Tevfik Oğurel

Intravitreal Bevacizumab for Diabetic Papillopathy

A 43-year-old woman presented with a visual acuity of 1/10 in the right eye and 3/10 in the left eye. Ophthalmologic examination disclosed optic disc swelling on both sides with mild nonproliferative diabetic retinopathy. The pupils were equal and reactive without an afferent pupillary defect. Visual field testing showed no significant defect in both eyes. Systemic investigations revealed no abnormality. The patient was injected with bevacizumab intravitreally with the diagnosis of diabetic papillopathy (DP). Three weeks later, the vision increased to 7/10 in the right eye and optic disc edema disappeared. Intravitreal injection of bevacizumab effectively treated DP.

Short-term effect of topical brinzolamide on human central corneal thickness.

Purpose To investigate the effect of short-term brinzolamide application on human central corneal thickness (CCT). Methods Seventeen eyes of 16 patients who underwent neodymium:YAG laser posterior capsulotomy were included in the study group. Twenty-two subjects served as controls. Brinzolamide twice daily and fluorometholone four times daily were initiated after the procedure. Corneal thickness was evaluated with an ultrasound pachymetry from the central region. CCT measurements were performed before the procedure, at first day, and at the end of first week. Results The mean baseline CCT value was 535.1±37.8 μm. In comparison to the control group (546.4±22.2 μm), there was no statistically significant difference (p=0.248). After brinzolamide instillation, the mean CCT values at first day and at first week was measured as 545.1±40.1 μm and 538.8±39.4 μm, respectively. The difference at first day was statistically significant when compared to the baseline values (p=0.00017). When compared to the control group, no statistically significant difference was observed for the mean CCT values of the first day and first week (p=0.906 and p=0.484, respectively). In the fellow eyes, mean CCT values increased following the dorzolamide instillation (529.3±42.6 μm, 534±41.7 μm, and 533±41.9 μm, respectively). No statistically significant difference was observed between the control group and fellow eye group when compared (p=0.162, p=0.247, p=0.270, respectively). Conclusions Brinzolamide may cause a short-term increase in the human CCT, particularly on the first day.

Effect of intravitreal bevacizumab on retrobulbar blood flow of patients with diabetic macular edema.

Purpose To determine the effect of intravitreal bevacizumab on retrobulbar blood flow of patients with diabetic macular edema. Methods Peak systolic velocity, end-diastolic velocity, resistance, and pulsatility indices of central retinal artery (CRA), nasal posterior ciliary artery (NPCA), temporal posterior ciliary artery (TPCA), and ophthalmic artery (OA) were assessed by color Doppler ultrasonography in injected and uninjected eyes of 37 patients at baseline and at day 1 and day 7 after the injection. Results At day 1 after the injection, peak systolic and end diastolic velocities of the CRA and NPCA in the injected eyes and peak systolic velocity of NPCA in the uninjected eyes decreased significantly (p<0.05, p = 0.025, respectively). Peak systolic and end diastolic velocities were not significantly different in the injected and uninjected eyes at day 7 after the injection (p>0.05). In the injected eyes, there was no significant change in resistance and pulsatility indices (p>0.05), but a decrease in resistance index of NPCA and resistance and pulsatility indices of TPCA occurred in uninjected eyes at day 7 after the injection (p = 0.016, p = 0.023, and p = 0.025, respectively). Conclusions Intravitreal bevacizumab affects retrobulbar blood flow in injected and uninjected eyes of patients with diabetic macular edema.

An oculomotor palsy developing immediately after a spinal tap in a 6-year-old child

