Oral Carbonic Anhydrase Inhibitors Research Articles

Rheumatoid arthritis- associated corneal perforation

1) To describe the association between rheumatoid arthritis and corneal perforation. 2) To review the aetiology and management of rheumatoid arthritis -associated Peripheral ulcerative keratitis (PUK). Patient and methods: A 35-year-old female presented with a five days history of decreased vision, pain, and watering and foreign body sensation in her left eye. She is a known case of Rheumatoid arthritis, which was quiescent at the time of presentation, and for which she is taking oral prednisolone, methotrexate, and etanercept and folic acid supplements. She never had any prior consultation with an ophthalmologist. The patients' visual outcomes and the development of any significant systemic complications were recorded. Slit-lamp examination in right eye showed mild meibomian gland dysfunction, central corneal thinning of about 60%, and also inferonasal thinning. Anterior chamber was of normal depth. Pupil was round and reacting, lens clear. Left eye had inferonasal corneal perforation, less than 2mm in maximum diameter, with iris prolapsed. There was no infiltration around the perforation and no corneal edema. Seidel test was positive in left eye. Corneal vascularization was noticed at 3’clock position. Anterior chamber was shallow with inferior iridocorneal touch. Pupil was peaked inferiorly, lens being clear. Patient was admitted to ward started oral Carbonic anhydrase inhibitors, T. acetazolamide 250mg, four times per day for five days and artificial tears hourly. Perforation was sealed with cyanoacrylate glue with bandage contact lens. Patient was discharged after week. Conclusion. PUK associated with rheumatoid arthritis often has a poor visual outcome and its appearance may herald the transformation of a patient's RA into the systemic vasculitic phase. RA-associated PUK should be managed with aggressive immunosuppression if the associated morbidity and mortality are to be avoided.

Comparison of Efficacy and Complications of Cyclophotocoagulation and Second Glaucoma Drainage Device After Initial Glaucoma Drainage Device Failure

Compare intraocular pressure (IOP) control and complication rates of a second glaucoma drainage device (GDD) to diode transscleral cyclophotocoagulation (TSCPC) following failure of an initial GDD. Eyes with 1 GDD that required a second GDD or TSCPC for glaucoma control were included. Exclusion criteria were a cyclodestructive procedure before initial GDD, no light perception vision, or follow-up <1 year. Failure was defined as ≥1 of (1) reoperation for lowering IOP; (2) explantation of second GDD; (3) persistent hypotony; (4) use of oral carbonic anhydrase inhibitor for lowering IOP in the study eye; or (5) loss of light perception. Reoperation for lowering IOP included additional GDD implantation or additional cyclodestruction, except if additional cyclodestruction was within 6 months of the initial session. A total of 75 eyes (35 in second GDD; 40 in TSCPC) were included (mean follow-up, 25.5 mo). Both procedures lowered IOP [-11.4 mm Hg (±13.6) for second GDD and -7.8 mm Hg (±11.8) for TSCPC groups] and decreased the number of IOP-lowering medications at the last visit. The second GDD group had significantly greater mean survival time [45.0 mo (±4.2)] than the TSCPC group [26.5 mo (±2.8)] but significantly more postoperative complications (60% of eyes) and non-IOP-related procedures (40% of eyes) than the TSCPC group (20% for postoperative complications and 18% for non-IOP-related procedures). Although both second procedures are efficacious in lowering IOP and number of IOP-lowering medications, TSCPC failed earlier, whereas a second GDD had significantly more complications.

Efficacy of carbonic anhydrase inhibitors in management of cystoid macular edema in retinitis pigmentosa: A meta-analysis.

BackgroundCarbonic anhydrase inhibitors (CAI) are often used in the treatment of cystoid macular edema (CME) in retinitis pigmentosa (RP) patients. The aim of this meta-analysis is to gain a better understanding of the overall efficacy of CAI treatment.MethodsDatabases including PubMed, EMBASE, and Cochrane Library were searched to identify relevant studies. Eligible studies were clinical trials of patients with RP assigned topical or oral CAIs such as dorzolamide and acetazolamide. Changes in central macular thickness (CMT) by OCT in μm and best-corrected visual acuity (BCVA) in log MAR equivalents were extracted and results compared between baseline and after treatment.Results11 clinical reports were identified which included a total of 194 patients (358 eyes) available for analysis, with 59 patients (115 eyes) assigned oral CAI treatment and 135 patients (243 eyes) assigned topical CAI treatment. The combined results showed a significant reduction of macular edema, as calculated by baseline and final central macular thickness (CMT) based on OCT examination (46.02μm, 95%CI: -60.96, -31.08, I2 = 65%). However, the effect on visual acuity was inconsistent across studies.ConclusionBased on non randomized controlled clinical studies, RP patients with CME who were treated with CAIs had better anatomical outcomes, but the effect on visual acuity was contradictory across studies. Multicenter prospective randomized controlled trials would be ideal to definitively test its clinical efficacy in RP patients.

