Tsunehiko Ikeda

Spontaneous Disappearance of Traumatic Macular Holes in Young Patients

PURPOSE To report the disappearance of traumatic macular hole in three eyes of three patients. METHODS Clinical data of the patients were reviewed. RESULTS The three patients were relatively young, ranging in age from 12 to 18 years old. In one eye of each patient, a small traumatic macular hole was observed at the first visit. Visual acuities ranged from 20/100 to 20/40. The macular holes resolved spontaneously 3 to 4 months after the trauma, and final visual acuity improved to 20/20 in all patients. CONCLUSION Small traumatic macular holes in young patients can resolve spontaneously, and this can be associated with good visual recovery.

Vitrectomy for rhegmatogenous or tractional retinal detachment with familial exudative vitreoretinopathy

OBJECTIVE To examine the anatomic features and surgical indications of familial exudative vitreoretinopathy (FEVR) complicated with rhegmatogenous or tractional retinal detachment. DESIGN Retrospective noncomparative case series. PARTICIPANTS Twenty-eight eyes of 25 patients who had either clinically suspected or fully diagnosed FEVR. Of these, 25 had rhegmatogenous retinal detachment, 2 had tractional retinal detachment, and 1 had tractional retinal detachment plus vitreous hemorrhage. INTERVENTIONS The authors carefully observed the vitreoretinal interface during surgery, studied the clinical and anatomic features of FEVR, and then evaluated the surgical results. RESULTS The vitreoretinal adhesions were so strong in the peripheral avascular area that iatrogenic retinal breaks easily occurred in 22 of 28 eyes. In all cases, the bimanual technique with vitreous scissors and forceps was required to dissect the posterior vitreous membrane from the retinal surface. The retina was reattached in 24 of 28 cases (85.7%), and visual acuity improved in 20 eyes (71.4%). CONCLUSION Dissection of the vitreous in the peripheral avascular area is very difficult in FEVR, and those patients for whom this procedure was not successfully performed may have a poorer prognosis.

Soluble Fas ligand expression in the ocular fluids of uveitis patients

Purpose. The expression of Fas ligand (FasL) in ocular tissues is thought to play a critical role in maintaining immune privilege in the eye. In this study, to clarify the involvement of the Fas-FasL system in inflammatory processes of the eye,we examined soluble FasL (sFasL) in ocular inflammation. Methods. Using ELISA systems recently developed, sFasL concentrations in aqueous humor (AH) and/or vitreous fluid (VF) were measured. AH was obtained from 17 eyes of 17 uveitis patients and from 12 eyes of 12 non-uveitis (cataract) patients. VF was obtained from 22 eyes of 22 uveitis patients and 7 eyes of 7 non-uveitis (macular hole) patients. Serum levels of sFasL were also determined. Results. sFasL in AH and VF was below the detection limit of the ELISA systems in all non-uveitis eyes. On the other hand, sFasL was detected in AH from uveitis patients where it measured 367.0 ± 154.7 pg/ml (mean ± SEM). sFasL was also detected in VF from uveitis patients where it measured 1132.2 ± 281.7 pg/ml. None of the sera from patients with or without uveitis contained a detectable level of sFas L. Conclusions. sFasL levels in AH and VF are elevated in the eye during ocular inflammation. Fas-FasL mediated apoptosis may play an important role in the regulation of inflammation during uveitis.

Retinal Cytokine Response in Mouse Alkali-Burned Eye

The kinetics of inflammatory cytokines in sensory retina of mice with corneal alkali-burned eyes were examined. Retinal samples were collected from ICR mice with unburned and alkali-burned eyes from day 3 to day 14. Enzyme-linked immunosorbent assay was used to quantitate the expression levels of interleukin-1α (IL-1α), IL-1β and IL-6. Concentrations of IL-1β and IL-6 were significantly elevated at day 3 after alkali burn, and reduced to normal level by day 7. The concentration of IL-1α was below assay sensitivity at all times. A significant elevation of IL-1β and IL-6 in the sensory retina may contribute to the retinal inflammatory response in the alkali-burned eyes. This is the first report suggesting that the retina is involved in the damage process of alkali burn.

Tractional retinal detachment after branch retinal vein occlusion. Influence of disc neovascularization on the outcome of vitreous surgery

