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Biomedical subjects

Susumu Ishida

Publications and source records attributed to Susumu Ishida.

At least 19 recordsLinked to original sources
PubMed2007

Detecting vitreomacular adhesions in eyes with asteroid hyalosis with triamcinolone acetonide.

BACKGROUND: To report the incidence of posterior vitreous detachments (PVDs) and the surgical results of vitrectomy with intravitreal triamcinolone acetonide (TA) to detect vitreomacular adhesions in eyes with asteroid hyalosis (AH). METHODS: Ten eyes of nine patients with AH underwent vitrectomy, six eyes with TA and four without TA. The presence of a PVD was determined preoperatively by ultrasound echography (USE) and intraoperatively by microscopic observations. The postoperative best-corrected visual acuities (BCVA) were evaluated. RESULTS: The BCVA was improved by >2 Snellen lines in nine eyes and maintained at 20/20 with symptomatic improvements in the other eye. A vitreomacular adhesion was clearly seen during TA-assisted vitrectomy, and none was seen when TA was not used, even though preoperative USE showed an incomplete PVD in all eyes. The BCVA was not significantly better in eyes with TA-assisted vitrectomy than without TA-assisted vitrectomy. In one eye with vitrectomy without TA, a second surgery was required for a persistent cystoid macular edema and an epiretinal membrane. The BCVA and the edema in this eye improved after removing the epiretinal membrane. CONCLUSIONS: All (ten) of the eyes with AH were found to have a vitreomacular adhesion by preoperative USE and intraoperative microscopic observations. The residual vitreous over the macula is more easily detected and removed after intravitreally injected TA, but the visual acuities were not significantly different from eyes without TA.

Aged↗
PubMed2007

Role of nonproteolytically activated prorenin in pathologic, but not physiologic, retinal neovascularization.

PURPOSE: Recently, it was revealed that the inhibition of nonproteolytic activation of prorenin led to significant suppression of ocular inflammation in endotoxin-induced uveitis. The purpose of the present study was to investigate whether nonproteolytically activated prorenin plays a role in ischemia-induced retinal neovascularization. METHODS: C57BL/6 neonatal mice were reared in an 80% concentration of oxygen from postnatal (P) day 7 to P12, followed by room-air breathing to P17 to induce ischemia-initiated retinal neovascularization. Tissue localization of activated prorenin and prorenin receptor was examined by immunohistochemistry. Animals received intraperitoneal injections of handle-region peptide (HRP), a decoy peptide corresponding to the handle region of prorenin, which inhibits prorenin receptor-mediated upregulation of the renin-angiotensin system (RAS). A concanavalin A lectin perfusion-labeling technique was used to evaluate the areas of physiologic and pathologic retinal new vessels and the number of leukocytes adhering to the vasculature. Retinal mRNA expression and protein levels of intercellular adhesion molecule (ICAM)-1, vascular endothelial growth factor (VEGF), VEGF receptor (VEGFR)-1, and VEGFR-2 were examined by RT-PCR and ELISA. RESULTS: Retinal vessels in ischemic retinopathy eyes were positive for activated prorenin and prorenin receptor. Pathologic, but not physiologic, retinal neovascularization was significantly attenuated in HRP-treated mice compared with vehicle- or control peptide-treated animals. The number of adherent leukocytes was also significantly reduced. Retinal mRNA expression and protein levels of ICAM-1, VEGF, VEGFR-1, and VEGFR-2 in ischemic retinopathy were also significantly suppressed by the application of HRP. CONCLUSIONS: The present findings suggest that nonproteolytic activation of prorenin selectively promotes pathologic, but not physiologic, retinal neovascularization through the inflammatory processes related to pathologic neovascularization.

Animals↗
PubMed2006

SOCS3 is required to temporally fine-tune photoreceptor cell differentiation.