Fulminant Idiopathic Intracranial Hypertension and Venous Stasis Retinopathy Resulting in Severe Bilateral Visual Impairment

To report a complicated case of fulminant idiopathic intracranial hypertension and concomitant venous stasis retinopathy leading to postpapilledema optic atrophy. Case report. A 34-year-old morbidly obese woman with a history of idiopathic intracranial hypertension (IIH) presented with a 1-month history of bilateral vision loss, diplopia, and left eye pain after being lost to follow-up for 6 years. Fundus examination revealed florid papilledema with venous tortuosity bilaterally. Brain and orbit magnetic resonance imaging showed bilateral globe flattening, intraocular optic nerve swelling in both eyes, and no abnormality on magnetic resonance venography. After additional workup including lumbar puncture with an opening pressure of 55 cm H2O, a diagnosis of IIH was confirmed. Medical treatment with oral carbonic anhydrase inhibitors was initiated, followed by same-day bilateral optic nerve sheath decompression and ventriculoperitoneal shunt placement the following week. Fundus examination 2 months later revealed a persistent blood and thunder fundus suggestive of bilateral central retinal vein occlusions. Over the course of 6 months, both eyes displayed postpapilledema optic atrophy with light perception and hand motion vision in the right and left eyes, respectively. On Goldmann perimetry, the patient had vague limited isolated responses in both eyes to the largest target. Fulminant IIH can present with profoundly blinding complications recalcitrant to aggressive medical and surgical intervention. Central retinal vein occlusion is an uncommon blinding complication of IIH.

Postsurgical Cystoid Macular Edema.

Cystoid macular edema (CME) is a primary cause of reduced vision following both cataract and successful vitreoretinal surgery. The incidence of clinical CME following modern cataract surgery is 0.1-2.35%. Preexisting conditions such as diabetes mellitus and uveitis as well as intraoperative complications can raise the risk of postsurgical CME. The etiology of CME is not completely understood. Prolapsed or incarcerated vitreous and postoperative inflammatory processes have been proposed as causative agents. Pseudophakic CME is characterized by poor postoperative visual acuity. Fluorescein angiography shows the classical perifoveal petaloid staining pattern and late leakage of the optic disk. Optical coherence tomography is a useful diagnostic tool, which displays cystic spaces in the outer nuclear layer. The most important differential diagnoses include age-related macular degeneration and other causes of CME such as diabetic macular edema. Most cases of pseudophakic CME resolve spontaneously. The value of prophylactic treatment is doubtful. First-line treatment of postsurgical CME should include topical nonsteroidal anti-inflammatory drugs and corticosteroids. Oral carbonic anhydrase inhibitors can be considered complementary. In cases of resistant CME, periocular or intraocular corticosteroids present an option. Antiangiogenic agents, though experimental, should be considered for nonresponsive persistent CME. Surgical options should be reserved for special indications.

Association between topiramate use and serum bicarbonate levels in a veteran population.

