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Biomedical subjects

Charanjit Sethi

Publications and source records attributed to Charanjit Sethi.

5 recordsLinked to original sources

Intraretinal and periretinal pathology in anterior proliferative vitreoretinopathy.

OBJECTIVES: To determine the intraretinal and periretinal pathological changes in early anterior proliferative vitreoretinopathy (APVR). DESIGN: Observational case series. PARTICIPANTS: Eighteen patients undergoing retinectomy for APVR. METHODS: Retinectomy specimens removed at vitrectomy surgery were analysed by (a) semithin light microscopy, (b) immunohistochemistry and (c) electron microscopy. RESULTS: The specimens showed consistent outer retinal degenerative changes, marked Muller cell hypertrophy and glial continuity to epiretinal membranes. Photoreceptor outer and inner segments were markedly disrupted and occasional photoreceptor nuclear had pyknosis and chromatin clumping consistent with apoptosis. Muller cells expressed upregulated levels of glial fibrillary acid protein (GFAP) and extended through glial bridges to complex epiretinal membranes which in some areas had a bilaminar structure with a glial-negative inner lamina. CONCLUSION: Retinal degeneration and photoreceptor apoptosis occur in retinal detachment complicated by proliferative vitreoretinopathy (PVR), although during the early stages of the process neural retinal cells remain present, suggesting potential for recovery. The intraretinal glial response appears to be centrally involved in the formation of contractile epiretinal membranes. The retina retains the capacity for a degree of functional recovery following surgery for PVR. Surgical separation of anterior epiretinal membranes in PVR may be difficult and incomplete and alternative surgical strategies may be necessary to prevent recurrence.

Adolescent↗

Staining and peeling of the internal limiting membrane in the cat eye.

PURPOSE: To investigate the cat vitreomacular interface using trypan blue (TB) and indocyanine green (ICG) and to determine the validity of the cat model in terms of staining and peeling of the internal limiting membrane (ILM). METHODS: Lensectomy and vitrectomy were performed in four eyes of two cats. The ILM of two eyes was stained with TB (0.15%). ILM peeling was performed in one eye. Two eyes were stained with ICG (0.5%). One eye was illuminated for 3 min. Light and transmission electron microscopy and confocal microscopy were performed. RESULTS: Clinically, both dyes stained the cat ILM similar to human ILM. TB staining resulted in a normal ultrastructure and antigenity of the retina. ILM peeling was associated with intraretinal bleeding. There were fragments of Müller cells adherent to the retinal side of the ILM, and Müller cell endfeet were ruptured and avulsed. ICG staining of the ILM followed by illumination caused severe inner retinal damage. ICG without illumination resulted in focal ILM detachments associated with tearing of Müller cell endfeet. CONCLUSIONS: The cat can be used as a model to study the effect of TB and ICG on the central area of the cat retina, as previous results from clinical and experimental postmortem settings in human eyes were confirmed in the current study. Peeling of the ILM as a sheet as performed in human macular surgery is not feasible. Differences in the ultrastructure of the ILM and a strong adhesion of the ILM to Müller cell endfeet may account for this observation.

Animals↗

Posterior vitreous detachment induced by microplasmin.

PURPOSE: To demonstrate the efficacy of microplasmin in inducing posterior vitreous detachment (PVD) and to evaluate the human and the feline retina after treatment. METHODS: Thirteen human donor eyes were injected with 62.5, 125, or 188 micro g microplasmin. The 13 fellow eyes received balanced salt solution. Four of the microplasmin-treated eyes received an additional intravitreal gas injection. After incubation at 37 degrees C for 30 minutes, all globes were placed in 4% paraformaldehyde. Retinal specimens were processed for scanning (SEM) and transmission (TEM) electron microscopy. Five feline eyes were injected with 14.5- or 25- micro g microplasmin. Animals were killed after 1 day, 3 days, or 3 weeks, and retinal specimens were evaluated by electron and confocal microscopy. RESULTS: In all control eyes, SEM demonstrated the cortical vitreous covering the inner limiting membrane (ILM). Intravitreal injection of 125 or 188 micro g microplasmin resulted in complete PVD. After treatment with 62.5 micro g microplasmin, SEM revealed collagen fibrils covering the ILM. Additional gas injection did not change the dose necessary for PVD. In vivo in cats, 25 micro g microplasmin resulted in complete PVD after 3 days. After 3 weeks, there was complete PVD with both doses of microplasmin. The retina and the ILM were well preserved in all eyes. CONCLUSIONS: Both after death and in vivo, microplasmin induces a dose-dependent cleavage between the vitreous cortex and the ILM without morphologic alterations of the retina. In the feline eye, there is no cellular response of retinal glial cells or neurons.

Adult↗

Acute macular pucker.

PURPOSE: To describe the presenting features, histopathology, and surgical outcome in a group of patients with rapidly progressive macular pucker. DESIGN: Retrospective interventional noncomparative case series. PARTICIPANTS: Five patients. METHODS: Review of case notes and the existing literature. RESULTS: All five patients had rapidly progressive visual loss and metamorphopsia over 2 weeks to 3 months, secondary to macular pucker after retinal tears or detachment. Vitrectomy and epiretinal membrane removal was performed within 1 month of diagnosis. In the absence of complications, there was rapid recovery of the visual acuity with resolution of metamorphopsia within 6 weeks to 3 months. Surgical complications limited the visual outcome in two cases. Histopathologic examination of epiretinal membrane removed from two of the cases suggests that these tend to form tubuloacinar structures and contain more retinal pigment epithelium-derived cells than tissue excised from cases with idiopathic macular pucker. CONCLUSIONS: Patients with acute macular pucker have precipitous visual loss caused by epiretinal membrane formation after retinal tear or detachment. Early surgery in these patients results in rapid recovery of visual acuity and resolution of metamorphopsia. The clinical features and comparative immunohistochemistry suggest that acute macular pucker is a distinct clinicopathologic entity.

Acute Disease↗

Matrix metalloproteinases in disease and repair processes in the anterior segment.

The pathogenesis of many anterior segment disorders and ocular complications following surgery are secondary to the wound healing response. The extent of clinical damage observed is closely related to the amount of scarring and tissue contraction. Matrix metalloproteinases (MMPs) are a family of enzymes that play a vital role in all stages of the wound healing process. They degrade all extracellular matrix components and also have the ability to synthesize collagen and extracellular matrix members, and are therefore important in the remodeling of a wound. Overexpression of MMPs results in excessive extracellular matrix degradation, leading to tissue destruction and loss of organ function. In the case of the anterior segment, this may mean the loss of visual function. This review focuses on the role MMPs have in the development of various anterior segment disorders. The importance of MMPs in the wound healing response and its potential modulation to manipulate the scarring response is being recognized, and current developments will be described.

Anterior Eye Segment↗