OBJECTIVE This study aimed to investigate the influence of disc neovascularization on the outcome of vitreous surgery for tractional retinal detachment (TRD) after branch retinal vein occlusion (BRVO). DESIGN The study design was a retrospective case series. PARTICIPANTS Twenty-two eyes of 22 patients who had undergone vitrectomy for TRD after BRVO at the Osaka National Hospital (Osaka, Japan) or the Surugadai Hospital of Nihon University (Tokyo, Japan) between 1985 and 1995 participated. Seven (32%) of 22 eyes had a TRD secondary to neovascularization of the optic disc (NVD) and neovascularization elsewhere (NVE; group I), and 15 (68%) had a TRD with NVE without NVD (group II). MAIN OUTCOME MEASURES Visual acuities and retinal reattachment rates were measured. RESULTS Sixteen (73%) of the 22 study eyes showed severe vitreous hemorrhage before surgery, and 11 eyes (50%) had received laser photocoagulation treatment before surgery. Fourteen (64%) of the study eyes achieved total retinal reattachment after initial vitrectomy, and 19 eyes (86%) were reattached completely at final examination. Thirteen eyes (59%) achieved a visual acuity of better than 0.1. Group I patients had a significantly higher rate of recurrent combined traction rhegmatogenous retinal detachment (P = 0.01) and a significantly worse final visual outcome (P = 0.01). CONCLUSIONS Better surgical results are expected in eyes without NVD than with NVD among patients who undergo vitrectomy for TRD after BRVO. Although the authors were unable to determine the reason for this difference in the current study, they speculate that the degree of retinal nonperfusion, diffusible angiogenic factors, and distance of the site of occlusion from the disc may each affect visual and anatomic outcomes in these eyes.

Association of Eosinophil Granule Major Basic Protein With Atopic Cataract

PURPOSE To investigate the mechanism of atopic cataract development, we examined a tissue-destroying major basic protein, derived from eosinophils, in the anterior capsule of cataractous lenses and the aqueous fluid of atopic dermatitis patients. METHODS Major basic protein deposition in anterior capsule tissues was evaluated immunohistochemically using anti-major basic protein monoclonal antibody in three consecutive eyes from three atopic cataract patients and three consecutive eyes from three senile cataract patients. Also, major basic protein concentration in aqueous fluid obtained during cataract surgery was measured by radioimmunoassay in 12 consecutive eyes from 11 atopic cataract patients and 15 consecutive eyes from 15 senile cataract patients. RESULTS Immunohistochemical investigation demonstrated lens epithelial major basic protein deposition in all three atopic cataracts but not in any of the senile cataracts. Major basic protein was detected in the aqueous fluid by radioimmunoassay in four of the 12 atopic cataract eyes and ranged in concentration from 11 to 70 ng/ml. No major basic protein was detected in the aqueous fluid of the 15 senile cataract eyes. CONCLUSION Major basic protein in anterior capsule tissues and in the aqueous fluid of eyes with atopic cataract may be associated with the pathogenesis of atopic cataract.

Retinal Detachment after Branch Retinal Vein Occlusion: Influence of the Type of Break on the Outcome of Vitreous Surgery

BACKGROUND Branch retinal vein occlusion (BRVO) is occasionally complicated by two types of retinal breaks (retinal holes without vitreous traction or retinal traction tears) that may lead to a rhegmatogenous retinal detachment (RRD). The authors describe surgical results of vitrectomy for RRD after BRVO and investigate whether there is any difference between clinical features or surgical results from eyes with the two types of retinal breaks. PATIENTS AND METHODS The authors retrospectively studied 25 patients (25 eyes) who underwent vitrectomy for RRD after BRVO. Twelve of 25 eyes (48%) had a detachment secondary to one or more retinal holes (group I), and 13 of the eyes (52%) had one or more retinal tears (group II). RESULTS Seventeen of the eyes (68%) achieved total retinal reattachment after the initial surgery; 22 (88%) did so by the time of final examination. Patients with retinal holes achieved more favorable final vision than those with retinal tears (P = 0.0391). A higher rate of preoperative macular detachment (P = 0.0112) and a higher rate of recurrent retinal detachment after initial vitrectomy (P = 0.0302) were the factors associated with the reduced final visual acuity in patients with retinal tears. The increased rate of recurrent retinal detachment in patients with retinal tears was associated with a higher rate of existing preretinal neovascular membranes (P = 0.0112) and a trend toward an increased incidence of intraoperative iatrogenic retinal breaks. CONCLUSION Among patients who undergo vitrectomy for RRD after BRVO, better surgical results are expected in eyes with retinal holes without vitreous traction than in those with retinal traction tears. This difference is thought to be due to the difference in vitreoretinal anatomy between eyes with the two types of retinal breaks.

Multiple cranial arteriovenous malformations in a child with eventual blindness in the affected eye.

PURPOSE To report a case of multiple cranial arteriovenous malformations involving the orbit and retina. METHOD Case report. We treated a 7-year-old girl who was diagnosed with a left submaxillary, a left retinal, a left orbital, and a middle subdural arteriovenous malformation. RESULTS Enlargement of the arteriovenous malformations, except for the retinal arteriovenous malformation, was observed. After external carotid artery embolizations and radiation therapy for uncontrolled oral cavity bleeding, loss of light perception in the affected eye occurred, but no marked changes occurred in the retinal arteriovenous malformation. CONCLUSION This rare case suggests that the clinical finding of a stable retinal arteriovenous malformation may be associated with enlargement of arteriovenous malformation lesions at other sites.