SIR—A 6-year-old boy was admitted to our hospital with fever, headache, and vomiting. On admission, his body temperature was 37.7 C. Blood pressure, pulse rate, and respiratory rate were all normal. Initially, he was suspected as acute bacterial meningitis and treated with i.v. antibiotics. A brain computerized tomography revealed no pathologic findings like cerebral edema. Lumbar puncture was planned to diagnose and treat central nervous system infection. The child was seen before the procedure for fundoscopy and ophthalmologic examination was found to be normal. He developed a complete oculomotor nerve palsy immediately after lumbar puncture. On examination, he had a right-sided ptosis with a dilated pupil which was unresponsive to light. The eye was deviated laterally and inferiorly. Fundus examination showed normal optic discs. Visual acuities were 10 ⁄ 10 on both sides. Color vision was in normal limits with Ishihara plates. Magnetic resonance imaging performed on the same day showed findings suggestive of meningitis. The cerebrospinal fluid tests confirmed the diagnosis of bacterial meningitis and i.v. ceftriaxone with vancomycin were started. In 3 days oculomotor nerve palsy began to resolve and improved during the following 4 weeks (Figure 1). Palsies of cranial nerves are well-recognized complications after lumbar puncture. Sixth nerve palsies are the most common. They normally occur 4–14 days after the lumbar puncture and spontaneously recover in a few weeks or months (1). The occurrence of a fourth nerve palsy following lumbar puncture is rare (2). To our knowledge, oculomotor nerve palsy of this etiology has not previously been reported. In childhood, involvement of third cranial nerve most often is congenital or results from neonatal trauma. The child did not have a history of trauma. However, he had clear signs of meningitis on admission. There are a few reports in the current literature of oculomotor palsy complicating bacterial meningitis. Ing et al. (3) have reported seven eyes with infection-related oculomotor palsy in children. Kazmi et al. (4) have demonstrated a case of bacterial meningitis presenting with ptosis. Imaging of brain and orbit did not reveal any mass lesions during the course. Oculomotor nerve palsy occurred immediately after lumbar puncture in our patient. Therefore, we propose that third nerve palsy was caused by spinal tap and associated mechanisms. A magnetic resonance imaging study has shown that lumbar puncture with overdrainage of the cerebrospinal fluid leads to intracranial hypotension with descent of the brain, thereby causing traction of the cranial nerves (5). The stretching of the nerve is thought to cause local ischemia as well as nerve dysfunction. In conclusion, cranial nerve palsies may occur as complications of lumbar puncture. Although the most frequently reported nerve palsy involving ocular motility is that of the sixth nerve, a third nerve palsy may develop in children following lumbar puncture. Kemal Örnek Tevfik Oğurel Department of Ophthalmology, School of Medicine, Kırıkkale University, Kırıkkale, Turkey (email: kemalornek@hotmail.com)

Fracture of hydrophilic acrylic intraocular lens during cataract surgery.

Kemal O¨ rnek,MD,AhmetErgin,MD,TevfikOg˘urel,MDA 23-year-old man with bilateral posterior polarcataract was admitted for cataract surgery. Clearcorneal incisions, continuous curvilinear capsulo-rhexis, hydrodelineation, and aspiration of the softlens material were performed successfully. Afterthe corneal incision was enlarged, a hydrophilicacrylic intraocular lens (IOL) (C22 diopters) wasfolded using a lens folder (Alcon) and gently pickedup with a tying forceps. However, the IOL did notmaintain the folded position between the tips ofthe forceps. A large central fracture was noticed un-der the microscope. The optic separated spontane-ously into 2 pieces (Figure 1).Intraoperative cracking of poly(methyl methacry-late) IOLs and acrylic and silicone foldable IOLshave been reported.

Effect of intravitreal bevacizumab on macular and peripapillary choroidal thickness in injected and fellow eyes of patients with diabetic macular oedema