Suppressor of cytokine signaling 3 (SOCS3) is an intracellular, ligand-induced negative feedback modulator of STAT3 activation that acts during inflammation. Here, we demonstrate that SOCS3 expression is important for normal retinal development in the perinatal period. STAT3 is highly activated in the late-embryonic retina, then downregulated at postnatal day 0 (P0), presumably by the depletion of upstream ligands. We found that SOCS3 was required after P0 to shut down the residual STAT3 activation; this loss of activated STAT3 leads to Rhodopsin expression and rod photoreceptor cell differentiation. SOCS3 deficiency failed to terminate STAT3 activation, thereby delaying expression of Rhodopsin and its upstream transcription factor, crx. Development subsequently continued, but its course was temporally erratic, probably because of faulty compensation. Interestingly, SOCS3 protein expression was first detected postnatally, after STAT3 activation was mostly downregulated. It initially appeared in some of the presumptive photoreceptor cells and gradually spread. SOCS3 mRNA level was constant from the late-embryonic to early-postnatal period. Post-transcriptional inhibition of SOCS3 protein expression maintains a high STAT3 activation during late embryogenesis, and after P0, releasing from the inhibition promptly terminates STAT3 activation. Thus, SOCS3 can act as a temporal fine-tuner of STAT3 activation during photoreceptor cell differentiation.

Animals↗
PubMed2006

Angiotensin II type 1 receptor-mediated inflammation is required for choroidal neovascularization.

BACKGROUND: Choroidal neovascularization (CNV) is a critical pathogenesis in age-related macular degeneration, the most common cause of blindness in the developed countries. The aim of the current study was to determine the involvement of the renin-angiotensin system (RAS) with the development of CNV, using human surgical samples and the murine model of laser-induced CNV. METHODS AND RESULTS: In the human and murine CNV tissues, the vascular endothelium expressed angiotensin II type 1 receptor (AT1-R), AT2-R, and angiotensin II. The CNV volume was significantly suppressed by treatment with an AT1-R blocker telmisartan, but not with an AT2-R blocker. AT1-R signaling blockade with telmisartan inhibited various inflammatory mechanisms including macrophage infiltration and upregulation of VEGF, intercellular adhesion molecule-1 (ICAM-1), MCP-1, and IL-6 in the retinal pigment epithelium-choroid complex. A PPAR-gamma antagonist partially but significantly reversed the suppressive effect of telmisartan on in vivo induction of CNV and in vitro upregulation of ICAM-1 and MCP-1 in endothelial cells and IL-6 in macrophages, showing the dual contribution of PPAR-gamma-agonistic and AT1-R-antagonistic actions in the telmisartan treatment. CONCLUSIONS: AT1-R-mediated inflammation plays a pivotal role in the development of CNV, indicating the possibility of AT1-R blockade as a novel therapeutic strategy to inhibit CNV.

Angiogenesis Inducing Agents↗
PubMed2006

Suppression of ocular inflammation in endotoxin-induced uveitis by inhibiting nonproteolytic activation of prorenin.

PURPOSE: A recent study revealed that angiotensin receptor signaling mediates ocular inflammation and neovascularization. It was also found that prorenin undergoes nonproteolytic activation leading to upregulation of the renin-angiotensin system (RAS) when prorenin receptor interacts specifically with the handle region of prorenin. The purpose of the present study was to elucidate the role of the receptor-dependent nonproteolytic activation of prorenin in ocular inflammation in endotoxin-induced uveitis (EIU). METHODS: EIU was induced in Long-Evans rats by a single intraperitoneal injection of 100 microg lipopolysaccharide (LPS). Tissue localization of total prorenin, prorenin receptor, and activated prorenin in the EIU retina was examined by immunohistochemistry. To inhibit the prorenin receptor-mediated upregulation of the RAS, a decoy handle-region peptide (HRP) was intraperitoneally administered 24 hours before and immediately after the injection of LPS. Twenty-four hours after LPS injection, leukocyte adhesion to the retinal vasculature was evaluated with a concanavalin A lectin perfusion-labeling technique. In addition, leukocyte infiltration into the vitreous cavity and protein concentration in the anterior chamber were also measured. Retinal mRNA and protein levels of intercellular adhesion molecule (ICAM)-1, interleukin (IL)-6, and C-C chemokine ligand (CCL) 2/monocyte chemotactic protein (MCP)-1 were examined by RT-PCR and ELISA. RESULTS: Retinal vessels in rats with EIU were strongly positive for total prorenin, prorenin receptor, and activated prorenin. Systemic treatment with HRP resulted in dose- and time-dependent inhibition of the leukocyte adhesion and infiltration and the protein leakage, all of which were increased by the induction of EIU. Retinal mRNA expression and protein levels of ICAM-1, CCL2/MCP-1 and IL-6, induced in rats with EIU, were also significantly suppressed with application of HRP. CONCLUSIONS: These findings demonstrate for the first time that nonproteolytically activated prorenin plays a significant role in the development of ocular inflammation in the EIU model. The present study suggests the potential use of HRP, a decoy peptide binding to the prorenin receptor, as a therapeutic agent to reduce ocular inflammation.

