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OBJECTIVE: To describe the clinical presentation and management of erosion and intrusion of silicone rubber implants that are used in scleral buckling procedures for the treatment of retinal detachment. METHODS: The authors identified four patients from their practices during the last 20 years (1978-1998) who had erosion or intrusion of silicone rubber scleral buckles that were used to manage retinal detachment. Approximately 4400 scleral buckling procedures were performed during this period. A retrospective review of the medical records of all patients was performed. Factors that influenced management decisions concerning the intruding buckle are emphasized. RESULTS: All four patients had myopia. The interval between placement of the scleral buckle and development of intrusion ranged from 1 to 20 years. The buckles were intrascleral in three cases and episcleral in one. Recurrent detachment and vitreous hemorrhage were indications for surgical intervention in three cases. After the surgical removal of buckling elements, visual acuity stabilized in all patients and the retina remained attached in all cases. CONCLUSIONS: Erosion and intrusion of scleral buckle are rare complications of scleral buckling procedures. The intruding buckle may be left intact unless there is significant threat to the integrity of ocular structures, recurrent detachment, or hemorrhage. Manipulation of the encircling band or buckle does not necessarily alter the visual acuity or the status of the retina.

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Assessment of ocular blood flow using laser based instruments is a rapidly emerging area of ophthalmic diagnosis. In this article, six specific laser based instruments are described and compared in terms of appropriate target vasculature and measured hemodynamic parameters. Described are retinal laser Doppler instruments, laser Doppler instruments for assessment of the optic nerve head microcirculation, and laser speckle instruments. © 1998 Society of Photo-Optical Instrumentation Engineers.

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BACKGROUND AND OBJECTIVE: The goal was to utilize ultrasound-guided cryotherapy as an immediate, low-risk, noninvasive, precise method of treating retinal tears obscured by vitreous hemorrhage. PATIENTS AND METHODS: Eleven patients with sudden onset of vitreous hemorrhage were referred for diagnosis and management. Ophthalmoscopy with scleral depression was unsuccessful at localizing peripheral retinal tears, and all of the patients were examined with ultrasound using the techniques of standardized echography. The cryoprobe was positioned for cryotherapy using both transverse and longitudinal B-scan approaches following the indentation of the globe as it appeared on the oscilloscope. RESULTS: On follow-up examination after the vitreous hemorrhage cleared, 10 of the 11 tears were examined by ophthalmoscopy and were thought to have been adequately treated. One patient had a retinal detachment after remaining stable for 3 months. Two patients were treated with laser to enhance the cryotherapy seal. One patient was observed by another physician and underwent vitrectomy due to vitreous hemorrhage that persisted 2 months following cryotherapy. After vitrectomy, the physician reported a successful cryotherapy reaction at the treated tear. One final patient in the series required vitrectomy and scleral buckle before the hemorrhage had cleared, and the treatment did not appear to be complete. CONCLUSION: Ultrasound-guided cryotherapy provides a noninvasive, inexpensive treatment alternative for retinal tears obscured by vitreous hemorrhage.

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BACKGROUND: The pathogenesis of idiopathic macular breaks is still uncertain. Their formation has been ascribed to anteriorly oriented intravitreous traction and to shrinkage of the prefoveal cortical vitreous. The validity of both hypotheses is considered in this paper. METHODS: In order to clarify the pathogenesis of idiopathic macular breaks 127 consecutive patients had their vitreous examined and photographed with the El Bayadi-Kajiura precorneal lens and a slit-lamp microscope. RESULTS: A comparison with 127 matched controls demonstrated that the vitreous was significantly more often attached in eyes with a macular break than in controls (P < 0.01). In eyes with a macular break the vitreous was significantly more often attached in early cases (Gass stage 1) than in Gass stages 3 and 4 (P < 0.01). Still photographs and observation of the movements of the operculum demonstrated that, in some cases of stage 3 and also in stage 4, it moved inside the partially liquefied posterior vitreous, anteriorly to the retinal surface and frequently without evidence of posterior vitreous detachment over the macular area. The following anatomical features characterize the vitreomacular area: extremely thin hyaloid membrane (< 100 microns) and inner limiting lamina (10 nm) that adhere strongly to each other and to the underlying Mueller cells. There is no evidence that these structures can shrink selectively to cause a macular break. The premacular vitreous gel contains collagen fibers that attach posteriorly to the macula and anteriorly to the vitreous base. CONCLUSIONS: Our working hypothesis is that when detachment of the posterior vitreous is abnormally delayed, anteroposterior traction by collagen fibers may pull a foveal operculum off the retina. Our observations make this hypothesis attractive. However, the generally accepted hypothesis of Johnson and Gass cannot be entirely dismissed. In reality, since the two hypotheses are not mutually exclusive, they may both the partially correct.

