Hugo Quiroz-Mercado, MD. Dolores Alvarez-Celorio, MD. Susana Martinez-Jardon, MD. Jose Luis Guerrero-Naranjo, MD. Felix Gil-Carrasco, MD. Soledad Solis ...
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Pars Plana Vitrectomy and Lamina Cribrosa Puncture in Absolute Glaucoma Hugo Quiroz-Mercado, MD Dolores Alvarez-Celorio, MD Susana Martinez-Jardon, MD Jose Luis Guerrero-Naranjo, MD Felix Gil-Carrasco, MD Soledad Solis, MD Osman Cekic, MD
Abstract. Two patients with refractory end-stage glaucoma who had no light perception underwent pars plana vitrectomy and lamina cribrosa puncture to relieve pain and decrease intraocular pressure. The patients presented with blind, painful eyes and high intraocular pressure (> 40 mm Hg). After the procedure, the pain was relieved and the intraocular pressure was lowered in both cases. The patients remained asymptomatic. Pars plana vitrectomy and lamina cribrosa puncture might be related to the decrease of intraocular pressure, probably by facilitating drainage of aqueous humor through the optic nerve. [Ophthalmic Surg Lasers Imaging 2004;35:244-246.] INTRODUCTION
Pars plana vitrectomy and lamina cribrosa puncture have been suggested for the treatment of central retinal vein occlusion.1 In our clinical trial of radial optic neurotomy and lamina cribrosa puncture for From the Asociación Para Evitar la Ceguera en México, Hospital Dr. Luis Sánchez Bulnes, México City, México. Presented at the annual meeting of the Association for Research in Vision and Ophthalmology, May 7, 2003, Fort Lauderdale, Florida. Address reprint requests to Hugo Quiroz-Mercado, MD, Asociacion Para Evitar la Ceguera en México, Hospital Dr. Luis Sanchez Bulnes, Vicente García Torres No. 46, Col. San Lucas Coyoacán, C.P. 04030 México, D.F. Delegación Coyoacán.
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central retinal vein occlusion, we noticed a decrease in IOP postoperatively.2 Pursuing this goal, we performed this procedure for a patient with refractory end-stage glaucoma who had no light perception. We report our results following pars plana vitrectomy and lamina cribrosa puncture in two patients with painful absolute glaucoma. The alternatives, potential benefits, risks, and complications of this surgical technique were explained in detail to both patients. They signed an informed consent approved by our Institutional Review Board. CASE REPORTS Case 1
A 31-year-old woman with a 2-year history of thyroid ophthalmopathy had been treated with topical steroids since her diagnosis. She presented to the glaucoma clinic of our hospital with a painful, red left eye and decreased visual acuity. At the time of presentation, she had been treated with timolol maleate twice a day and a combination of dexamethasone, neomycin, and polymixin once a day. Complete ophthalmic examination revealed no light perception in the left eye and a best-corrected visual acuity of 20/20 in the right eye. A restrictive, constant 30° exotropia was noted in the left eye. Afferent pupillary defect was present in the left eye. The IOP was 12 mm Hg in the right eye and 44 mm Hg in the left eye. Results of slit-lamp examination of the right eye were normal. The patient had deep hyperemic conjunctiva and flare in the anterior chamber of the left eye. The angle was open IV/IV 360° in both eyes with gonioscopy. On ophthalmoscopic examination, the right optic disc had a 5:10 cup-todisc ratio and the left optic disc had a 10:10 cup-todisc ratio (Fig. 1A). Because the patient’s symptoms were refractory to combined therapy (timolol maleate plus atropine), she was offered the option of undergoing lamina cribrosa puncture combined with extraocular muscle surgery for the left eye. She underwent correction of exotropia. Immediately after that, three-port
OPHTHALMIC SURGERY, LASERS & IMAGING · MAY/JUNE 2004 · VOL 35, NO 3
Figure 1. (A) Preoperative fundus photograph of case 1 showing the optic nerve appearance. (B) Postoperative fundus photograph 3 months after lamina cribrosa puncture (black arrow).