Animals↗
PubMed2006

Neuroprotective effects of angiotensin II type 1 receptor (AT1R) blocker, telmisartan, via modulating AT1R and AT2R signaling in retinal inflammation.

PURPOSE: To investigate the retinal neural damage that occurs during inflammation and the therapeutic effects of the angiotensin II type 1 receptor (AT1R) blocker, telmisartan, using a model of endotoxin-induced uveitis (EIU). METHODS: The localization of AT1R and AT2R was shown by immunohistochemistry. EIU was induced by intraperitoneal injection of lipopolysaccharide (LPS). Animals were treated with telmisartan for 2 days and were evaluated 24 hours later. Expression levels of angiotensin II, STAT3 activation induced by inflammatory cytokines, and retinal proteins essential for neural activities (e.g., synaptophysin, rhodopsin) were analyzed by immunoblot. An AT2R antagonist was administered to evaluate the contribution of AT2R signaling in this therapy. Dark-adapted full-field electroretinography (ERG) was also performed. RESULTS: AT1R and AT2R were expressed in presynaptic terminals in most of the retinal neurons. AT1R was also expressed in Müller glial cells. During inflammation, angiotensin II expression was elevated, STAT3 was activated, and synaptophysin and rhodopsin expression were reduced. The expression of glial fibrillary acidic protein (GFAP), downstream of STAT3 activation, was induced in Müller glial cells. However, treatment with telmisartan successfully avoided all these changes. An AT2R antagonist lowered synaptophysin expression despite the treatment. STAT3 activity was negatively correlated with rhodopsin expression. Furthermore, ERG responses, which were mostly prevented by telmisartan, were disturbed during inflammation. CONCLUSIONS: Retinal protein expression and visual function are both disturbed by inflammation. Treatment with the AT1R blocker telmisartan efficiently prevented these signs of retinal neural damage through the reduction of local angiotensin II expression, the blockade of AT1R, and the relative upregulation of AT2R function.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Pars plana vitrectomy with internal limiting membrane removal for macular hole associated with proliferative diabetic retinopathy.

BACKGROUND: We describe the outcome of vitreous surgery in three eyes of three patients with macular hole associated with proliferative diabetic retinopathy (PDR) in the absence of fibrovascular proliferation, a combination of conditions where efficacy is incompletely known. METHODS: The patients, all male were 62, 65, and 66 years old. Panretinal photocoagulation had been performed preoperatively in all, and one eye had undergone vitreous surgery. No fibrovascular tissue causing macular traction was observed in any case. Fluorescein angiography and optical coherence tomography (OCT) demonstrated persistent diabetic macular edema surrounding the hole. Affected eyes were treated with vitrectomy including internal limiting membrane (ILM) peeling; 20% sulfur hexafluoride gas (SF(6)) was introduced for tamponade. RESULTS: Anatomical closure of the macular hole as well as resolution of macular edema was achieved in all cases, and vision improved considerably by more than two Snellen lines. CONCLUSIONS: Vitreous surgery with ILM peeling was effective for macular hole associated with PDR, attaining not only macular hole closure but also resolution of persistent diabetic macular edema.

Aged↗
PubMed2005

Intraocular lens implantation after atopic cataract surgery decreases incidence of postoperative retinal detachment.