Topiramate has been associated with metabolic acidosis secondary to decreased serum bicarbonate. Product labeling recommends serum bicarbonate monitoring at baseline and periodically thereafter. The study objective was to assess changes in serum bicarbonate within the first year of topiramate use in an outpatient veteran population. This was a single-center, retrospective study conducted at the Iowa City Veterans Affairs Health Care System. Inclusion criteria required a minimum of 1 topiramate outpatient prescription between October 1, 1999, and August 31, 2012, and at least 1 serum bicarbonate level within 12 months prior to topiramate initiation. Patients with topiramate nonadherence, concurrent use of sodium bicarbonate or oral carbonic anhydrase inhibitors, and individual serum bicarbonate values obtained during inpatient hospitalizations were excluded. Change in bicarbonate was evaluated using a paired t test. Decreases in bicarbonate of ≥5 mEq/L, values <20 mEq/L, days to lowest value, and correlation between adverse drug reactions (ADRs) and topiramate discontinuation were evaluated. Of 546 patients reviewed, 350 were included in the analysis. There was a statistically significant decrease of 2.7 mEq/L in bicarbonate following initiation of topiramate. Only 1 patient had a bicarbonate value <17 mEq/L. There was no association between bicarbonate decrease ≥5 mEq/L and ADRs. A statistically significant reduction in bicarbonate levels occurred with topiramate, which was clinically insignificant. ADR occurrence did not correlate with bicarbonate levels <17 mEq/L or a decrease ≥5 mEq/L. Our results indicate that serum bicarbonate levels should only be monitored before topiramate initiation and in patients presenting with symptoms suggestive of acidosis.

DECREASED MACULAR THICKNESS IN NONPROLIFERATIVE MACULAR TELANGIECTASIA TYPE 2 WITH ORAL CARBONIC ANHYDRASE INHIBITORS

To evaluate whether carbonic anhydrase inhibitors reduce the macular thickness and/or cystic spaces in patients with macular telangiectasia (MacTel) Type 2. Retrospective review of patients with nonproliferative cystoid changes associated with MacTel seen at the University of Iowa between 2009 and 2012. Carbonic anhydrase inhibitors were used in 8 patients with MacTel Type 2. Five patients with MacTel Type 2 were observed during this period. Initial and final visual acuities were documented. The presence of cystic spaces and the retinal thickness were measured with spectral-domain optical coherence tomography. Patients treated with oral carbonic anhydrase inhibitors showed significant reduction in both the cystoid cavities and central macular thickness when compared with the patients who were observed (-12.2 μm; P = 0.020). The reduction in retinal thickness was more pronounced in patients receiving acetazolamide (-20.13 μm; P = 0.007) compared with methazolamide (-6.25 μm; P = 0.177). There was no significant change in visual acuity in patients receiving carbonic anhydrase inhibitors. Five patients with MacTel Type 2 did not receive treatment and demonstrated no change in visual acuity, cystoid cavities, or central macular thickness. Oral carbonic anhydrase inhibitors, particularly acetazolamide, may decrease macular cystic cavities and reduce central macular thickness but does not appear to improve visual acuity. These findings have yet to be confirmed with a prospective treatment trial.

Toxic Epidermal Necrolysis in a Patient with HLA-B*5901 Haplotype Caused by Topical and Oral Carbonic Anhydrase Inhibitors.