Histopathological findings in proliferative membrane from a patient with sarcoid uveitis.

BACKGROUND Sarcoid uveitis is occasionally accompanied by proliferative changes, such as retinal neovascularization and vitreous hemorrhage. Steroid administration, retinal photocoagulation, and vitrectomy may be indicated in such proliferative cases. CASE A 19-year-old woman presented with proliferative sarcoid uveitis accompanied by recurrent vitreous hemorrhage. OBSERVATIONS At the initial examination, bilateral vitreous opacity, retinal exudates, mild vitreous hemorrhage, retinal vasculitis, and neovascularization of the retina and optic disc were observed. Although prednisolone was administered and panretinal photocoagulation was performed several times, recurrent vitreous hemorrhage continued. Since the vitreous hemorrhage was not absorbed, pars plana vitrectomy and lensectomy were performed. After surgery, neovascularization and intraocular inflammation decreased, and the corrected visual acuity in the right eye improved to 20/50. Histopathologic analysis of the proliferative membrane removed during surgery revealed substantial neovascularization and numerous neutrophils in the vessels. CONCLUSIONS Based on these findings, an inflammatory reaction as well as retinal ischemia were thought to be involved in the proliferative changes in this patient.

Subretinal haemorrhage after granulocyte colony-stimulating factor

Haemopoietic colony-stimulating factors (CSFs) have been known to worsen autoimmune disorders, whereas granulocyte-macrophage colony-stimulating factor and granulocyte colony-stimulating factor (G-CSF) activate preexisting inflammatory eye disease or even induce the disease. We report here a girl in whom G-CSF induced subretinal haemorrhage resulting in irreversible loss of vision. A 4-year-old girl with a neuroblastoma, diagnosed in July, 1995, received filgrastim for neutropenia and for mobilising peripheral blood stem cells after chemotherapy. On April 16, 1996, during chemotherapy, she complained of right ocular pain and had conjunctival hyperaemia, compatible with acute haemorrhagic corneoconjunctivitis. Antibiotic and corticosteroid eyedrops were effective and her symptoms disappeared within a week. Despite negative results for cultures and serological tests, viral infection was thought likely. After chemotherapy, filgrastim 250 mg/m was administered from May 5, 1996 (leucocytes 0·1 10/L). She complained of sensitivity to light and ocular pain again in the right eye. While she continued to receive filgrastim for collection of peripheral blood stem cells, her ocular symptoms progressed despite local treatment with eyedrops for suspected infectious conjunctivitis. Ophthalmological examination revealed massive vitreous haemorrhage with increased intraocular pressure. 5 days after intensive treatment with intravenous haemostatics and diuretics, after discontinuation of filgrastim, the intraocular haemorrhage became inactive and intraocular pressure decreased. Since retinal detachment appeared progressive, vitrectomy and retinal photocoagulation were carried out. However, her right vision did not return to normal. Pathological evaluation of a specimen taken from the subretinal mass revealed hyaline tissue with minimal inflammatory cell infiltration, suggesting degenerated haematoma. Thereafter, she received another G-CSF (nartograstim 150 mg/m) from June 28 (leucocytes 0·1 10/L with 0% neutrophils) after chemotherapy. On July 22 (leucocytes 2·4 10/L with 79% neutrophils, platelets 36 10/L), conjunctival hyperaemia and mild vitreous haemorrhage recurred in the right eye. Soon after subsequent discontinuation of nartograstim, her occular symptoms disappeared under local treatment. On August 14 (leucocytes 1·9 10/L with 88% neutrophils, platelets 44 10/L), just 2 days after starting G-CSF (filgrastim) for febril neutropenia (less than 0·4 10/L), sensitivity to light, conjunctival hyperaemia, and floaters in the anterior chamber of her right eye suggested iridocyclitis. Since the ocular involvement was each time associated with administration of G-CSF, it was discontinued. Her symptoms disappeared without progression to subretinal haemorrhage. However, she subsequently lost the vision in her right eye. Over this period of time, no other haemorrhagic episodes were observed and her blood clotting studies remained normal. In animal models, pretreatment with G-CSF worsens intraocular inflammation through local production of tumour necrosis factor activated by G-CSF. In our case, it was likely that the primary, probably infectious, ocular inflammation was reactivated by G-CSF and progressed to subretinal haemorrhage, because all episodes occurred in the accelerated phase of granulocyte recovery induced by GCSF. Upon reporting the ocular complications observed in our case, we have obtained details from the manufacturers of subretinal bleeding possibly induced by G-CSF in at least four patients in Japan and the USA (unpublished cases). Two of them had a history of cytomegalovirus retinitis complicated with AIDS; two other cases with lymphoma and neuroblastoma did not have pre-existing ocular inflammation. At least two of these patients have subsequently lost vision (unilateral and bilateral). Taken together, upon administrating CSFs, ophthalmological examination should be done to prevent progression to serious ocular involvement, particularly in patients with a history of inflammatory eye disease.