PURPOSE: To investigate the efficacy of intraocular lens (IOL) implantation in reducing the incidence of postoperative retinal detachment after cataract surgery in patients with atopic dermatitis. DESIGN: Retrospective review. PARTICIPANTS: One hundred sixty-nine eyes of 126 patients who underwent cataract surgery for atopic cataract were followed for more than 1 year. None of the eyes previously had a retinal detachment or retinal detachment surgery. METHODS: The eyes were divided into 132 eyes of 95 patients with an IOL implantation (IOL group) and 37 eyes of 31 patients without an IOL implantation (aphakia group). The postoperative visual acuity and incidence of postoperative retinal detachment were compared between the 2 groups. The effects of the location of the causative retinal breaks, intraoperative posterior capsule rupture, and postoperative posterior capsulotomy on the incidence of retinal detachments were evaluated. MAIN OUTCOME MEASURES: The postoperative corrected visual acuity, incidence of postoperative retinal detachment, and influence of intraoperative posterior capsule rupture on the retinal detachment. RESULTS: The final visual acuity was better than or equal to 20/20 in 128 eyes (97.0%) of the IOL group and in 29 eyes (78.4%) of the aphakia group (P = 0.0007). Retinal detachment after an uncomplicated cataract surgery occurred in 3 eyes (2.3%) of the IOL group and in 8 eyes (25.8%) of the aphakia group (P<0.0001, Mantel-Cox). Two of 3 eyes (66.7%) in the IOL group and 1 of 8 eyes (16.7%) in the aphakia group that later developed a retinal detachment had an intraoperative posterior capsule rupture. Posterior capsulotomy by yttrium-aluminum-garnet laser did not seem to alter the incidence of postoperative retinal detachment in either the IOL (2.0%) or the aphakia group (25.0%). CONCLUSIONS: The rate of postoperative retinal detachment in eyes with IOL and no intraoperative posterior capsule rupture seems to be low. Intraocular lens implantation with capsular bag fixation may reduce the incidence of postoperative retinal detachment triggered by lens surgery for atopic cataract.

Adolescent↗
PubMed2005

Selective suppression of pathologic, but not physiologic, retinal neovascularization by blocking the angiotensin II type 1 receptor.

PURPOSE: To investigate the anti-inflammatory and anti-angiogenic effects of telmisartan, an angiotensin II type 1 receptor (AT1-R) antagonist, on ischemia-induced retinal neovascularization. METHODS: C57BL/6 neonatal mice were reared in an 80% concentration of oxygen from postnatal day (P)7 to P12, followed by room-air breathing until P17, to induce ischemia-initiated retinal neovascularization (i.e., a murine model of ischemic retinopathy). Tissue localization of AT1-R was examined by immunohistochemistry for murine retinal wholemounts and human fibrovascular tissues excised at vitrectomy for proliferative diabetic retinopathy. Animals received intraperitoneal injection of telmisartan or vehicle. A concanavalin A lectin perfusion-labeling technique was used to evaluate the areas of physiological and pathologic retinal new vessels and the number of leukocytes adhering to the vasculature. Retinal mRNA and protein levels of intercellular adhesion molecule (ICAM)-1, vascular endothelial growth factor receptor (VEGFR)-1, and VEGFR-2 were examined by RT-PCR and ELISA. RESULTS: Vessels in human fibrovascular tissues and the murine retinas were positive for AT1-R. Pathologic (P < 0.01), but not physiologic (P > 0.05), retinal neovascularization was significantly suppressed in telmisartan-treated mice compared with vehicle-treated animals. The number of adherent leukocytes (P < 0.01) was also significantly reduced, together with retinal ICAM-1 levels (P < 0.01) in the telmisartan-treated group compared with the control group. No significant difference was detected in retinal VEGFR-2 levels between the two groups, whereas retinal VEGFR-1 levels in the telmisartan-treated group were significantly (P < 0.05) lower than in the vehicle-treated group. CONCLUSIONS: The present findings suggest that the AT1-R signaling blockade leads to the selective suppression of pathologic, but not physiological, retinal neovascularization through the inhibition of the inflammatory processes related to pathologic neovascularization.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Suppression of ocular inflammation in endotoxin-induced uveitis by blocking the angiotensin II type 1 receptor.

PURPOSE: To examine whether the angiotensin II type 1 receptor (AT1-R) signaling plays a role in ocular inflammation in endotoxin-induced uveitis (EIU). METHODS: EIU was induced in C57BL/6 mice by a single intraperitoneal injection of 150 mug lipopolysaccharide (LPS). Tissue localization, mRNA expression, and protein levels of AT1-R in murine retinas were examined by immunohistochemistry, RT-PCR, and Western blot analyses, respectively. Telmisartan, an AT1-R antagonist widely used as an antihypertensive agent, was administered intraperitoneally at a dose of 10 mg/kg daily for 5 days until the injection of LPS. Twenty-four hours after administration, leukocyte adhesion to the retinal vasculature was evaluated with a concanavalin A lectin perfusion-labeling technique. Retinal mRNA and protein levels of intercellular adhesion molecule (ICAM)-1 were examined by RT-PCR and ELISA, respectively. Protein concentration and inflammatory cells in the aqueous humor were also measured. RESULTS: Retinal vessels were positive for AT1-R. In mice with EIU, retinal AT1-R mRNA and protein levels were significantly increased when compared to the normal control. EIU animals also showed significant increases in the number of inflammatory cells infiltrating the anterior chamber and adhering to the retinal vessels and in retinal ICAM-1 levels. Administration of telmisartan to EIU mice resulted in significant suppression of retinal ICAM-1 expression and leukocyte adhesion and infiltration compared with vehicle treatment. Protein concentration in the aqueous humor of telmisartan-treated EIU mice tended to be lower than that of vehicle-treated EIU mice, but the difference was not statistically significant. CONCLUSIONS: AT1-R signaling blockade inhibited retinal ICAM-1 upregulation and leukocyte adhesion and infiltration in the EIU model. These results suggest the potential use of an AT1-R antagonist as a therapeutic agent to reduce ocular inflammation.

