Cause Of Permanent Loss Research Articles

The Visual Outcome of Gunshot Injury after Last Civil War in Tobruk-Libya: A Retrospective Study

Ocular trauma is one of the most common causes of acquired blindness. This study aims to determine the epidemiology of ocular trauma in all the age groups in Tobruk Medical Centre- Libya. A retrospective study was conducted in our hospital for one year and all the aged group presenting with ocular trauma in the Ophthalmology and Emergency Departments were enrolled in the study. Age, sex distribution, presentation duration, mode of injury, type of injury, and final visual outcome were analyzed. There were 201 patients, 76% of the patients were male. Injuries usually occurred at home (54%) followed by accidents at workplaces (18%), car accidents (10.5%), fighting (15%), and at school (2.5%). There were 100/201 patients (49%) of cases that required hospital admission and (40.8%) needed surgical interventions. The most common traumas were blunt trauma in 124/201 patients (61.7%). Penetrating trauma with an intraocular foreign body (IOFB) accounted for (11.5%) of cases. The visual outcome was recorded in 200 patients. 22/201 patients (11%) ended with severe impairment of vision (vision hand movement (HM) or less). Blindness with no perception of light (no PL) was the result in 3.5% of trauma cases, while 11/16 patients (86%) with gunshot injuries through fighting have complete irreversible blindness (no PL). We concluded, that most open-globe injuries can cause severe vision impairment. In this study, gunshot injury is the leading cause of permanent loss of vision.

Optimized convolutional neural network for glaucoma detection with improved optic-cup segmentation

Glaucoma is the foremost cause of permanent loss of visioahn; it develops slowly with no discernible sign. Early glaucoma recognition is critical because it might aid to slow the progression of the disease. Customary schemes are less precise and manual. As a result, automatic glaucoma analysis is required to identify glaucoma at the earliest with greater precision. The purpose here is to bring in a new scheme in which pre-processing is done using Gaussian filtering, which aids in the removal of unwanted noise in images. Then Optic Cup segmentation is performed using the Modified Level Set Algorithm. Followed by segmentation, the morphological features (disc area, cup area, and blood vessel), as well as non-morphological features (Color, Shape, and Modified LBP), are derived. The Blood vessel thickness is 5 to 100 micrometers. These features are then classified using the Optimized CNN framework, where the weights get optimized via the Self Adaptive Butterfly Optimization Algorithm (SA-BOA). The precision of the developed approach was 21.16%, 7.35%, 6.62%, 2.98%, 4.29%, 3.89%, 5.67%, 6.23%, 6.79%, and 1.63% better than the values obtained for conservative techniques Similarly, the adopted model's negative metrics show negligible values when compared to other models. Thus, the proposed method supremacy was validated successfully.

Looking Disease in the Eye.

The eyes are said to be the windows of the soul, but they are increasingly the door to diagnostic information that could transform the lives of millions of people. Age-related macular degeneration (AMD), diabetic retinopathy, and glaucoma are the big three causes of permanent loss of vision, while severe neurological diseases like Alzheimer's and Parkinson's are on the rise. Thanks to new technologies for imaging the eye, the early signs of all of them can be detected earlier.

JNK/c-Jun-driven NLRP3 inflammasome activation in microglia contributed to retinal ganglion cells degeneration induced by indirect traumatic optic neuropathy

BackgroundIndirect traumatic optic neuropathy (ITON) is a major cause of permanent loss of vision after blunt head trauma. Neuroinflammation plays a crucial role in neurodegenerative diseases. The present study concentrated on JNK/c-Jun-driven NLRP3 inflammasome activation in microglia during the degeneration of retinal ganglion cells (RGCs) in ITON. MethodsAn impact acceleration (IA) model was employed to induce ITON, which could produce significant neurodegeneration in the visual system. Pharmacological approaches were employed to disrupt JNK and to explore whether JNK and the microglial response contribute to RGC death and axonal degeneration. ResultsOur results indicated that the ITON model induced significant RGC death and axonal degeneration and activated JNK/c-Jun signaling, which could further induce the microglial response and NLRP3 inflammasome activation. Moreover, JNK disruption is sufficient to suppress NLRP3 inflammasome activation in microglia and to prevent RGC death and axonal degeneration. ConclusionsITON could promote JNK/c-Jun signaling, which further activates the NLRP3 inflammasome in microglia and contributes to the degeneration of axons and death of RGCs. JNK inhibition is able to suppress the inflammatory reaction and improve RGC survival. Although further work is needed to determine whether pharmacological inhibition of the NLRP3 inflammasome can prevent ITON, our findings indicated that such intervention could be promising for translational work.

Glaucoma management in Boston keratoprosthesis type I recipients

To review the literature on management of glaucoma in Boston keratoprosthesis type I recipients. Glaucoma is a prevalent and important cause of permanent loss of sight in Boston keratoprosthesis recipients. The management of glaucoma is challenging as there are no reliable and accurate means to monitor the intraocular pressure (IOP) in these patients, and no standardized protocols exist regarding management. Because a significant number of patients require glaucoma drainage device placement, further studies are needed to determine ways to reduce the risk of shunt-associated complications. Surgical adjustments including posterior shunt placement, adjunctive corneal patch graft, and selection of a different size bandage contact lens can help reduce shunt-associated complications. Anterior segment optical coherence tomography is useful in elucidating the mechanisms of failure to control IOP. Continual innovations in imaging and IOP measurement technologies will assist surgeons' preoperative planning and postoperative management. In keratoprosthesis recipients, glaucoma often leads to permanent loss of sight. It is imperative that these patients be monitored with vigilance by a multidisciplinary team to prevent progression. Pooled data from multiple centers and technologic innovations will assist the surgeon to design a surgical approach and postoperative management regimen for the individual recipient.