Dear Editor: Toxic epidermal necrolysis (TEN) and Stevens-Johnson syndrome (SJS) are severe life-threatening mucocutaneous diseases that involve different extents of epidermal detachment and severity1. Carbonic anhydrase inhibitors (CAIs) are used to decrease intraocular pressure (IOP) in glaucoma2 and may rarely induce TEN/SJS. Moreover, strong genetic associations between human leukocyte antigen (HLA)-B*5901HLA alleles and methazolamide-induced TEN/SJS have been discovered in Koreans3. Herein, we report a case of TEN in a Korean woman with HLA-B* 5901 haplotype, who had taken methazolamide for 1 day and instilled brinzolamide for 10 days. An otherwise healthy 33-year-old Korean woman presented with pruritic, multiple, coalescent, erythematous patches with vesicles on the face and trunk involving erosive oral mucosa (Fig. 1A). Twenty days prior, she visited an ophthalmic clinic complaining of blurred vision after taking phendimetrazine, an anorectic agent, for 2 days. Her IOP was elevated and was treated with methazolamide, brinzolamide 1%/timolol 0.5%, brimonidine 0.15%, and prednisolone 1% eye drops for 1 day. Nevertheless, her IOP remained elevated, and both eyes were treated with argon laser iridotomy. Brinzolamide 1%/timolol 0.5% and brimonidine 0.15% eye drops were administrated for an additional 9 days. Two days after stopping the eye drops, she noted pruritic erythematous macules on the face. Her cutaneous lesions were aggravated and expanded distally with conjunctival and oral mucosal involvements over several days. She had no history of drug allergies, including sulfonamide antibiotics. Personal and family histories were unremarkable. Routine laboratory test results were normal. HLA typing showed B*5901 and B*5204. She was initially treated with dexamethasone 10 mg daily for 2 days, but epidermal necrolysis worsened and became confluent (Fig. 1B, C). Intravenous immunoglobulin (3.5 g/day) was infused for 4 days. Her skin lesions gradually improved within 3 weeks. Fig. 1 (A) Coalescent erythematous macules, papules, and patches with vesicles on the face. (B) Widespread sheet-like epidermolytic detachment on the dorsum. (C) Histopathologic findings show subepidermal bullae, diffuse epidermal necrosis, and mild upper dermal ... In the present case, topical timolol and brimonidine were administrated for 10 days. However, there has been no report of timolol- or brimonidine-associated TEN/SJS. Moreover, neither timolol nor brimonidine appears to cause TEN/SJS, because the relative risk of timolol or brimonidine for TEN/SJS is much lower than that of CAIs. Therefore, CAIs appear to have induced TEN in this patient. Twelve days before the first cutaneous manifestations, she took methazolamide for 1 day while simultaneously instilling brinzolamide for 10 days. Therefore, it is reasonable to postulate that 2 types of CAIs contributed to the induction of TEN in this patient, because either topical or oral CAIs can induce TEN/SJS4. The first methazolamide administrated appears to have played a role in initial phase of sensitization, whereas continual brinzolamide administration appears to have played crucial roles in maturation and/or the initial phase. TEN/SJS encompass idiopathic hypersensitivity reactions to specific drugs and usually occur in people with a genetic predisposition1. A strong and unique genetic association between HLA alleles and drug-induced TEN/SJS has been discovered. In Koreans, HLA-B*5901 is strongly associated with methazolamide-induced TEN/SJS3. The gene frequency of HLA-B*5901 allele in the Korean population is reported to be 2.06%5 and HLA-B*5901 allele was detected in this patient. In summary, both topical and oral CAIs should be administrated cautiously in Koreans.

Cystoid macular edema in a patient with Danon disease

To report a patient with Danon retinopathy with cystoid macular edema treated with topical dorzolamide 2% eye drops and oral acetazolamide. A 37-year-old Caucasian man with Danon disease treated with topical and oral carbonic anhydrase inhibitors participated in the study. Examinations performed before and during treatment included visual acuity (VA), spectral-domain optical coherence tomography, and electroretinography. Following total 48 weeks of treatment, VA decreased from 20/30 OD, 20/200 OS, to 20/40 OD, CF OS. The mean central retinal thickness was unchanged from baseline 263 μm OD, 226 μm OS, after treatment 283 μm OD and 202 μm OS. In our case, carbonic anydrase inhibitors were not effective. However, a general recommendation cannot be given based on a single case.

Glaucoma management: relative value and place in therapy of available drug treatments

Lowering intraocular pressure (IOP) is the only proven therapeutic intervention for glaucomatous optic neuropathy. Despite advances in laser and microsurgical techniques, medical IOP reduction remains the first-line treatment option for the majority of patients with open-angle glaucoma. Prostaglandin analogs are the most efficacious topical agents and carry a remarkable safety profile. Topical beta-blockers, alpha-agonists, and carbonic anhydrase inhibitors are often employed as adjunctive agents for further IOP control. Newer preserved and nonpreserved formulations are available and appear to be less toxic to the ocular surface. Oral carbonic anhydrase inhibitors, miotic agents, and hyperosmotics are infrequently used due to a host of potentially serious adverse events. Medical therapies on the horizon include rho-kinase inhibitors, neuroprotective interventions, and gene therapies.

Hemorrhagic choroidal detachment after use of anti-glaucomatous eye drops: case report

Eighty-two-year-old patient with a pacemaker using warfarin due to arrhythmia and having an intraocular lens in the right eye, developed spontaneous hemorrhagic choroidal detachment one day after the use of combined preparation of 0.5% timolol maleate and 0.004% travoprost, due to primary open-angle glaucoma. Hemorrhagic detachment was detected by anterior and posterior segment examination, as well as B-scan ultrasonography. After the detachment, excessive increased intraocular pressure was controlled with oral carbonic anhydrase inhibitor, cycloplegic and steroid therapy. After four months, visual acuity was 20/20 and the intraocular pressure was under control with 0.5% timolol maleate and 1% brinzolamide. Controlled reduction of the intraocular pressure should be considered, particularly in older patients under anticoagulant therapy and that had undergone prior ocular surgery.

