To report observations of horizontal corneal diameter (HCD) and central corneal thickness (CCT) changes in premature infants with stable optic disc cupping and intraocular pressures (IOPs). The HCD and CCT at term serve as a baseline for premature infants.Sixty-three premature infants were enrolled in a prospective case series. HCD, CCT, and IOP were measured. RetCam images of the optic discs were used to evaluate the cup-disc ratio (CDR) and read by an independent masked observer. Data were collected at between preterm (32–36 weeks) and again at term (37–41 weeks) postconceptual age. Left eye measurements were used for statistical analysis. Left eye findings were combined to construct predictive models for HCD and CCT.The mean HCD was 9.1 mm (standard deviation [SD] = 0.7 mm) at preterm and 10.0 mm (SD = 0.52 mm) at term. The mean CCT preterm was 618.8 (SD = 72.9) μm and at term 563.9 (SD = 50.7) μm, respectively. The average preterm CDR was 0.31 and at maturity was 0.33. Average IOP of preterm and term was 13.1 and 14.11 mm Hg, respectively. There was significant linear correlation between HCD with the postmenstrual age (r = 0.40, P < .01) and the head circumference (r = 0.33, P < .05). Predictive models were constructed for HCD (R2 = 0.52, 0.2 mm/wk) and CCT (R2 = 0.23, −11.4 μm/wk) with postconceptual ages.The HCD and CCT variation did not affect IOP reading over time. CCT was not correlated with birth parameters and decreased as the infant reached term. Corneal diameter correlated with gestational age at birth and head circumference.

BackgroundTo report the rate of cystoid macular oedema (CMO) as detected by spectral-domain optical coherence tomography (SD-OCT) after intraoperative complication during phacoemulsification. The secondary objectives include comparing mean macular thickness and best-corrected visual acuity (BCVA) between those who developed postoperative CMO against those who did not.MethodsThis is a prospective cohort study conducted in a tertiary hospital between July 2009 and June 2010. Serial SD-OCT and BCVA were performed at baseline, 1 week, 6 weeks and 16 weeks postoperatively.ResultsSingle eyes from 47 subjects were analyzed; of these 16 (34%) eyes developed CMO. In the CMO group, mean macular thickness (±SD) increased sharply by 56 μm from 273 ± 24 μm at baseline to 329 ± 31 μm at 16 weeks; whereas in the non-CMO group, macular thickness showed a slight increase of 14 μm from 259 ± 21 μm to 272 ± 20 μm. In the CMO group, mean BCVA (in logarithm of minimum angle of resolution) improved modestly from 0.92 ± 0.66 to 0.66 ± 0.41 at week 16; while in the non-CMO group, mean BCVA improved markedly from 0.98 ± 0.59 to 0.21 ± 0.13. The two groups differed significantly in mean macular thickness (p < 0.001) and mean BCVA (p < 0.001) at 16 weeks.ConclusionAs detection rate of CMO is high, postoperative OCT monitoring for patients with intraoperative complications allows earlier diagnosis and treatment.

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Leber’s hereditary optic neuropathy (LHON) is a maternally inherited mitochondrial disease caused by several point mutations in mitochondrial DNA. We present the case of a healthy 12-year-old Chinese boy who presented with bilateral, painless, subacute loss of central vision (more severe in the left eye the than right eye) for 1 week. No abnormalities were detected on magnetic resonance imaging of the brain and orbit. Serial Humphrey visual field tests initially showed a centrocaecal scotoma that worsened progressively. Cerebrospinal fluid samples and blood investigations showed normal results. A trial of steroid therapy was commenced with not much improvement in the patient’s vision. A blood sample was then sent for LHON genetic testing and a mitochondrial DNA (mtDNA) G11778A pathogenic mutation was detected. The same mutation was also present in the patient’s mother.

Tazocin showed good ocular penetration and was effective in treatment of Pseudomonas induced keratitis in rabbits.

We reported a rare case of neuroretinitis secondary to cat scratch disease, which was successfully treated with steroids and antibiotic. A healthy young lady presented with a 6-day history of central blurring of vision over her right eye (OD) after an episode of flu. Visual acuity over the OD was 6/60 with positive relative afferent pupillary defect. There were no features of anterior uveitis. Fundus of the OD showed swollen, hyperemic optic disc with disc hemorrhages and early macular star but clear vitreous, with the absence of retinochoroiditis or vasculitic changes. The serum Bartonella henselae immunoglobulins M and G were raised. Magnetic resonance imaging of the brain and orbit showed a normal result. Our impression was neuroretinitis secondary to cat scratch disease. Her OD’s vision improved to 6/9 after completing a course of doxycycline and systemic corticosteroids. Early commencement of antibiotic and corticosteroids is essential to impede potentially blinding ocular complications despite its rarity.

Objective To report a rare complication of oculomotor and trochlear nerve neuritis following botulinum toxin injection for masseter hypertrophy. Case Presentation A previously healthy 31-year-old man presented with a two-week history of left eye (OS) ptosis and diplopia, following botulinum toxin injection over the masseter area for masseter hypertrophy at an aesthetic centre. He had no proptosis or facial asymmetry. Visual acuity was 6/6 in the right eye (OD) and 6/9 in the OS. There was anisocoria, with pupils measuring 3 mm in the OD and 5 mm in the OS but no relative afferent pupillary defect. OS appeared hypertropic in primary gaze with impaired intorsion. Extraocular movement of the OS was restricted in all gazes, except for laevoversion; that of the OD was normal. This was associated with diplopia in all gazes except on laevoversion. Both eyes’ anterior and posterior segment examinations were otherwise unremarkable. Besides the oculomotor and trochlear nerve, the other cranial nerves and neurological examinations were normal. Investigations including blood and cerebrospinal fluid, magnetic resonance imaging and angiography of the brain, were normal. Our impression was left oculomotor and trochlear nerve neuritis secondary to botulinum toxin injection. He was started on oral prednisolone 1 mg/kg daily and tapered by 5 mg per week. His condition improved gradually with no residual ptosis or anisocoria after three months. Extraocular movements normalised except for minimal residual restriction on depression. Conclusion Oculomotor and trochlear nerve neuritis can occur following botulinum toxin injection over the masseter area. Healthcare professionals should be aware of this potential complication before offering the injection.