Macular pucker after retinal detachment surgery.

To better understand postsurgical macular pucker in rhegmatogenous retinal detachment, we reviewed a consecutive series of 277 eyes in 268 patients in whom retinal detachment had spared the macular area and in whom no preretinal membrane with distortion of the retinal vessels had been present preoperatively. Postoperatively, 17 eyes (6.1%) developed obvious macular pucker; 260 eyes (93.9%) did not. Using the Mantel-Haenszel chi-square test, we found that patient age, preoperative vitreous hemorrhage, large retinal breaks of more than three disc diameters, and cryoapplication were significant precipitating factors of postoperative macular pucker. These findings are consistent with the view that dispersion of retinal pigment epithelial cells through the retinal break into the vitreous cavity is the major cause of this disorder. Minimal use of cryotherapy is recommended in treating elderly patients who have a large retinal break or a preoperative vitreous hemorrhage.     

Prognosis of foveal splitting rhegmatogenous retinal detachments

Retrospectively reviewing 4,966 patients with rhegmatogenous retinal detachments, we identified 21 patients with foveal split detachments who had no coexisting macular disease and who had been followed at least 6 months postoperatively. All detached retinas were anatomically reattached with one operation. The average preoperative and postoperative visual acuity was 20/50. Because eyes with foveal split detachments have a good visual prognosis when the retinas are anatomically reattached, we recommend that they be treated urgently, as if they had a macular-spared detachment.     

Retinal detachment in Morning Glory syndrome

A 9-year-old girl with bilateral Morning Glory syndrome developed bilateral bullous retinal detachment. There was a small break on the temporal margin of the disc in the left eye. The retinal detachment in this eye was successfully treated by drainage of the subretinal fluid, vitrectomy, intravitreal air injection, and photocoagulation around the edge of the anomalous disc. It is suggested that some retinal detachments in the Morning Glory syndrome may be rhegmatogenous in nature.     

The relationship between retina surgery and preretinal macular fibrosis

A prospective study of 440 eyes of 220 patients following successful operations for primary rhegmatogenous retinal detachment (132 eyes) and prophylactic operations for retinal breaks (103 eyes) revealed an incidence of preretinal macular fibrosis (PRMF) of 47% after scleral buckling surgery and 42% after prophylactic laser or cryopexy. The incidence of PRMF was significantly greater in aphakic vs phakic detachments, in detachments with operculated vs horseshoe breaks, in detachments with horseshoe breaks vs lattice degeneration, in detachments involving the macula, after scleral buckling with cryotherapy vs diathermy, and after prophylactic treatment of retinal breaks of fellow eyes with retinal detachment or retinal breaks that had developed postoperative PRMF. Analysis of the data suggests that PRMF is most likely a result of the retinal break, detachment, and subsequent treatment.     

Nd:YAG laser augmented pneumatic retinopexy

We present the first ten consecutive cases of rhegmatogenous retinal detachment treated by one surgeon using pneumatic retinopexy with Nd:YAG laser disruption of vitreoretinal adhesions. In nine cases the retina has remained reattached, after a follow-up period of 11 to 18 months. The use of the Nd:YAG laser to disrupt vitreoretinal adhesions at the sites of retinal tears is discussed.     

In vitro modulation of tubular cyst regression in murine polycystic kidney disease

Recent studies in a murine model of genetically-determined polycystic kidney disease, the CPK mouse, have suggested that alterations in renal Na-K ATPase activity in concert with tubular epithelial hyperplasia have pathogenic import in proximal tubular cyst formation. In the current study, we therefore studied the relative roles of Na-K ATPase activity, tubular epithelial hyperplasia, and basal lamina alterations during in vitro modulation of proximal tubular cyst regression during serum-free organ culture of newborn CPK kidneys. Under basal in vitro conditions, regression of CPK proximal tubular cysts was demonstrated in association with progressive decreases in Na-K ATPase activity and tubular epithelial hyperplasia. The pattern of proximal tubular cyst regression was modified by: a) Na-K ATPase activity induction with triiodothyronine, which promoted proximal tubular cystogenesis; and b) Na-K ATPase activity inhibition with ouabain, which blocked the effects of T3 on the process of cyst formation. Modulation of proximal tubular cystogenesis by Na-K ATPase induction and inhibition were accomplished without significant changes in proximal tubular epithelial hyperplasia or expression of basal lamina components. We conclude that increased Na pump activity may have a significant role in proximal tubular cyst formation and progressive enlargement in the CPK mouse.     