Angiotensin II Type 1 Receptor Blockers↗
PubMed2005

Hypoxia induces the expression of membrane-type 1 matrix metalloproteinase in retinal glial cells.

PURPOSE: Fibrovascular tissue formation in diabetic retinopathy necessitates not only angiogenic activity but also proteolytic activity, which is at least in part attributable to the induction of membrane-type 1 matrix metalloproteinase (MT1-MMP) in retinal glial cells. However, little is known about the triggers for MT1-MMP induction in the diabetic retina. In the present study, the effect of tissue hypoxia on MT1-MMP expression in retinal glial cells was investigated. METHODS: Retinal glial cells were isolated from the rabbit retina and cultured under either normoxic (20% O(2)) or hypoxic (1% O(2)) conditions in the presence or absence of the inhibitor for vascular endothelial growth factor (VEGF) receptor signal transduction or a neutralizing antibody against VEGF. The expression level of MT1-MMP in retinal glial cells was analyzed by reverse transcription-polymerase chain reaction (RT-PCR), real-time PCR, Western blot analysis and immunocytochemistry. Expression of VEGF and VEGF receptors, VEGFR-1 and VEGFR-2, was also examined by RT-PCR. RESULTS: RT-PCR and real-time PCR analyses showed a 2.3-fold induction of MT1-MMP expression in retinal glial cells under hypoxic conditions. VEGF, especially its isoform VEGF(165), and VEGFR-2 were also upregulated in retinal glial cells by hypoxia, and hypoxia-induced MT1-MMP expression was inhibited in the presence of the VEGFR-2 inhibitor SU1498 or the anti-VEGF antibody. CONCLUSIONS: Hypoxia can induce MT1-MMP expression in retinal glial cells, and the hypoxia-induced expression of MT1-MMP is mediated by VEGF in an autocrine fashion.

Animals↗
PubMed2004

A clinicopathologic case report on macular hole associated with von Hippel-Lindau disease: a novel ultrastructural finding of wormlike, wavy tangles of filaments.

BACKGROUND: We describe a novel ultrastructural finding observed in an epiretinal membrane excised from a patient with von Hippel-Lindau disease. METHODS: This interventional case report presents a 45-year-old woman who noted decreased vision in her right eye and was referred for treatment of a macular hole secondary to von Hippel-Lindau disease. Blindness had occurred previously in the left eye because of exudative retinal detachment. Funduscopic examination revealed a macular hole associated with a delicate epiretinal membrane, multiple retinal angiomas, and multiple old laser scars. Vitrectomy was performed in her right eye. The epiretinal membrane was peeled off and processed for light and electron microscopy. RESULTS: Postoperatively the macular hole was successfully closed, and vision recovered to 20/20 from 20/40. In the excised epiretinal membrane, flattened glial cells and extracellular matrix containing fibrous elements formed a multilayered pattern. Ultrastructurally, the fibrous elements appeared as wormlike, wavy tangles of filaments (WWTF) with an orientation parallel to the surface of the epiretinal membrane. Just above the WWTF, flattened glial cells frequently extended thin cytoplasmic processes with pinocytotic vesicles. CONCLUSION: The ultrastructure suggested that retinal glial cells had induced a remodeling of the collagenous stroma in the posterior vitreous cortex, resulting in tangential macular traction.

Basement Membrane↗
PubMed2004

Novel 473-bp deletion in XLRS1 gene in a Japanese family with X-linked juvenile retinoschisis.

