Kazushi Tamai

Retention of dye after indocyanine Green-assisted internal limiting membrane peeling ☆

PURPOSE To describe the long-term retention of indocyanine green (ICG) in the fundus after ICG-assisted internal limiting membrane peeling. DESIGN Case report. Two patients underwent vitrectomy including ICG-assisted internal limiting membrane peeling. The fundus was examined with a 780-nm infrared illumination of a scanning laser ophthalmoscope after surgery. RESULTS No ICG staining of the fundus was visible ophthalmoscopically. Examination with a scanning laser ophthalmoscope, however, detected fluorescence from residual ICG until 6 months after surgery in case 1 and 9 months in case 2. No complication related to the residual ICG was observed. CONCLUSIONS The results suggested that ICG remains in the fundus for a long period after surgery. Clearance of the dye from the diabetic retina may be prolonged.

Local hypothermia protects the retina from ischaemic injury in vitrectomy

AIMS Hypothermic irrigating solutions were used during vitrectomy in pressure induced ischaemic eyes so that their effects on retinal function and histological changes could be investigated. METHODS After anaesthetised albino rabbits underwent closed vitrectomy, their vitreous cavities were continuously irrigated for 30 minutes at a perfusion pressure of 140 mm Hg. The rabbits were divided into three groups according to their intraocular perfusion temperatures—8°C, 22°C, and 38°C. Electroretinograms were taken before and after irrigation. Glutamate levels in the vitreous were examined after irrigation. Eyes were enucleated on the seventh postoperative day and examined histologically. RESULTS On the seventh postoperative day, the recovery rate of a-wave amplitudes was significantly lower in the 38°C group than in the 8°C group, and that of b-wave amplitudes was significantly lower in the 38°C group than in either the 8°C or 22°C group. Retinal damage in the 38°C group revealed more severe histological impairment than in either the 8°C or 22°C group. Oedema of the inner retinal layer was significant in both the 22°C and 38°C groups. Glutamates reached peak values 30 minutes after the end of ischaemia in the 38°C group. However, no significant glutamate increases were detected 15 to 60 minutes after ischaemia in either the 8°C or 22°C group. CONCLUSION Local hypothermia during vitrectomy in acute ischaemic eyes appears to decrease retinal damage.

Lipid hydroperoxide stimulates leukocyte-endothelium interaction in the retinal microcirculation.

Leukocyte dynamics were evaluatyed in vivo in rat retinal microcirculation following exposure to lipid hydroperoxide (LHP) in the vitreous.Various amounts (1, 5, 10 or 100 microg) of LHP (18:2) dissolved in 5 microl of sodium borate buffer (SBB, 0.02M) were injected into the vitreous of Brown-Norway rats. As a comparative study, 10 microg of linoleic acid (LA) dissolved in 5 microl of SBB was injected in the same way. Rats that did not undergo injection were evaluated as un-treated. At 2 to 48 hr after LHP exposure, the following were examined: (1) the flux of rolling leukocytes along the major retinal veins, (2) the number of leukocytes that accumulated in the retinal microvasculature using acridine orange digital fluorography and (3) the diameter of major retinal vessels. In the LHP-treated eyes, leukocyte rolling along the major retinal veins was observed and the number increased in a dose-dependent manner ( 1 to 10 microg). The flux of rolling leukocytes peaked at 6 hr after LHP (10-100 microg) injection. No rolling leukocytes were observed in LA-treated or un-treated eyes. The number of accumulated leukocytes started to increase at 4 hr and peaked at 24 hr after LHP (10 microg) injection. This number was significantly higher than that in LA-treated and un-treated eyes. Venous dilation was seen from 4 hr after LHP (10 microg) injection and became significant at 6 and 24 hr as compared with LA-treated and un-treated eyes. The results indicate that increased LHP levels in the vitreous due to oxidative stress enhance leukocyte-enothelium interaction in the retinal microcirculation.

Hypercholesterolemia induces leukocyte entrapment in the retinal microcirculation of rats

Purpose. To evaluate leukocyte dynamics in the retinal microcirculation of hypercholesterolemic rats in vivo using acridine orange digital fluorography. Methods. 18 male pigmented rats were divided into 3 groups according to their diet; (A) control diet (0.1% cholesterol) for 8 weeks, (B) control diet for an initial 4 weeks followed by a high-cholesterol (HC) diet (5% cholesterol) for another 4 weeks and (C) HC diet for 8 weeks. Leukocyte dynamics were observed with acridine orange digital fluorography. The diameter of major retinal vessels and the number of leukocytes trapped in the retina were evaluated quantitatively. Results. Both groups B and C showed approximately 4-fold higher serum cholesterol levels than in group A. The diameters of retinal arteries and veins were not significantly different among the three groups. Also, no rolling leukocytes were observed in any of the groups. In the retinal microcirculation at 30 minutes after acridine orange injection, the density of trapped leukocytes in both groups B and C was significantly greater than in group A (23.19 ± 2.13, 28.56 ± 1.96 and 13.67 ± 1.45 cells/mm 2, respectively, p < 0.01). Furthermore, group C exhibited a significantly greater number of trapped leukocytes than in group B (p < 0.01). Conclusion. Enhanced leukocyte entrapment in the retinal microcirculation was induced in the early stage of hypercholesterolemia. Entrapment was increased as the period of hypercholesterolemia was prolonged. Leukocyte accumulation in the retina may be an early vascular dysfunction leading to arteriosclerosis in hypercholesterolemia.

Pachymeningitis with pseudo–Foster Kennedy syndrome

PURPOSE To report a case of pachymeningitis with pseudo-Foster Kennedy syndrome in a patient who was positive for perinuclear antineutrophil cytoplasmic antibody. METHODS Case report. A 44-year-old man was examined for headache and diplopia. RESULTS Left eye showed limitation of abduction. Ocular fundus, computed tomography (CT), and magnetic resonance imaging (MRI) of the head and orbits were normal. The diplopia subsided spontaneously. Six months later, he noticed sudden visual loss in the left eye. The left eye showed optic disk atrophy and episcleritis, and the right eye showed papilloedema. Computed tomography and MRI exhibited thickened dura mater. Serum perinuclear antineutrophil cytoplasmic antibody level was highly increased. CONCLUSION Pachymeningitis with ocular involvement sometimes requires repeated CT or MRI for diagnosis. This disorder may be caused by microvasculitis.

Long-term retention of dye after indocyanine green-assisted internal limiting membrane peeling.

PurposeTo evaluate dye retention in the fundus after indocyanine green (ICG)-assisted internal limiting membrane peeling.MethodsTen eyes with stage 3 or 4 nondiabetic idiopathic macular hole (MH group) and six eyes with diffuse diabetic macular edema (DM group) were studied. The fundus was examined with 780-nm infrared illumination by a scanning laser ophthalmoscope (SLO) after ICG-assisted internal limiting membrane peeling. The postoperative follow-up period ranged from 6 to 12 months (mean ± SD, 3.7 ± 2.6 months).ResultsFluorescence from ICG was detected in all studied eyes in both groups up to 6 months after surgery. At 9 months after surgery, ICG fluorescence was visible in all eyes of the DM group, but in only one-third of eyes of the MH group. No fluorescence was detected in fellow eyes that had not been operated on.ConclusionThe present study using SLO revealed that ICG remains in the fundus for over 6 months after surgery. The results also suggested that a longer time might be required for dye clearance from the diabetic retina than from the nondiabetic retina. Jpn J Ophthalmol 2006;50:349–353