one-sided anterior necrotizing scleritis with no known systemic rheumatological disorder. Initially, the patient complained about anterior scleral and conjunctival injection and little pain of the left eye, headache and subjectively unaltered vision of 0.7 decimal. The patient received local steroid therapy, which did not alter the disease. Two weeks later the patient presented with massive disease progression, including thinning of the sclera. Treatment was then increased to systemic steroid therapy (40 mg methylprednisolone daily, weekly reduced by 10 mg), which showed no beneficial effect. In accordance with rheumatological recommendations, therapy was escalated to anti-TNF-a (Infliximab) application. This treatment still did not change the course of disease and vision even dropped to 0.5 decimal. As scleritis worsened and necrosis increased, in April 2012 (see Fig. 1) an interdisciplinary inpatient therapy was initiated. The combination of anti-IL-6 (Tocilizumab 480 mg every month) and steroid bolus (Prednisolone 500 mg for 3 days, 250 mg for 2 days, then slowly reducing) showed to be effective. The patient was dismissed from the clinic with reduced scleritis and stopped necrosis 1 week after the anti-IL-6 treatment was started. After the sixth Tocilizumab infusion, in September 2012, the patient presented with no inflammatory signs. Steroid therapy was reduced and discontinued in February 2014. Until now, the patient has been free from any relapse of disease; the decimal visual acuity is 0.8. Within the last 6 years, 9of 10patients with anterior necrotizing scleritis at our clinic received multiple anti-inflammatory and immunosuppressive drugs, four of which did not benefit frommost of the currently available treatments. AntiTNF-a agents showed no effect in 3 of 4 cases. Anti-CD20 Rituximab did not help in 2 of 2 cases. Cyclophosphamide did not stop necrosis in 2 of 4 patients (J. Tode, unpublished). The presented single case report indicates a putative alternate therapy regime for patients with treatmentresistant anterior necrotizing scleritis. It provides evidence that anti-IL-6 therapy with Tocilizumab can be an effective drug in alleviating this rare disease. However, from this case one cannot differentiate whether Tocilizumab alone, the steroid bolus therapy or the combination of both is the driving mechanism to the cure. Not much is known about anti-IL-6 treatment in autoimmune inflammation of the eye. There are no data about Tocilizumab treatment in scleritis and only little data about Tocilizumab treatment in uveitis (Tappeiner et al. 2012). One can only assume that autoimmune scleritis is linked to processes known from autoimmune uveitis and non-articular manifestations of arthritis and that IL-6 could play an important role in this disease. The presented case report is to date the first case of anti-IL-6 treatment in anterior necrotizing scleritis. It shows the need for further research and shall put emphasis on the possibility of Tocilizumab treatment in rare autoimmune eye diseases. The potential of anti-IL-6 therapy is large, as side-effects are estimated to be little and the need for new therapeutic alternatives is unmatched.

Cystoid macular edema following selective laser trabeculoplasty in a patient with ocular hypertension

PurposePresentation of a case with ocular hypertension who developed cystoid macular edema (CME) following selective laser trabeculoplasty (SLT).Case reportA 62-year-old male patient who had undergone phacoemulsification surgery for traumatic cataract 9 years ago was on ocular hypertension treatment for the last 5 years. Due to uncontrolled intraocular pressure and side effect of medications, a 360° SLT was performed. The patient returned with decrased visual acuity 1 week after the procedure. There was CME in the treated eye. It healed completely after topical prednisolone acetate QID and nepafenac QID for 1 week, and no recurrence was observed during follow-ups.ConclusionCystoid macular edema may occur following SLT treatment in patients with previous traumatic cataract surgery which responds to topical treatment.

Endophthalmitis after tooth extraction in a patient with previous perforating eye injury

The aim of this stuty is to describe a case of endophthalmitis after tooth extraction in a patient with previous perforating eye injury. 50 years old male patient attempted to our clinic with complaints of sudden severe pain, reduced vision, light sensitivity and redness in the right eye. The patient stated that severe pain in his eye began approximately 12 hours following tooth extraction. The patients ocular examination revealed a visual acuity of hand motion in the right eye. Anterior segment examination of the right eye showed intense conjunctival hyperemia, chemosis, a fine keraticprespitat and corneal edema. Dental procedures of the patients who had recently underwent ocular surgery or trauma should be done in a more controlled manner under anti -infective therapy or should be postponed in elective procedures.

Branch Retinal Artery Occlusion following Dental Extraction.

Aim. To describe a case of branch retinal artery occlusion following dental extraction and to point out the ophthalmic complications of dental procedures to ophthalmologists and dentists. Case. A 51-year-old woman was referred to our clinic with painless sudden visual loss in her left eye after tooth extraction two days ago. In her left eye the best corrected visual acuity was 6/30 and fundus examination revealed peripapillary flame-shaped hemorrhages and pale retina in the upper temporal arcuate. The right eye examination was unremarkable. Conclusion. Dental procedures can lead to miscellaneous ophthalmic complications possibly due to the close proximity of the anatomic structures. Retinal arterial occlusion is a rare but serious cause of permanent visual loss among these dental procedures where the exact pathologic mechanism is still obscure.