PURPOSE: To present the clinical features of two brothers with molecularly confirmed X-linked juvenile retinoschisis (xlRS) but with non-characteristic electrophysiological findings. METHODS: Comprehensive ophthalmological examinations were performed. The electroretinograms (ERGs) were recorded under ISCEV standards, and ERGs elicited by long-duration stimuli were also evaluated. Standard genetic analysis of peripheral blood leukocytes was performed. RESULTS: Molecular testing revealed a novel 473-bp deletion including exon 4 in the XLRS1 gene in both siblings. This resulted in a frameshift mutation and a premature termination at codon 78. The scotopic and photopic ERGs were reduced, but the "negative-type" ERG, characteristic of xlRS, was not observed. Flicker ERGs were also highly reduced. Long-duration stimuli elicited ERGs with a complete loss of the b-wave and a preservation of the off-response, i.e., negative-type ERG. The phenotype/genotype relationship was not determined. CONCLUSION: The consistency of the ERGs elicited by long-duration stimuli in xlRS patients suggests that this type of stimuli provides responses that are a better indicator for the progression or stage of the disease.

Adult↗
PubMed2004

Cerebral fat embolism diagnosed by magnetic resonance imaging at one, eight, and 50 days after hip arthroplasty: a case report.

PURPOSE: To describe cardiovascular collapse during a cemented hip hemiarthroplasty in a patient who, despite a successful cardiopulmonary resuscitation, remained in a persistent vegetative state due to cerebral fat embolism diagnosed by magnetic resonance imaging (MRI). CLINICAL FEATURES: A 75-yr-old woman with no medical history underwent cemented hip hemiarthroplasty under spinal anesthesia for a right femoral neck fracture. Shortly after insertion of the prosthesis, a sudden oxygen desaturation, hypotension, bradycardia, and cardiac arrest occurred. The patient was successfully resuscitated, but did not regain consciousness. The patient developed high-grade fever, thrombocytopenia, anemia, and oliguria. MRI scans of the brain revealed multiple high intensity signals throughout the white matter, the basal ganglia, the cerebellum, and the brain stem. The diagnosis of fat embolism was made on the basis of clinical findings and MRI images. Although her cardiorespiratory status improved over the next week, the patient remained in a persistent vegetative state. CONCLUSION: When fat embolism is suspected, serial MRI scans of the brain should be performed to diagnose the etiology of cerebral embolism as well as to evaluate the severity of brain damage.

Aged↗
PubMed2004

Successful treatment of subfoveal choroidal neovascularization associated with combined hamartoma of the retina and retinal pigment epithelium.

PURPOSE: To describe a patient with subfoveal choroidal neovascularization (CNV) associated with combined hamartoma of the retina and retinal pigment epithelium (CHRRPE), treated successfully by submacular surgery. DESIGN: Interventional case report. METHODS: A 12-year-old girl was referred to our clinic for evaluation. Visual acuity was 20/30 in the affected left eye. Ophthalmoscopy disclosed juxtapapillary CHRRPE and subfoveal pigmented CNV. Vitreous surgery was carried out because of visual deterioration to 20/60. RESULTS: The posterior vitreous was strongly attached to glial tissue at the superior margin of the optic disk in the CHRRPE region. The CNV, which was not connected with the CHRRPE, was carefully removed, resulting in visual improvement to 20/20 5 months after surgery. Histologically, the excised membrane showed fibroblast-rich cellular component and a type 2 configuration. CONCLUSION: Submacular surgery can be effective for the treatment of secondary CNV associated with CHRRPE.

Child↗
PubMed2004

Intraoperative breakage of a 25-gauge vitreous cutter.

PURPOSE: To report breakage of a 25-gauge vitreous cutter during vitreous surgery. DESIGN: Interventional case report. METHODS: A 60-year-old woman was referred for management of an epiretinal membrane at the macula. Visual acuity was 20/100 in the affected left eye. Vitreous surgery using a 25-gauge vitrectomy system was carried out with a combination of conventional cataract surgery. RESULTS: The vitreous cutter was lodged within the sclerotomy cannula after peripheral vitrectomy and was pulled together with the cannula. The cannula was reinserted by trocar, but as the floating peeled epiretinal membrane was dissected with the vitreous cutter, the tip of the cutter was broken and was aspirated with the membrane. Stereoscopic microscopy and scanning electron microscopy demonstrated that the edge that had broken at the cutter port was smooth. CONCLUSION: Although 25-gauge instruments remain useful, care should be taken against rare surgical complications related to their fragility.

Catheterization↗