Red blood cell phosphatidylserine exposure is responsible for increased erythrocyte adhesion to endothelium in central retinal vein occlusion

Retinal vein occlusion (RVO) is a common cause of permanent loss of vision. The pathophysiology is uncertain, although enhanced erythrocyte aggregation and blood hyperviscosity have been observed. Increased red blood cell (RBC) adhesion has been associated with vascular complications in several diseases, such as sickle cell anemia, diabetes mellitus or polycythemia vera. To measure RBC adhesion to endothelial cells in RVO and to explore the molecular basis of the adhesion process. We assessed RBC adhesion to endothelial cells and adhesion molecule expression among 32 patients with RVO. Patients with disease known to alter RBC adhesion were excluded (n = 8), and further investigation was conducted in 20 patients with central retinal vein occlusion (CRVO) and four patients with retinal artery occlusion (RAO), compared with 25 normal subjects. Under static conditions, adhesion of CRVO RBC was increased (135 ± 7 × 10(2) mm(-2)) compared with RAO RBC (63 ± 5 × 10(2) mm(-2)) (P < 0.01) and normal control RBC (37 ± 3 × 10(2) mm(-2)) (P < 0.001). Under flow conditions, CRVO RBC adhered in greater numbers than normal RBC (P < 0.001). Phosphatidylserine (PS) expression on CRVO RBC was 2.4-fold higher than controls and correlated with RBC adhesion (P = 0.001). In static conditions, specific antibodies against PS receptor and annexin V inhibited RBC adhesion. In flow conditions, the inhibitory effect was in the same range with antibodies but was 2-fold higher with annexin V. Increased CRVO RBC adhesion is mediated by PS RBC and endothelial PS receptor. This phenomenon may be one of the factors responsible for CRVO.

Aniridie-Intraokularlinsen bei Augen mit traumatischen Irisdefekten

Globe injuries frequently are the cause of permanent loss of visual function. Especially ruptures of the globe have a 50 times lower chance of achieving a final visual acuity better than 20/200 as compared to contusions of the globe. Besides injury to the retina and choroids, injury of the iris-lens diaphragm plays an important role for visual rehabilitation (10% iris defects and 1% aniridia after blunt trauma). Against this background the surgical results after implantation of aniridia intraocular lenses were investigated. Eleven patients (41.9+/-19.6 years of age) after globe injury (three ruptures of the globe, eight penetrating injuries with trauma of the iris) were implanted with an aniridia IOL. The implantation of an aniridia IOL was performed on average 1.0+/-0.6 years (range: 0.4-2.3 years) after the primary injury. In ten eyes an aniridia IOL model HMK ANI 2 (Ophtec/Polytech) was implanted and in one eye an aniridia IOL model 67 (Morcher). Most patients were very satisfied with the results achieved (average corrected visual acuity 0.48; 0.05-1.0). Of the operated eyes, 63% reached a visual acuity > or = 0.4. All patients noticed a significant reduction in glare disability as compared to the preoperative condition. The incidence of secondary glaucoma remained unchanged after the secondary implantation. One patient demonstrated retinal detachment 3 months after receiving the secondary implant, which was successfully treated with vitrectomy and gas tamponade. The implantation of aniridia IOLs seems to be a beneficial therapeutic option in post-traumatic eyes with partial or complete aniridia and aphakia with good visual recovery. During the postoperative follow-up special attention must be paid to sufficient regulation of intraocular pressure and to the retinal situation.

Peritoneal transport in CAPD patients with permanent loss of ultrafiltration capacity

During a 10 year period, 14 out of 227 patients (6.2%) undergoing continuous ambulatory peritoneal dialysis (CAPD) developed permanent loss of ultrafiltration capacity (UFC). The risk of UFC loss increased from 2.6% after one year to 30.9% after six years of treatment. A six hour, single dwell study with glucose 3.86% dialysis fluid was carried out in nine of the UFC loss patients and in 18 CAPD patients with normal UFC. Intraperitoneal dialysate volumes were calculated using 131I-tagged albumin (RISA) as volume marker with a correction applied for its elimination from the peritoneal cavity. The RISA elimination coefficient (KE), which can serve as an estimation of the upper limit of the lymphatic flow, was also calculated. Diffusive mass transport coefficients (KBD) for investigated solutes (glucose, creatinine, urea, potassium, total protein, albumin and beta 2-microglobulin) were calculated during a period of dialysate isovolemia. Two patterns of UFC loss were observed: (a) seven patients had high KBD values for small solutes resulting in rapid uptake of glucose, whereas KBD values for proteins were normal; (b) two patients had normal KBD values but a threefold increase both in the fluid reabsorption rate and KE. We conclude that loss of the osmotic driving force (due to increased diffusive mass transport for small solutes) and increased fluid reabsorption (possibly due to increased lymphatic reabsorption) are the two major causes of permanent loss of UFC in CAPD patients.