Topical steroidal and nonsteroidal antiinflammatory drugs for the treatment of cystoid macular edema in retinitis pigmentosa.

Oral carbonic anhydrase inhibitors have been the treatment of choice for managing cystoid macular edema (CMO) in retinitis pigmentosa. We report a case illustrating the effectiveness of topical steroidal and nonsteroidal antiinflammatory drugs (NSAIDs) in managing CMO in a patient with retinitis pigmentosa, who is unable to take oral carbonic anhydrase inhibitor because of chronic renal impairment. An 85-year-old woman with retinitis pigmentosa-related CMO in the left eye was prospectively followed up after treatment with a 4 times daily regimen consisting of a topical steroid (prednisolone acetate 1%) and an NSAID (ketorolac trometamol 0.5%). The right eye showed no evidence of CMO. Oral acetazolamide was avoided as the patient had chronic renal impairment. Three months after treatment, best-corrected visual acuity in the left eye improved from 20/200 to 20/60, and spectral domain optical coherence tomography showed complete resolution of CMO. Topical steroid and NSAID were therefore stopped. However, 6 months later, left best-corrected visual acuity was reduced to 20/120 and spectral domain optical coherence tomography showed recurrence of CMO. This was managed with the same treatment regimen of topical steroid and NSAID, which resulted in complete resolution of CMO with best-corrected visual acuity in the left eye improving to 20/80 after 3 months. To our knowledge, this is the first report that demonstrates the effectiveness of topical steroids or NSAIDs in managing CMO in a retinitis pigmentosa patient with chronic renal impairment who is unable to take a carbonic anhydrase inhibitor because of chronic renal impairment.

Argon laser peripheral iridoplasty versus systemic intraocular pressure-lowering medications as immediate management for acute phacomorphic angle closure.

BackgroundThe purpose of this study was to compare the efficacy and safety of argon laser peripheral iridoplasty (ALPI) and systemic intraocular pressure (IOP)-lowering medications in the immediate management of acute phacomorphic angle closure.MethodsConsecutive cases of acute phacomorphic angle closure were randomized to receive ALPI and an intravenous or oral carbonic anhydrase inhibitor as initial treatment. Intravenous mannitol was administered for presenting IOP > 60 mmHg or IOP > 40 mmHg 2 hours posttreatment in both arms.ResultsOf 10 consecutive cases, six received medical therapy and four received ALPI. Fifty percent in the medical group and none in the ALPI group required intravenous mannitol. The ALPI group took less time to achieve IOP < 25 mmHg (18.8 ± 7.5 minutes versus 115.0 ± 97.0 minutes, P = 0.001, F test); had a greater IOP reduction within 30 minutes (69.8% ± 7.7% versus 40.9 ± 23.9%, P = 0.03, t-test); and had a consistently smaller post-attack cup to disc ratio (0.50 ± 0.02 versus 0.60 ± 0.20, P = 0.002, F test).ConclusionALPI offers greater safety, consistency, and efficacy than systemic IOP-lowering medications as initial treatment for phacomorphic angle closure.

London 2012: prescribing for athletes in ophthalmology

Prescribing for athletes requires an up-to-date knowledge of the World Anti-Doping Agency's list of prohibited substances. As the London 2012 Olympic Games attract athletes from around the world, we review the current guidelines with respect to all medications licensed for ophthalmic use in the United Kingdom. We describe the process that an ophthalmologist can use to check for permissible medications and also highlight treatments that are contraindicated. We systematically reviewed all 77 drugs listed in Section 11 of the British National Formulary (Issue 63) for use in the treatment of ophthalmic conditions, and referenced these against the 2012 Prohibited List published by the World Anti-Doping Agency. The majority of ophthalmic preparations are suitable for use in- and out-of-competition. Some preparations, such as glucocorticoids, are prohibited when administered systemically but permitted for topical administration. Beta-blockers are prohibited in-competition and oral carbonic anhydrase inhibitors are prohibited in- and out-of competition. The 2012 Prohibited List has important implications for the pharmacological treatment of ophthalmic conditions in athletes. Clinicians prescribing for athletes have a duty to familiarize themselves with the list in order to avoid causing significant damage to their patient's career and reputation.