pars plana vitrectomy, posterior hyaloid membrane removal, and lamina cribrosa puncture using a fine sapphire tip (360 µm) were performed. There were no complications and she was prescribed topical atropine 1% and prednisolone. On the first postoperative day, the IOP was 14 mm Hg and pain resolved. The IOP remained low (10 to 14 mm Hg) during the first postoperative month and the patient remained asymptomatic. The IOP was 26 mm Hg after the first postoperative month and then started to increase. At 3 months of follow-up, she presented with an IOP of 37 mm Hg with a pain-free orthophoric left eye without treatment. Fundus examination and optical coherence tomography revealed the site of the lamina cribrosa puncture (Figs. 1B and 2). Case 2
A 63-year-old man with a 5-month history of type 2 diabetes mellitus presented to the retina clinic of our hospital complaining of sudden visual loss in his right eye and a red, painful eye for 9 weeks. He was treated with oral acetazolamide and timolol maleate. Complete ophthalmic examination revealed no light perception in the right eye and a best-corrected visual acuity of 20/60 in the left eye. Afferent pupillary defect was found in the right eye. The IOP was 46 mm Hg in the right eye and 11 mm Hg in the left eye. The patient had deep hyperemic conjunctiva and flare in the anterior chamber of the right eye. Rubeosis iridis was present and the angle was closed. Fundus examination revealed diffuse retinal whitening, arteriole constriction, and segmentation. Results of slit-lamp examination of the left eye were normal with diabetic retinopathy absent. Central retinal artery occlusion and secondary
Figure 2. Optical coherence tomography of case 1 showing the site of lamina cribrosa puncture.
neovascular glaucoma were diagnosed in the right eye. Because his symptoms were refractory to combined therapy (topical timolol maleate plus atropine), the patient was offered the option of undergoing conventional therapies along with lamina cribrosa puncture. Three-port pars plana vitrectomy, posterior hyaloid membrane removal, endophotocoagulation, and lamina cribrosa puncture using a fine sapphire tip (360 µm) were performed. There were no complications and the patient was prescribed topical atropine 1% and prednisolone. On the first postoperative day, the IOP was 22 mm Hg and pain resolved. The IOP was 33 mm Hg 2 weeks after the procedure, and remained at this level (32 to 33 mm Hg) for 4 months with a pain-free right eye with no medication. DISCUSSION
Cyclodestruction and retrobulbar alcohol are used for painful absolute glaucoma but have undesirable
complications. After noticing a decrease in IOP following radial optic neurotomy and lamina cribrosa puncture,2 we performed lamina cribrosa puncture in one eye with absolute glaucoma to reduce IOP and prevent discomfort. Because IOP is stronger than the cerebrospinal fluid, a pressure gradient exists in the anterior part of the optic nerve.2 Rodriguez-Peralta found that intravitreal tracers moved further posteriorly through the optic nerve in the presence of increased IOP.3 However, in glaucomatous eyes, alterations in the lamina cribrosa structure disturb the physiologic flow through it.2 Lamina cribrosa puncture might create an alternative method for drainage of aqueous humor in vitrectomized eyes. In fact, posterior flow of fluid has already been shown to occur from vitreous through the optic nerve.3 Lamina cribrosa puncture probably decreases IOP by enhancing this backflow. Moreover, some of this fluid is eliminated by the vessels in the optic nerve head.4 Hofman et al.5 showed that microvessels in the prelaminar region lack blood–brain barrier characteristics and display nonspecific permeability. According to Hayreh,4 this fluid drains into the orbit by following loose perivascular spaces in the optic nerve. On the other hand, a free diffusion between the cerebrospinal fluid in the optic nerve sheath and the optic nerve may also be assumed.4,6 It is already known that aqueous humor has a composition similar to cerebrospinal fluid. IOP decreased in the immediate postoperative period, probably by facilitating drainage of aqueous humor through the optic
nerve. We are aware that the results of these two cases do not scientifically prove our theory, but they may be helpful for further studies. In our patients, a cicatrization process probably occurred and partially obstructed this communication, which may explain the increase in IOP at the last follow-up visit. If our theory is correct, perhaps a tube placed within this puncture would maintain the desired effects for a longer period. REFERENCES
1. Lit ES, Tsilimbaris M, Gotzaridis E, D’Amico DJ. Lamina puncture: pars plana optic disc surgery for central retinal vein occlusion. Arch Ophthalmol. 2002;120:495-499. 2. Martínez-Jardón CS, Dalma-Weiszhausz J, MoralesCanton V, et al. Radial optic neurotomy for ischemic central vein occlusion. Presented at the annual meeting of the Association for Research in Vision and Ophthalmology; May 7, 2003; Fort Lauderdale, Florida. Abstract No. 4053. 3. Rodriguez-Peralta LA. Hematic and fluid barriers in the optic nerve. J Comp Neurol. 1966;126:109-121. 4. Hayreh SS. Fluids in the anterior part of the optic nerve in health and disease. Surv Ophthalmol. 1978;23:1-25. 5. Hofman P, Hoyng P, Vanderwerf F, Vrensen GF, Schlingemann RO. Lack of blood-brain barrier properties in microvessels of the prelaminar optic nerve head. Invest Ophthalmol Vis Sci. 2001;42:895-901. 6. Tso MOM, Shih CY, McLean IW. Is there a bloodbrain barrier at the optic nerve head? Arch Ophthalmol. 1975;93:815-825.
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