Sodium-potassium ATPase activity mediates cyst formation in metanephric organ culture

To study the possible role of altered transtubular transport in renal tubular cyst formation, the ontogeny of renal Na-K ATPase was studied during glucocorticoid-induced cystic metanephric tubular development in serum-free, murine organ culture (SFMOC). Utilizing an enzyme-linked kinetic microassay, a developmental profile of total ATPase and specific Na-K ATPase activity was established for control (CON) and glucocorticoid-induced cystic organ culture (CY) explants. During 120 hr of CON and CY organ culture nephrogenesis total Na-K ATPase activity, specific Na-K ATPase activity, and the Na-K ATPase: total ATPase ratio progressively increased, simulating normal in vivo murine enzyme development. However, from 48 to 120 hr of organ culture, CY showed significant increases in Na-K ATPase activity when compared to CON at similar stages of development. Na-K ATPase activity (expressed as nmoles . min-1 . mg protein -1, mean +/- SD) was, at: 48 hr, CY 13.1 +/- 0.7 vs. CON 11.0 +/- 0.9 (P less than 0.01); 72 hr, CY 16.4 +/- 1.1 vs. CON 12.2 +/- 0.7 (P less than 0.001); 96 hr, CY 35.4 +/- 4.9 vs. CON 13.7 +/- 0.4 (P less than 0.001); and 120 hr, CY 26.1 +/- 1.4 vs. CON 16.3 +/- 0.9 (P less than 0.001). The initial differences in CY enzyme activity preceded the earliest ultrastructural evidence of cyst formation by 18 to 24 hr, while subsequent increases in Na-K ATPase activity in CY paralleled progressive tubular cyst formation. Tubular cyst formation in CY could be largely prevented by daily incubation of explants with ouabain, 0.2 mM (final concentration) X 120 min, without deleterious effects on overall metanephric development.(ABSTRACT TRUNCATED AT 250 WORDS)     

BB-gun injuries to the eye

Thirteen patients with BB-gun injuries to the eye are reported. Included are nine instances of double perforation, one case of vitreous hemorrhage, a case of late rhegmatogenous retinal detachment, one of retinitis sclopetaria, and a case of an intraocular shell casing introduced indirectly via an inadvertant BB-gun discharge into a drawer of bullets. Among the nine globes with double perforation, seven eyes were irreparably damaged and eventually enucleated, while two remained with hand motions vision. Despite modern vitrectomy techniques, double perforating BB-gun injuries to the globe imply a grim prognosis.     

Intravitreous silicone balloon: an experimental study.

A specially designed silicone balloon, expanded in vivo with normal saline, was tested for possible use as a retinal tamponade in desperate cases of rhegmatogenous retinal detachment. In six pigmented rabbits there were extensive postoperative complications, but in eight owl monkeys results were noticeably better. When the seam of the balloon was in contact with the retina there were adverse effects; seamless areas of the balloon did not appear to disturb the retina. Histopathologic studies indicated that excessive expansion of the balloon can cause significant damage, but that carefully controlled expansion can probably minimize complications. The presence of the balloon appears to alter electroretinographic response, but without necessarily causing histopathologic changes. Balloons of this type have been used in treatment of a small number of otherwise inoperable cases of retinal detachment with promising results.     

Sudden vision loss following retinal detachment surgery.

A 22-year-old man with Eales' disease with secondary rhegmatogenous retinal detachment with a break five disc diameters from the disc underwent radial scleral buckling using a silicone sponge episcleral explant with local cryopexy. Five hours after surgery the patient had no light perception. There was no intraoperative or postoperative rise of intraocular pressure or central retinal artery ischemia. Immediate removal of the explant brought a return of light perception and postoperative visual acuity improvement. The episcleral explant may have caused the direct optic nerve trauma that resulted in loss of vision.     

Phospholipase-C and Na-K ATPase activation by cyclosporine and FK506 in LLC-PK1, cells. Possible implications in blood pressure regulation.

