Purpose: To investigate the cytokine concentrations of aqueous humor in patients with exudative age-related macular degeneration (AMD) and diabetic macular edema (DME). Methods: Fifty-seven subjects were included in the exudative AMD, DME and control groups, each group has 19 patients. Aqueous levels of cytokines epidermal growth factor (EGF), vascular endothelial growth factor-C (VEGF-C), monocyte chemoattractant protein-1 (MCP-1), hepatocyte growth factor (HGF), interleukin (IL)-3, IL-8, IL-6, IL-12p40, intercellular adhesion molecule 1 (ICAM-1) were investigated in each groups. Kruskal-Wallis test and Mann-Whitney U test were performed to compare cytokine concentrations. Results: Aqueous levels of EGF, VEGF-C, MCP-1, HGF, IL-3, IL-8 were significantly higher in exudative AMD group than control group (p = < 0.0001, < 0.0001, 0.004, 0.015, < 0.0001, 0.014) and EGF, VEGF-C, IL-3, IL-8 were significantly higher in DME group than control group (p = < 0.0001, < 0.0001, < 0.0001, 0.005). In the comparison between the exudative AMD and DME groups, EGF was significantly higher in the exudative AMD group (p = 0.001). Conclusions Various cytokines were increased in patients with exudative AMD and DME. In particular, EGF showed a higher level in exudative AMD than in DME.

Purpose: To report a case of massive retinal hemorrhage during epiretinal membrane (ERM) peeling in a patient with iron deficiency anemia (IDA).Case summary: A 59-year-old female presented with gradually decreasing visual acuity and dysmorphopsia in the right eye for several months. She had a history of chronic IDA due to subtotal gastrectomy from gastric cancer 20 years prior. The patient was diagnosed as having macular ERM and underwent vitrectomy. During ERM peeling with intraocular forceps, we found a massive retinal hemorrhage which was presumed to have originated from the superotemporal branched retinal artery. After hemostasis, the operation was completed without critical complications. However, 2 months after surgery, the patient presented with decreased visual acuity once again. In fundus examination, diffuse macular tractional ERM was evident in the proximity of the previous intraoperative hemorrhage site. The patient underwent tractional membrane and internal limiting membrane removal surgery. The patient is currently undergoing follow-up without complications to date following the second surgery. Conclusions Our case study describes a patient having experienced massive retinal hemorrhage presumably having originated from a superotemporal branched retinal artery during ERM peeling. We speculate that the endothelial cells of retinal vessels are more vulnerable than normal in patients with severe chronic IDA.

Purpose: To report a case of massive retinal hemorrhage during epiretinal membrane (ERM) peeling in a patient with iron deficiency anemia (IDA).Case summary: A 59-year-old female presented with gradually decreasing visual acuity and dysmorphopsia in the right eye for several months. She had a history of chronic IDA due to subtotal gastrectomy from gastric cancer 20 years prior. The patient was diagnosed as having macular ERM and underwent vitrectomy. During ERM peeling with intraocular forceps, we found a massive retinal hemorrhage which was presumed to have originated from the superotemporal branched retinal artery. After hemostasis, the operation was completed without critical complications. However, 2 months after surgery, the patient presented with decreased visual acuity once again. In fundus examination, diffuse macular tractional ERM was evident in the proximity of the previous intraoperative hemorrhage site. The patient underwent tractional membrane and internal limiting membrane removal surgery. The patient is currently undergoing follow-up without complications to date following the second surgery. Conclusions Our case study describes a patient having experienced massive retinal hemorrhage presumably having originated from a superotemporal branched retinal artery during ERM peeling. We speculate that the endothelial cells of retinal vessels are more vulnerable than normal in patients with severe chronic IDA.

Purpose: To report a case of ischemic optic neuropathy caused by iron deficiency anemia (IDA) accompanied by ethambutol-induced toxic optic neuropathy.Case summary: A 64-year-old female patient presented with declining visual acuity. Four months prior, she had been taking ethambutol daily for tuberculosis. Corrected visual acuity was 0.3 in both eyes and a central visual field defect was revealed in visual field tests. In the color vision test, the right eye scored three and the left eye scored two. Ethambutol was stopped immediately under suspicion of toxic optic neuropathy; however, the corrected visual acuity gradually worsened to 0.05 in the right eye and the finger count was 50 cm in the left eye. The patient’s blood test showed signs of IDA. After 5 months of IDA treatment, the blood test results returned to the normal range and corrected visual acuity improved to 0.5 in both eyes. However, focal atrophy of the ganglion cell-inner plexiform layer was observed, requiring close monitoring of optical coherence tomography findings. Conclusions Ischemic optic neuropathy due to IDA may occur in a short period of time and may be difficult to diagnose if accompanied by ethambutol-induced toxic optic neuropathy. In the case of patients with progressive vision loss, prompt diagnosis and careful monitoring in follow-up evaluations are required.

Purpose: To investigate the effect of blunt ocular trauma (BOT) on foveal circulation, and in particular the foveal avascular zone (FAZ), using optical coherence tomography angiography (OCTA). Methods: This retrospective study consisted of 96 eyes (48 traumatized eyes and 48 nontraumatized eyes) from 48 subjects with BOT. We analyzed the FAZ area of deep capillary plexus (DCP) and superficial capillary plexus (SCP) immediately after BOT and at 2 weeks after BOT. We also evaluated the FAZ area of DCP and SCP in patients with and without blowout fracture (BOF). Results: There were no significant differences in FAZ area between traumatized and nontraumatized eyes at DCP and SCP in the initial test. In traumatized eyes, the FAZ area at SCP was significantly reduced on follow-up when compared to initial test (p = 0.01). In case of eyes with BOF, there was no significant differences in FAZ area between traumatized and nontraumatized eyes at DCP and SCP on initial test. No significant difference of FAZ area was found on follow-up relative to the initial test, whether in the DCP or SCP. In case of eyes without BOF, there was no significant differences of FAZ area between traumatized and nontraumatized eyes at DCP and SCP in initial test. Also, no significant difference of FAZ area at DCP was found on follow-up test compared to initial test. However, the FAZ area at SCP was significantly reduced in follow-up test compared with that in the initial test (p = 0.04). Conclusions Temporary microvascular ischemia occurs in the SCP of patients after BOT. Patients should be warned of transient ischemic changes that may occur after trauma. OCTA can provide useful information regarding the subacute changes in the FAZ at SCP after BOT, even without evident findings of structural damage on fundus examination.

Purpose: To report a case of ischemic optic neuropathy caused by iron deficiency anemia (IDA) accompanied by ethambutol-induced toxic optic neuropathy.Case summary: A 64-year-old female patient presented with declining visual acuity. Four months prior, she had been taking ethambutol daily for tuberculosis. Corrected visual acuity was 0.3 in both eyes and a central visual field defect was revealed in visual field tests. In the color vision test, the right eye scored three and the left eye scored two. Ethambutol was stopped immediately under suspicion of toxic optic neuropathy; however, the corrected visual acuity gradually worsened to 0.05 in the right eye and the finger count was 50 cm in the left eye. The patient’s blood test showed signs of IDA. After 5 months of IDA treatment, the blood test results returned to the normal range and corrected visual acuity improved to 0.5 in both eyes. However, focal atrophy of the ganglion cell-inner plexiform layer was observed, requiring close monitoring of optical coherence tomography findings. Conclusions Ischemic optic neuropathy due to IDA may occur in a short period of time and may be difficult to diagnose if accompanied by ethambutol-induced toxic optic neuropathy. In the case of patients with progressive vision loss, prompt diagnosis and careful monitoring in follow-up evaluations are required.