Endoscopic Cyclophotocoagulation (ECP) in the Management of Uncontrolled Glaucoma With Prior Aqueous Tube Shunt

To evaluate the efficacy and safety of endoscopic cyclophotocoagulation (ECP) in the treatment of uncontrolled glaucoma with a prior aqueous tube shunt. A prospective, nonrandomized, interventional clinical trial with up to 2 years of follow up included 25 eyes of 25 consecutive glaucoma patients with a previous tube shunt and uncontrolled intraocular pressure (IOP) despite medical therapy. Patients had IOP greater than 21 mm Hg on maximal medications or IOP ≤21 mm Hg but intolerant to medications or using an oral carbonic anhydrase inhibitor. Application of ECP over 360 degrees was performed and subjects were followed for 6 months minimum. Main outcome measures were mean reduction in IOP and medications at 12 months. Success was defined as reduction in IOP of 3 mm Hg and discontinuation of nontolerated glaucoma medications. A failure was defined as continued uncontrolled IOP, vision loss to no light perception, or additional medications or glaucoma surgery required. At 12 months, the mean IOP dropped from 24.02 to 15.36 mm Hg. The mean of the differences was -7.77 mm Hg (-30.8%). The mean number of medications was 3.2 before laser and 1.5 at 12 months (P<0.001). The success rate at 12 months (n=18) was 88% and remained at that level until the end of the follow-up period of 2 years (n=11, P<0.00005). There were no serious complications. ECP seems to be a safe and effective treatment in patients with uncontrolled IOP with a prior aqueous tube shunt, and is a reasonable option in this group of refractory glaucoma patients.

Postsurgical Cystoid Macular Edema

Cystoid macular edema (CME) is a primary cause of postoperative reduced vision. It may occur even when the intraoperative course is successful for operations such as cataract and vitreoretinal surgery. Its incidence following modern cataract surgery is 0.1%-2.35%. This risk is increased if there are certain preexisting systemic or ocular conditions and when there are intraoperative complications. The etiology of CME is not completely understood. Prolapsed or incarcerated vitreous and postoperative inflammatory processes have been proposed as causative agents. Pseudophakic CME is characterized by poor postoperative visual acuity. Fluorescein angiography is indispensable in the workup of CME, showing the classical perifoveal petaloid staining pattern and late leakage of the optic disk. Optical coherence tomography is a useful diagnostic tool, which displays cystic spaces in the outer nuclear layer. The most important differential diagnoses include age-related macular degeneration and other causes of CME such as diabetic macular edema. Most cases of pseudophakic CME resolve spontaneously. The value of prophylactic treatment is doubtful. First-line treatment of postsurgical CME should include topical nonsteroidal anti-inflammatory drugs and corticosteroids. Oral carbonic anhydrase inhibitors can be considered complementary. In cases of resistant CME, periocular or intraocular corticosteroids present an option. Antiangiogenic agents, though experimental, should be considered for nonresponsive persistent CME. Surgical options should be reserved for special indications.

Promising complexes of acetazolamide for topical ocular administration

Importance of the field: Acetazolamide (ACZ), a carbonic anhydrase inhibitor (CAI), and other oral CAIs have been an integral part of antiglaucoma therapy for > 40 years. ACZ is used orally for the reduction of intraocular pressure in patients suffering from glaucoma. However, this treatment leads to unpleasant systemic side effects. The answer to the undesirable effects of ACZ is the topical delivery of this drug into the eye, where it could elicit its physiological action. However, the development of a topical formulation of ACZ is limited by its poor ocular bioavailability, which can be largely attributed to its poor penetration coefficient and poor biphasic solubility.Areas covered in this review: This review offers an overview of different approaches to delivering ACZ to the eye, highlighting the potential of the ternary system ACZ:HP-β-CD:TEA as a tool for formulating aqueous ACZ eye drop solutions.What the reader will gain: A critical analysis is provided to highlight the key issues to design formulations containing hydrophilic cyclodextrins.Take home message: The ACZ:HP-β-CD:TEA complex is an important new approach to improve the ocular bioavailability of this drug. This approach may be applied to other CAIs in the future.