Enhanced Na+ and water reabsorption by proximal tubular epithelial cells plays an important role in the development of systemic hypertension associated with cyclosporine immunosuppression. Since such Na+ reabsorption is subserved by sodium-potassium adenosine triphosphatase (Na-K ATPase), the current study compared the acute effects of hydrocortisone (H), cyclosporine, and FK506 on cultured LLC-PK1 cell viability and on Na-K ATPase activity. Phospholipase-C (PL-C) activity was also investigated because of its possible regulatory effect on Na-K ATPase activity. Culture medium containing low (5 nM, 4.1 ng/ml) or high (10 nM) concentrations of FK506 plus cyclosporine at 415 microM (500 ng/ml) resulted in cell death, whereas cyclosporine concentrations of 83 microM plus 5 nM or 10 nM FK506, or isolated use of the two drugs at high dosages, did not affect cell viability. As compared with controls, cyclosporine increased Na-K ATPase activity, particularly with addition of H (P less than 0.01). In contrast, FK506 reduced the specific activity of both PL-cyclosporine and Na-K ATPase (P less than 0.001-0.01); addition of H to FK506 resulted in an even greater fall in both the enzyme activities (P less than 0.001). Na-K ATPase activity increased in cell homogenates briefly incubated with cyclosporine in the ATPase reaction mixture (P less than 0.05) while FK506 reduced such enzyme activity (P less than 0.05), suggesting a direct effect of these agents on pump activity. These data in LLC-PK1 cells pocessing proximal tubular epithelial cell characteristics indicate that the combined use of cyclosporine plus FK506 may be very deleterious to viability in such cells. The opposing effects of cyclosporine and FK506 on PL-cyclosporine and Na-K ATPase activities and the possible potentiating effect of H on such responses are speculated to affect Na+ and water homeostasis in a manner that may explain differences in systemic blood pressure due to these agents.     

Significant difference in the effect of acute saline loading on plasma Na-K ATPase inhibitor and blood pressure between children and adults with essential hypertension.

Twenty-one male children and 3 male adults with essential hypertension were infused with physiological saline solution (15 ml/kg/hr) for 1 hr after they had been supine for 90 min. The blood pressure and heart rate were monitored, and blood was taken twice before and after the infusion to measure the plasma Na-K ATPase inhibitor. After saline infusion, both the plasma Na-K ATPase inhibitor and blood pressure increased significantly in the hypertensive adults, and the number of Na pump sites decreased. However, such changes were not observed in the hypertensive children. These findings suggest that circulating Na-K ATPase inhibitor may not appear following acute saline infusion in hypertensive children unlike in hypertensive adults, and that the mechanisms regulating cell membrane sodium transport and high blood pressure may differ between hypertensive children and adults.     

Anemia and left ventricular hypertrophy in chronic kidney disease populations: a review of the current state of knowledge

The increasing awareness of the high prevalence of cardiovascular disease (CVD) in the dialysis population has led clinical nephrologists and researchers to focus their attention on processes and factors that are present in patients prior to dialysis. It is clear that many of the risk factors for kidney disease and cardiovascular disease are similar: This may account for the high prevalence of CVD within the dialysis population. However, it is evident that there are unique risk factors for CVD that are present in patients with chronic kidney disease (CKD). These unique uremia-related risk factors for CVD include anemia, hyperparathyroidism, abnormalities of mineral metabolism, and acidosis. Of note, the association of anemia, or lower levels of hemoglobin, have been consistently described in all populations with kidney disease. Left ventricular hypertrophy has long been known as an independent risk factor for death and CV events, in both the dialysis and general populations. There have been accumulating data that LVH and left ventricular (LV) growth occur prior to dialysis in patients with kidney disease, and that the prevalence of LVH in that group of patients is caused by, conventional risk factors for LVH (e.g., hypertension) as well as nonconventional risk factors such as anemia.     

