Koichi Shimizu

Midperipheral Fundus Involvement in Diabetic Retinopathy

We evaluated the topologic distribution of vaso-occlusive and vasoformative lesions in 119 eyes with diabetic retinopathy using our newly developed super-wide (130 degrees) fluorescein angiographic montage technique. A numeric coding system was applied to assess the vaso-occlusive lesions by dividing each fundus maximally into 418 blocks. We demonstrated that the midperipheral retina was far more prone to undergo capillary nonperfusion than the posterior retina. The extent of capillary nonperfusion was more pronounced in eyes with neovascularization from (in ascending order): the retina, the optic disc, and in the chamber angle.

Persistent and bilateral choroidal vascular abnormalities in central serous chorioretinopathy.

BACKGROUND To clarify the role of choroidal vascular abnormalities in central serous chorioretinopathy (CSC) in active stage, remission, and recurrence. METHODS Indocyanine green angiography and fluorescein angiography were performed in 105 eyes (104 patients) with active CSC. Forty-six patients were followed up for 6 to 48 months (mean +/- standard deviation, 22.5 +/- 8.9 months) with repeated angiography (mean +/- standard deviation, 3.5 +/- 1.5 times). Indocyanine green angiography and fluorescein angiography also were performed during remission in all 46 eyes with CSC and during recurrent CSC in 6 eyes. Unaffected fellow eyes underwent angiographic examinations in all patients. RESULTS In active CSC, indocyanine green angiography showed a choroidal filling delay (71%), venous dilation (61%), and focal choroidal hyperfluorescence (96%) surrounding leakage from the retinal pigment epithelium. Focal choroidal hyperfluorescence was present in unaffected areas of affected eyes (55%). The choroidal venous dilation (36%) and choroidal hyperfluorescence (62%) were noted even in unaffected fellow eyes. These choroidal abnormalities persisted during remission after leakage ceased throughout the follow-up period. In the six patients with recurrent CSC, new leakage developed in the areas of persistent choroidal hyperfluorescence. Central serous chorioretinopathy developed in the unaffected fellow eye in one of these six patients. CONCLUSION Choroidal vascular abnormalities persist in both eyes even after leakage from the retinal pigment epithelium ceases. Central serous chorioretinopathy may recur in areas of choroidal vascular abnormalities.

Vitreous cortex remnants at the fovea after spontaneous vitreous detachment

We performed a scanning electron microscopic observation of the posterior retinal surface of 59 autopsy eyes with spontaneous vitreous detachment. In 26 eyes (44%), there were remnants of the posterior vitreous membrane in the foveal area. These vitreous cortex remnants formed three basic patterns. They appeared either as disc-shaped collagenous membranes covering the fovea, as rings along the foveal margin, or forming a structure that resembles a cyst. Each of these patterns seemed to have a counterpart to various known clinical situations.These findings imply that remnants of the vitreous cortex membrane frequently remain attached to the fovea after apparent complete posterior vitreous detachment. The observed features would provide morphological basis for the interpretation of several clinical conditions that take place along the vitreoretinal interface at the fovea.

Distribution of Capillary Nonperfusion in Early-stage Diabetic Retinopathy

Using composite super-wide fluorescein angiography, 152 eyes with nonproliferative diabetic retinopathy were evaluated for capillary nonperfusion. Four basic types of eyes were distinguished according to the location of capillary nonperfusion: peripheral type 4 eyes, midperipheral type 93 eyes, central type 40 eyes and generalized type 15 eyes. The rate of enlargement of nonperfused area was more rapid in peripheral type, midperipheral type, central type and the generalized type in the ascending order. Eyes belonging to midperipheral and central types evolved into other, usually generalized type during the course of observation. There is a positive correlation between the initial site of occurrence of capillary nonperfusion and its progression in nonproliferative diabetic retinopathy. A proper recognition of the typing is claimed to be of prognostic value.