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PURPOSE: To evaluate the mechanism of spontaneous resolution of foveal detachments and idiopathic macular breaks. METHODS: We reviewed the records of 139 consecutive eyes (94 patients) with either a foveal detachment or a macular break in patients who were examined between 1989 and 1992. There were 26 men and 68 women (mean age, 66.9 +/- 6.9 years). They were either unoperated on or observed during the period that preceded surgery. Each patient underwent complete ophthalmic examination in addition to slit-lamp photography of the vitreomacular interface and microperimetry with the scanning laser ophthalmoscope. RESULTS: Eight eyes demonstrated spontaneous resolution. A foveal detachment was noted in five eyes (five patients) and a stage 2 macular break in three eyes (three patients). The mean duration of observation was 33 months (range, one to 144 months). Resolution of the foveal detachments occurred without the development of posterior vitreous detachment. In each eye, the presence of a pseudo-operculum, indicating vitreofoveal separation, was accompanied by flattening of the foveal detachment without detectable posterior vitreous detachment. The three eyes with stage 2 macular break resolved after premature development of a posterior vitreous detachment. CONCLUSIONS: Foveal detachment and macular break resolution seem to result from the release or weakening of vitreous traction on the fovea. Reattachment of the foveal retina preserves fair to good visual acuity. Surgical intervention is contraindicated (1) in eyes in which foveal detachment flattens and develops a pseudo-operculum and (2) when a posterior vitreous detachment develops in an eye with a stage 2 macular break. Careful biomicroscopic vitreous examination and microperimetry with the scanning laser ophthalmoscope are extremely useful methods for adequate examination of these patients.

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We used vitreous videography in conjunction with the scanning laser ophthalmoscope (SLO) to evaluate the pathogenesis of idiopathic macular breaks. The fundamental aspect of this method is videographic documentation of the mobile posterior vitreous and an operculum. The high reflectivity from the vitreous gel using the SLO clearly showed the mobility of the operculum and the posterior vitreous in the idiopathic macular breaks. In some cases without posterior vitreous detachment, the operculum initially was suspended superior to the macular break and anterior to the retinal surface. Upon ocular movement, the operculum moved down smoothly in front of the macular break. The findings of these vitreous videographs using the SLO suggest that anteriorly oriented vitreous traction is one cause of idiopathic macular breaks.

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Three patients, 2 males and 1 female, with intrasellar, hypersecretive pituitary adenoma were studied. Blood hypertension was present in all and hyperglycemia in 2 (1 male, 1 female). None had neurological signs of compression of the optic disk or chiasma. One patient showed bilateral circumpapillary and multiple retinal pigment epithelium (RPE) detachment with pooling defects and intraretinal leakage from small retinal arterioles. Another had loss of foveolar, macular and retinal reflexes in the right eye; negligible RPE changes became visible with fluorescein angiography. The third, who had developed malignant hypertension, manifested bilateral hypertensive neuroretinopathy and papilledema. The simultaneous improvement of general and ocular symptoms after removal of the pituitary tumor makes a causal relationship possible and even very likely, between the underlying disorder and fundus abnormalities.

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PURPOSE: To investigate the relationship between the defect in the premacular cortical vitreous detached from the retina and the development of idiopathic premacular fibrosis. METHODS: One hundred six consecutive patients (106 eyes) with posterior vitreous detachment but no other ocular disorders were prospectively studied. All follow-up periods were longer than 6 months. The vitreous condition was studied using an aspherical, +58.6-diopter preset lens with a slit-lamp. RESULTS: The detached premacular cortical vitreous was a continuous, unbroken sheet in 93 (88%) of the 106 eyes; in 13 (12%) eyes, the detached premacular cortical vitreous had an oval or round defect ranging from 4 to 7 disc diameters over the macula. At the study's conclusion, 36 (34%) of the 106 eyes had idiopathic premacular fibrosis; 70 (66%) eyes did not. The defect in the detached premacular vitreous was observed in 9 (25%) of the 36 eyes that eventually developed idiopathic premacular fibrosis and in 4 (6%) of the 70 eyes that did not undergo such development. The incidence of the defect in the detached premacular cortical vitreous was significantly higher in eyes with idiopathic premacular fibrosis than in eyes without (P = 0.011). Nine (69%) of thirteen eyes with the defect in the detached premacular cortical vitreous developed premacular fibrosis, whereas only 25% of eyes without the defect developed it. Twenty-seven (75%) of thirty-six eyes with premacular fibrosis did not have a defect in the detached premacular cortical vitreous. CONCLUSIONS: The defect in the detached premacular cortical vitreous probably occurs because the premacular cortical vitreous remains attached to the internal limiting lamina when a posterior vitreous detachment develops. The vitreous that remains attached to the macula may be related to the development of idiopathic premacular fibrosis.