Relative afferent pupillary defect in eyes with retinal detachment

Relative afferent pupillary defects were measured before and after surgery in 38 patients with unilateral rhegmatogenous retinal detachment. All 38 patients were measured preoperatively and the mean (+/- SD) pupillary defect was 1.4 +/- 0.7 log units. The afferent pupillary defect decreased in 36 of the 38 patients after successful scleral buckling operations (postoperative mean = 0.4 +/- 0.3 log units). Twenty patients had defects postoperatively of 0.3 log units or less, and seven of these had no measurable defects at all. A prediction model, using the variables of total number of peripheral quadrants detached and whether the macula was detached, yielded the following prediction equation: Relative afferent pupillary defect (log units) = 0.35 X (total quadrants) + 0.68 X macula detachment. This means that the detachment of each peripheral quadrant of retina caused about 0.35 log units of defect, whereas detachment of the macula caused 0.68 log units. The standard error of this estimate was rather large (+/- .65 log units); therefore, the size of the afferent pupillary defect can only roughly predict the extent of the retinal detachment and vice versa.     

Role of NHERF-1 in regulation of the activity of Na-K ATPase and sodium-phosphate co-transport in epithelial cells

Parathyroid hormone (PTH), acting at least in part through a cAMP signaling pathway, regulates three important transporters in the renal proximal convoluted tubule, namely Na-H exchanger 3, Na-K ATPase, and type IIa sodium phosphate cotransporter (NaPi IIa). The regulation of Na-H exchanger 3 by protein kinase A requires a protein co-factor from the sodium-hydrogen exchanger regulatory factor (NHERF) family of proteins (NHERF-1 and NHERF-2). However, the role of NHERF in PTH regulation of Na-K ATPase and NaPi IIa has not been explored. For studying the role of NHERF-1 on PTH regulation of these transporters, wild-type mNHERF-1 (1-355) or mNHERF-1 (1-325) lacking the ezrin-binding domain were expressed in proximal tubule-derived opossum kidney cells. PTH inhibited Na-K ATPase activity in cells expressing wild-type NHERF-1 associated with increased serine phosphorylation of the alpha subunit of the transporter. By contrast, in cells expressing mNHERF (1-325), the phosphorylation of the alpha subunit of Na-K ATPase was blunted and the activity of the transporter was stimulated in response to PTH. Basal sodium-dependent phosphate transport was lower in cells expressing mNHERF-1 (1-325) as compared with cells expressing mNHERF-1 (1-355). Nonetheless, there were no differences in PTH-associated inhibition of the activity or the decrease in membrane expression of the NaPi IIa in any of the cell lines. These experiments document for the first time an association between NHERF-1 and PTH regulation of Na-K ATPase in epithelial cells. These experiments also suggest that the mechanism for retrieval of NaPi IIa transporters from the apical membrane in response to cAMP does not require NHERF.     

Postoperative subretinal neovascular membrane at the drain site of a scleral buckle

A 57-year-old patient underwent a scleral buckle operation for a rhegmatogenous bullous retinal detachment. An episcleral buckle and cryotherapy were used. Drainage of subretinal fluid was performed beneath the buckle as well as posterior to the buckle, close to the posterior pole. The postoperative course was unremarkable. Eight months later, the patient developed a subretinal neovascular membrane at the drain site posterior to the buckle. This was documented by fluorescein angiography. Such membranes have not been previously documented at retinal drain sites in an ophthalmic journal.     

Age-related macular degeneration

EPIDEMIOLOGICAL AND PATHOGENIC DATA: Age-related macular degeneration (ARMD) is the first cause of blindness in industrialized countries in patients over the age of 55. Its prevalence increases with age, affecting up to 25% of the population aged over 75. The pathogenesis of this disease is not well known. Not only aging, but also other varying degrees of genetic and environmental factors are implied. CLINICAL ASPECTS: Precursors (first clinical signs of ARMD) can be observed on examination of the fundus: drusen (localized deposits of lipids and lipoproteins) and alterations in retinal pigment epithelium (RPE) (hypo- or hyperpigmentation). Two forms of complications are observed: atrophic (or "dry") and exudative (or "wet"). The atrophic form is defined by the presence of degeneration in the central RPE, choriocapillaris and photoreceptors, resulting from the enlargement and/or coalescence of small areas of peri-foveolar atrophy (or "geographic" atrophy). The exudative form, responsible for the majority of cases of blindness due to ARMD, is characterized by the appearance of choroidal new vessels, identifiable on fluorescein angiography and responsible for serous retinal detachment, edema and hemorrhage, leading to the destruction of the macular photoreceptors. FROM A THERAPEUTIC POINT OF VIEW: Treatment of the atrophic form is currently only palliative (visual aids and re-habilitation of low vision). Treatments of the exudative form having demonstrated their efficacy are laser photocoagulation and dynamic phototherapy with verteporfine, providing relative stabilization of visual acuity in around 2/3 of the eyes. Other treatments are under evaluation: anti-angiogenic treatments, surgical techniques (ablation of the new vessels, foveal translocation), new laser treatments (transpupillary thermotherapy, selective photocoagulation of the feeder vessels). Photoreceptor and pigment epithelium transplantations or implantation of microphotodiodes represent other long-term alternatives.     