The Role of the Premacular Liquefied Pocket and Premacular Vitreous Cortex in Idiopathic Macular Hole Development

PURPOSE To clarify the role of the vitreous in idiopathic macular hole formation. METHODS We prospectively evaluated the vitreous before and during vitreous surgery in 64 consecutive eyes of 62 patients (stage 1B, four eyes; stage 2, ten eyes; stage 3, 43 eyes; stage 4, four eyes) with macular holes; another three eyes underwent a second vitrectomy. After core vitrectomy, the premacular vitreous cortex was examined by applying gentle suction. The detached posterior hyaloid face was observed under endoilluminiation. RESULTS We observed in all eyes a liquefied lacuna anterior to the posterior fundus before and during vitreous surgery. The premacular vitreous cortex was extremely thin and elastic upon gentle suction. A premacular ring, the diameter two to four times that of the Weiss ring, was observed in 48 of 57 eyes (84%) with stages 1B, 2, and 3 macular hole. In most cases, the vitreous cortex within the premacular ring either was absent or had a break, resulting in a premacular round defect. The vitreous cortex peripheral to the premacular ring, which was thick and less deformed, never showed a break. In eyes that had undergone a second vitrectomy, we noted residual cortex or an epiretinal membrane around the macular hole. CONCLUSIONS The premacular vitreous cortex is extremely thin and elastic. It is sharply demarcated by a ring from the thick peripheral vitreous cortex. Tangential traction, which causes macular holes, appears to originate exclusively in the premacular vitreous cortex that forms the posterior wall of the premacular liquefied pocket.

Oval defect in detached posterior hyaloid membrane in idiopathic preretinal macular fibrosis.

We examined the vitreous of 71 eyes with idiopathic preretinal macular fibrosis and observed complete posterior vitreous detachment in 48 eyes (68%), partial posterior vitreous detachment in 16 eyes (22%), and no posterior vitreous detachment in seven eyes (10%). Among the 48 eyes with posterior vitreous detachment, we observed that the detached posterior hyaloid membrane had an oval or round defect in 31 eyes (65%) and a break in the premacular area in 12 eyes (25%). The size and the contour of the premacular defects in the posterior hyaloid membrane corresponded to those characteristic of premacular fibrosis. A premacular oval defect in the detached posterior hyaloid membrane indicates that the vitreous cortex is a structural component of idiopathic premacular fibrosis. We postulate that the thin, premacular vitreous cortex, which forms the posterior wall of the premacular liquefied pocket, plays a key role in the development of idiopathic preretinal macular fibrosis in eyes with or without posterior vitreous detachment.

Tractional Elevation of Henle's Fiber Layer in Idiopathic Macular Holes

PURPOSE We sought to clarify the morphologic features of macular hole development. METHODS Using scanning laser ophthalmoscopy, we examined 47 eyes with macular holes before and after vitrectomy. Cases included three eyes with stage 1B disease (foveal detachment), 14 with stage 2 (break at the fovea), 21 with stage 3 (full-thickness macular hole), and nine with stage 4 (detached operculum), according to Gasss classification. Ten eyes with central serous chorioretinopathy served as controls. RESULTS Radiating striae of Henles fibers were seen around the elevated rim of the macular cyst or hole when the intraretinal structures were illuminated by helium-neon laser. Granularity was observed on the macular hole floor. A granular reflex corresponding to the macular break or hole, but no radiating striae were seen by argon blue laser. In 40 eyes in which macular holes were successfully closed by vitrectomy, radiating striae of Henles fiber layer disappeared, and the normal foveal depression was restored. The ten eyes with central serous chorioretinopathy had a normal foveolar depression and no detectable radiating striae of Henles fiber layer, despite full-thickness retinal detachment in the macular area. CONCLUSIONS Tractional elevation of Henles fiber layer with intraretinal foveolar cyst formation is the initial feature of macular hole development. A macular hole is formed when the anterior cyst wall containing Henles fiber layer is operculated. Remnants of the photoreceptor cell layer remain on the hole floor in the early stage of macular hole development and subsequently degenerate.