Management of Neovascular Glaucoma

Management of NVG remains a therapeutic challenge. The diagnosis of NVG should be made as early as possible if the patient is to be provided the best chance to maintain vision. To achieve this goal, a high index of suspicion, a full ocular examination including undilated gonioscopy, and pupil examination are essential. There are two key aspects to the management of NVG: treatment of the underlying disease process responsible for rubeosis and treatment of the increased IOP. Treatment of rubeosis is directed at the ischemic retina in most cases. Panretinal photocoagulation (PRP) is considered the treatment of choice. However, other modalities such as panretinal cryotherapy, transscleral diode laser retinopexy, and panretinal diathermy have been described. Medical management of NVG consists of IOP-lowering agents, including topical �adrenergic antagonists, alpha-2 agonists, and topical and oral carbonic anhydrase inhibitors. However, once the angle is synechially closed, medical management becomes unsuccessful and one has to resort to surgical management. Although the ideal surgical procedure has yet to be determined, trabeculectomy with antimetabolite therapy, aqueous shunt implants, and diode laser cyclophotocoagulation are the best current surgical options. Studies have shown VEGF as a key molecule in ocular angiogenesis and direct targeting of VEGF might be another possible therapeutic strategy to treat neovascularization.

Oral versus topical carbonic anhydrase inhibitors in ocular hypertension after scleral tunnel cataract surgery

To compare the effect of oral acetazolamide and topical 2% dorzolamide in prevention of ocular hypertension after scleral tunnel cataract surgery. Ophthalmic department, Sana'a University, Yemen Sana'a from March 2007 to October 2007. This prospective double-blind, randomized study included 150 eyes undergoing scleral tunnel cataract surgery with hard posterior chamber intraocular implantation. Methylcellulose was used as the viscoelastic in all surgery cases. Patients were assigned to one of three groups: group 1: topical gentamicin eye drops (control; n = 52); group 2: systemic acetazolamide 250 mg (n = 45); and group 3: topical 2% dorzolamide (n = 53). Acetazolamide patients received one 250 mg tablet, one hour before surgery, then half a tablet every eight hours. A topical dorzolamide 2% or gentamicin was applied in one drop one hour before surgery then every eight hours, for three days postoperatively. Intraocular pressures (IOP) were measured by Goldman applanation tonometry one hour preoperatively and 16, 24, and 48 hours postoperatively. At 16 hours, IOP between the three groups increased significantly with a statistically significant p-value of 0.008, but the mean IOP of acetazolamide patients was less than other groups. IOP nearly returned to the normal level 24 and 48 hours postoperatively, but this was not statistically significant (p = 0.452 and 0.138, respectively). Acetazolamide offers better IOP control than topical dorzolamide 2% in preventing ocular hypertension after scleral tunnel cataract surgery.

Treatment of Adult-Onset Acute Macular Retinoschisis in Enhanced S-cone Syndrome With Oral Acetazolamide

To report on the efficacy of the oral carbonic anhydrase inhibitor (CAI) acetazolamide in treating macular retinoschisis (RS) in the rare vitreoretinal dystrophy best known as the enhanced S-cone syndrome (ESCS). Interventional case report. setting: University-based practice. patient: A 48-year old Jewish Italian male with clinically, functionally, and molecularly confirmed ESCS, attributable to homozygosity for the R311Q mutation in the NR2E3 gene, presented with sudden visual acuity (VA) loss (20/200) and metamorphopsia in the left eye resulting from acute, late-onset, asymmetric macular RS. intervention: Open-label, off-label treatment with the oral CAI acetazolamide. main outcome measure(s): Best-corrected VA, retinal thickness, and retinal microanatomy, assessed by Stratus optical coherence tomography (OCT) criteria. Following treatment, instituted one month after the acute-onset VA loss, retinal thickness and microanatomic profile normalized in the affected eye, with restoration of 20/20 corrected VA. The fellow eye, which had remained asymptomatic at 20/16 vision, had experienced mild paracentral macular RS evident by OCT criteria, which also resolved completely following oral CAI treatment. The outcome was maintained throughout the follow-up period at a low maintenance dose. Taken together with other recent reported benefits of topical and oral CAIs in the treatment of macular RS in X-linked retinoschisis, this interventional case report shows that CAIs can be used to treat effectively macular RS in general, and also specifically in ESCS.