Surgical repair of a traumatized shrunken eye.

A 50-year-old Japanese man underwent removal of a traumatic cataract with an intralenticular foreign body. Surgery was complicated by an unplanned extracapsular delivery of the lens and vitreous loss. Two years later, with a visual acuity of hand motions and signs of phthisis bulbi, he had a vitrectomy that cleared the media to reveal a rhegmatogenous retinal detachment. The detachment was treated by cryopexy, scleral buckling, and intraocular gas injection. One year after this combined procedure, his best corrected visual acuity was 20/400 with clear media and attached retina.     

Enzyme activity in obstructive uropathy: basis for salt wastage and the acidification defect

Unilateral ureteral obstruction results in marked changes in renal function throughout the nephron, including impaired acid and potassium secretion and salt wastage. The nephron site believed responsible for the acidification defect is the collecting duct. It has been presumed, although not demonstrated, that the cellular mechanism for the acidification defect is both a decrease in transepithelial voltage and a decrease in activity of the proton pump located at the luminal membrane. The mechanism for the abnormalities in sodium handling are thought due to alterations in Na-K ATPase activity. Our laboratory has recently mapped the profile of the N-ethylmaleimide (NEM)-sensitive ATPase and Na-K ATPase in microdissected rat nephron, documenting their presence throughout much of the nephron. In animals with acute unilateral ureteral obstruction for 18 to 24 hours, we measured NEM-sensitive ATPase and Na-K ATPase activities in several nephron sites. In all nephron segments Na-K ATPase activity was markedly decreased. In the medullary collecting duct, NEM-sensitive ATPase activity was also markedly reduced in animals with acute ureteral obstruction; in the cortical collecting duct, activity fell significantly, but to a lesser degree than was observed in the medullary collecting duct. NEM-sensitive ATPase activity was unchanged from control in the proximal convoluted tubule and in the medullary thick ascending limb; in the cortical thick ascending limb enzyme activity increased. These results demonstrate a change in both Na-K ATPase and NEM-sensitive ATPase activities as a direct consequence of a defect known to result in salt wastage and an acidification defect in humans and animals.(ABSTRACT TRUNCATED AT 250 WORDS)     

Relationship of extracranial carotid occlusive disease and central retinal artery occlusion

Central retinal artery occlusion usually results in blindness. The association between central retinal artery occlusion and extracranial carotid disease has not been clearly delineated. We reviewed the case reports of 62 patients with central retinal artery occlusion, 25 of whom underwent carotid angiography as part of the diagnostic evaluation. Fourteen of the 25 (56 percent) were found to have ipsilateral extracranial carotid disease. These patients did not generally have carotid bruits and had normal noninvasive carotid tests. Ten patients underwent ipsilateral carotid endarterectomy; these patients had either embologenic ulcerated plaque or tight stenosis of the carotid artery. There were 11 patients who showed no abnormalities on angiography. Thirteen patients who did not undergo angiography showed clinical evidence of etiologic factors, including vasculitis, an embolism of cardiac origin, and trauma. The remaining 24 patients had no diagnostic workup. Follow-up data were available in six of those patients who underwent carotid endarterectomy for a mean of 34 months; no strokes were reported. In conclusion, over half of patients with central retinal artery occlusion who undergo carotid angiography will have a carotid lesion on the ipsilateral side. This suggests that central retinal artery occlusion is a significant marker for extracranial carotid disease and should be an indication for complete carotid evaluation.