Ciliary Body and Choroidal Detachment after Laser Photocoagulation for Diabetic Retinopathy: A High-frequency Ultrasound Study

OBJECTIVE The purpose of the study is to clarify the manifestation of the ciliary body after retinal photocoagulation for diabetic retinopathy. DESIGN Ultrasound biomicroscopy (UBM) was applied to obtain the tomographic features of the anterior ocular segment. PARTICIPANTS Twenty-one eyes of 17 consecutive patients with diabetic retinopathy were included in this study. INTERVENTION These eyes were treated by panretinal photocoagulation divided in four sessions. In the first session, the nasal quadrant of the fundus was treated with argon or dye (590 nm) laser totaling 208 to 331 spots per eye. MAIN OUTCOME MEASURES The eyes were examined by UBM before, immediately after, 3, and 7 days after the first session of photocoagulation. RESULTS Three days after photocoagulation, ciliochoroidal detachment was observed in 19 eyes (90%). The detachment was present along the whole circumference. The ciliary detachment was most prominent in the pars plana in 19 eyes and extended to the pars plicata in 9 eyes. It spontaneously had disappeared 7 days after photocoagulation. CONCLUSIONS Ciliochoroidal detachment was a very frequent feature after sector photocoagulation in diabetic eyes. Although this complication was asymptomatic and transient so far, this potential hazard merits due attention in the planning of panretinal photocoagulation in diabetic eyes.

Fluorescein fundus angiography with scanning laser ophthalmoscope. Visibility of leukocytes and platelets in perifoveal capillaries.

The authors performed fluorescein fundus angiography in 130 eyes using a scanning laser ophthalmoscope (SLO). Capillaries were observed in the perifoveal area in 63 eyes. In these 63 eyes, numerous fluorescent dots were seen flowing through the capillaries. This feature allowed identification of the direction and velocity of blood flow in the retinal capillaries. The distance from 1 dot to the next was widely variable and averaged 100 microM. The velocity of flow was faster in precapillary arterioles, slower in capillaries, and again faster in postcapillary venules. The dots were much more numerous in an eye with leukemia and less numerous in an eye with idiopathic thrombocytopenic purpura. Staining of whole blood from three healthy persons with fluorescein sodium resulted in prompt and intense staining of leukocytes and platelets. These findings indicate that the observed fluorescent dots in perifoveal capillaries correspond to leukocytes and platelets in the circulating blood.

Formation of retinochoroidal collaterals in central retinal vein occlusion

PURPOSE To demonstrate the drainage routes that compensate the venous congestion in central retinal vein occlusion. METHODS Indocyanine green angiography was performed in 13 eyes of 13 patients with central retinal vein occlusion at the involutional stage using a scanning laser ophthalmoscope. The interval between onset of central retinal vein occlusion and indocyanine green angiography ranged from 1.0 to 9.3 years (mean, 3.6 years). Panoramic indocyanine green angiograms that covered the entire choroidal vasculature were produced by composing regional angiograms. RESULTS Retinochoroidal collateral routes were found in 10 eyes that had papillary vascular loops. They were not observed in three eyes that did not have the vascular loops. Papillary vascular loops served as the collaterals to connect retinal veins and choroidal veins. The blood in the retinal veins was drained through the papillary vascular loops into the choroidal veins. These choroidal veins were selectively dilated and acted as drainage routes to the vortex veins. Nasal vortex veins served as extraocular exits of the drainage routes in all 10 eyes, and temporal vortex veins served as extraocular exits of the drainage routes in three of the 10 eyes. CONCLUSIONS In central retinal vein occlusion with papillary loops, blood in the retinal veins ultimately drained into the vortex veins through the retinochoroidal collaterals.