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We retrospectively reviewed the eyes of 143 patients with tractional retinal detachment caused by diabetes that had been studied biomicroscopically, and, after some exclusions, divided them into two groups: those with retinal breaks (group 1) (16 patients, 16 eyes), and those without retinal breaks (group 2) (127 patients, 161 eyes). The group 1 eyes were further divided into three subgroups: those with retinal tears from limited anteroposterior vitreous traction (subgroup A), those with macular holes in an area without posterior vitreous detachment (subgroup B), and those with oval retinal holes anterior to the anteroposterior vitreous traction (subgroup C). Subgroup C comprised most of the eyes in group 1 (10 eyes) and was the only subgroup that we compared with group 2. Significant differences between subgroup C and group 2 were found in terms of the extent of tractional retinal detachment (P = .002) and the degree of preretinal fibrosis (P = .009). These data suggest that large tractional retinal detachments and extensive preretinal fibrosis are significant risk factors for the development of retinal breaks in proliferative diabetic retinopathy.

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PURPOSE: Variations in vitreomacular adhesions and the significance of a hole in the premacular hyaloid membrane were studied clinically to better understand vitreomacular pathology. METHODS: With an El-Bayadi-Kajiura aspheric preset lens, the authors used a vitreous examination technique on 96 eyes, which were divided into three groups. Findings were recorded photographically. RESULTS: Group 1 (25 eyes, 26%) included eyes with a partial posterior vitreous detachment and a residual vitreomacular attachment, but no hole in the premacular hyaloid. All eyes in this group, except one, showed another complication. Diabetic retinopathy and retinal vein occlusion were the most frequent problems noted. Premacular fibrosis, often present in these eyes, may have been precipitated by a vascular complication in the retina. In groups 2 and 3 (71 eyes, 74%), a hole was seen in the premacular hyaloid. Group 2 (46 eyes, 48%) comprised eyes showing a partial posterior vitreous detachment with a strand of vitreous that extruded through the hole in the posterior hyaloid and adhered to the macula. In group 3 (25 eyes, 26%), the hole in the premacular hyaloid was accompanied by a total posterior vitrous detachment. The most common complication noted in eyes in groups 2 and 3 was premacular fibrosis (34 of 71 eyes, 47.9%). The persistence of a residual vitreous attachment to the macula was accompanied by a significantly greater frequency of visual acuity equal to or worse than 20/200. CONCLUSIONS: Variations in vitreomacular pathology seem to result from differences in the strength of the vitreomacular adhesion and in the process of vitreous liquefaction and shrinkage. In patients with a hole in the premacular hyaloid membrane, the vitreomacular attachment is stronger than the vitreous attachment to other parts of the retina. The latter feature may cause visual acuity deterioration. When there is a hole in the premacular hyaloid membrane, the presence or absence of a vitreomacular adhesion may affect the prognosis for macular function.

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I present what, in my opinion, is the optimal technique of managing primary simple retinal breaks and retinal detachment. For the preoperative examination, I recommend indirect stereoscopic ophthalmoscopy with scleral depression. The macula and suspected small peripheral breaks are studied with the biomicroscope and a three-mirror contact lens. Retinal breaks without retinal detachment are treated with cryotherapy if they are located anteriorly; with laser photocoagulation if they are posterior. Breaks with frank detachment can be treated with Lincoff's balloon, a procedure I prefer over pneumatic retinopexy. Multiple retinal breaks and those associated with fairly extensive chorioretinal degeneration are best treated with a permanent scleral buckling, the various modalities of which, along with their indications, I discuss in some detail.

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The clinical entity of posterior vitreoschisis, splitting of the posterior cortical vitreous, is not well known. We confirmed its presence biomicroscopically in cases with posterior vitreous detachment and found it mostly associated with retinal vascular diseases, usually manifesting as two dense vitreous membranes with defects. When posterior vitreoschisis develops in an otherwise normal eye, it may not manifest as two membranes, but can form a crescent-shaped, optically empty space in the posterior vitreous cavity. Because its management is different, posterior vitreoschisis should be differentiated from other, apparently similar, conditions, especially posterior vitreous detachment.

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