophthalmology, 11-43 Bath Street, London, United Kingdom EC1V 9EL; e-mail: [email protected]

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Fig. 1. a, Slit-lamp photograph of the left eye taken 6 days after the initial pars plana vitrectomy showing a normal sized pupil and characteristic axial shallowing of the anterior chamber secondary to anterior iris–lens diaphragm displacement. Iris bombe´ and posterior synechiae were not present. b, Ultrasound B-scan of the left eye at this time performed with the patient in an erect position demonstrated a substantially reduced axial anterior chamber depth (1.4 mm). c, Ultrasound B-scan of the unaffected eye is shown for comparison (axial anterior chamber depth, 3.2 mm).

associated cystoid macular edema, a partial posterior vitreous detachment, and an acute temporal rhegmatogenous retinal detachment not involving the macula secondary to a U-shaped tear at the 3-o’clock position. Right fundal examination revealed a posterior vitreous detachment and macular drusen. Optic disks were healthy. Axial length was 22.03 mm in the left eye (partly reduced due to macular detachment resulting from vitreomacular traction syndrome) and 22.87 mm in the right eye. She underwent uneventful PPV, posterior hyaloid peeling, cryopexy, and 16% C3F8 gas insertion. On the first postoperative day, IOP was 44 mmHg, and the AC was deep. There was an 80% gas fill, and the retina was fully attached except for minimal residual subretinal fluid inferiorly. The patient responded to treatment with topical apraclonidine, levobunolol, and latanoprost and oral acetazolamide, and 4 hours later, IOP had fallen to 22 mmHg. Medications at discharge were topical chloramphenicol and prednisolone (0.5%) in addition to the above-mentioned topical medications, and she was instructed to posture right cheek to pillow. She returned 6 days after surgery with a 2-day history of increasing left eye pain, and vision was reduced to hand movements. She denied supine posturing and reported compliance with medication. There was epithelial edema, ⫹1 cells in the AC, marked anterior displacement of the lens–iris diaphragm (Fig. 1), IOP of 50 mmHg, and a unilateral closed drainage angle (Shaffer grade 0; grades 2 to 3 in the fellow eye). The pupil was of normal size and had a completely normal light response. There was no evidence of iris bombe´ or posterior synechiae. Gas fill was 70% (less than that 1 day after surgery). Funduscopy and B-scan ultrasonography further ruled out gas overfill, choroidal hemorrhage, and effusion. IOP was refractory to face down posturing combined with further topical, oral, and parenteral hypotensive treatments. AMS was diagnosed, following which C3F8 tamponade removal, phacoemulsification, posterior chamber intraocular lens insertion, anterior vitrectomy, peripheral iridocapsulohyaloidectomy, and retamponade with 30% SF6 were urgently performed. The following day, there was 80% gas fill, the AC was deep, and IOP had fallen to 18 mmHg. All glaucoma medications were discontinued. In 2 years of follow-up, there was no recurrence of AMS; IOP remained normal, the AC was deep, angles were open, and iridocapsulohyaloidectomy was patent (Fig. 2).

Discussion Although the precise mechanisms resulting in AMS are still unclear, it is postulated that apposition of the ciliary processes to the anterior vitreous causes diversion of aqueous into the vitreous. If this is associated with an abnormally impermeable anterior hyaloid face, then such misdirection would produce an expansion in vitreous volume with consequent anterior displacement of the lens–iris diaphragm, resulting in the characteristic axially shallow AC with a relentless increase in IOP. It is this axial AC shallowing, which is considered the hallmark of AMS because it does not occur in acute angle-closure glaucoma secondary to pupil block, that was demonstrated in our case. Additional signs consistent with AMS rather than pupil block were that our patient, in keeping with the four

Fig. 2. Slit-lamp photograph of the left eye taken 2 months after the second pars plana vitrectomy showing a deep anterior chamber and patent iridocapsulohyaloidectomy.

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previously reported cases, had no history or signs of angle-closure glaucoma, narrow angles, or a shallow AC.2– 4 There was also nothing to suggest angle-closure glaucoma secondary to gas overfill or ciliochoroidal elevation due to effusion or hemorrhage. Definitive treatment of AMS appears to require an unobstructed communication between the vitreous cavity and the AC. It is probable that “standard” PPV in which the anterior hyaloid is not deliberately disrupted would have been insufficient to terminate the aqueous misdirection in our patient, as appears to be the case in classical presentations of AMS. Adequate anterior hyaloid disruption must therefore be performed in these instances in combination with iris and capsular disruption to restore uninterrupted aqueous flow into the AC. To provide the optimal conditions for permanent restoration of aqueous flow and to minimize the risk of obstruction by residual cortical, capsular, zonular, or inflammatory fibrocellular material, we fashioned a sufficiently large iridocapsulohyaloidectomy, which was placed peripheral to the posterior chamber intraocular lens. It is perhaps not surprising that the success of single PPV in terminating persistent or recurrent AMS is substantially lower for phakic eyes (25–50%) than for pseudophakic eyes (67–90%) or when simultaneous cataract extraction and posterior capsulectomy are performed (83%).1,5 In such procedures, it is often challenging to completely remove the anterior hyaloid, particularly in phakic eyes. However, in three of the four previously reported cases, the patients were either pseudophakic or aphakic at the time of developing AMS,2– 4 and one could postulate that the anterior hyaloid was not initially intentionally excised. These patients also underwent expansile intraocular gas tamponade unlike eyes receiving PPV as treatment of classical AMS. It is conceivable that the combination of these two factors contributed to the development of AMS in predisposed eyes.

It is interesting that, although our patient was hyperopic, her eyes were not short, and her ACs were documented initially to be deep and not shallow. The refractive status in three of the previously reported cases was not stated3,4; however, in at least one of the previous cases, AMS developed in a very high myope (axial length, 30.64 mm).2 Therefore, it is possible that, unlike in classical presentations of AMS, hyperopia and a short axial length may not be as important risk factors for AMS complicating PPV. In addition, in our case, there was no evidence of fibrinous or other obstructive inflammatory debris that may have precipitated or contributed to the development of AMS, as may have been the case in at least one of the previously reported cases.3 This case highlights that AMS can indeed occur in vitrectomized eyes as a complication of PPV and without a history of AMS, angle-closure glaucoma, or narrow angles. AMS should therefore be considered as a potential cause of raised IOP in association with a shallow AC after vitrectomy. Key words: aqueous misdirection syndrome, malignant glaucoma, pars plana vitrectomy, retinal detachment. References 1.

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Tsai JC, Barton KA, Miller MH, et al. Surgical results in malignant glaucoma refractory to medical or laser therapy. Eye 1997;11:677–681. Francis BA, Babel D. Malignant glaucoma (aqueous misdirection) after pars plana vitrectomy. Ophthalmology 2000;107: 1220–1222. Massicotte EC, Schuman JS. A malignant glaucoma-like syndrome following pars plana vitrectomy. Ophthalmology 1999; 106:1375–1379. Zacharia PT, Abboud EB. Recalcitrant malignant glaucoma following pars plana vitrectomy, scleral buckle, and extracapsular cataract extraction with posterior chamber intraocular lens implantation. Ophthalmic Surg Lasers 1998;29:323–327. Byrnes GA, Leen MM, Wong TP, Benson WE. Vitrectomy for ciliary block (malignant) glaucoma. Ophthalmology 1995;102: 1308–1311.

Aqueous misdirection syndrome after pars plana vitrectomy for retinal detachment.

Aqueous misdirection syndrome (AMS) typically occurs after surgery for angle closure glaucoma, or surgery in hyperopic eyes with narrow angles. Pars p...
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