Clinical Study of Risk Factors for Diabetic Maculopathy

Aim:To determine the association between various systemic risk factors with diabetic maculopathy. Methodology:A prospective observational study was conducted on 50 patients having diabetic maculopathy. Patients with maculopathies secondary to Vitreous Haemorrhage, Ocular disorders like Glaucoma, Uveitis, Advanced Diabetic Eye Disease, Vitreo-macular traction, maculopathy along with proliferative diabetic retinopathy, ischemic maculopathy, and history of laser treatment in last six months were excluded from the study. Data was collected using a structured proforma that included name, age, sex, occupation, height, weight, history of other systemic diseases like hypertension, investigations and treatment taken in past, family history, duration of DM, smoking, hyperlipidemia, hyperglycemia and nephropathy. Results:Out of 50 patients, 38 (76%) were males and 12 (24%) were females suggestive of male predominance. Mean age of the patient was 57.36±11.65 years in males and 56.67±10.17 years in females. Among 50 patients, 19 patients had diabetes mellitus for 6-10 years duration, 14 patients had diabetes mellitus for 1-5 years, in 12 patients for 11-15 years, in 2 patients for 16-20 years, in 2 patients for 21-25 years and only 1 patient more than 25 years. Mean duration of DM was 12.2±6.1 years. Majority of patients having maculopathy had duration of DM up to 20 years. Among 50 patients, 27 patients (54%) had systemic hypertension, 37 patients (74%) had uncontrolled blood sugar level, 29 patients (58%) were found to have hyperlipidemia and 20 patients (40%) had nephropathy. Among 50 patients, pseudophakia was noted in 7 patients (14%), obesity was noted in 21patients (42%). Eleven patients (22%) were found to have anemia, 6 patients (12%) had family history of DM and 13 patients (26%) had history of smoking. Conclusion: Hyperglycemia, hypertension, duration of DM, hyperlipidemia are the major risk factors for the development and progression of diabetic maculopathy. While anemia, smoking, obesity and family history of DM is the less signi?cant risk factors

48-year-old female with sudden onset of painless diminution of vision in left eye

A 48-year-old female came to ophthalmology outpatient department with sudden onset painless diminution of vision in left eye since last 4 days, which was not associated with trauma, floaters, flashes of light, blurring of vision or any other ocular complaints. On general examination patient's pulse was 76/min that was regularly regular, and blood pressure was found to be 200/120. On ophthalmic examination, the distant vision in left eye was finger counting close to face that was not improved with refraction and in right eye was 6/6. In left eye, anterior segment examination was normal except for relative afferent pupillary defect and early cortical cataract, while fundus examination revealed findings shown in Figures 1 and 2

Endotracheal tuberculous stenosis: Ventilation rescue and bronchography guided stenting.

We present the case of a 16-year-old female patient who presented with dyspnoea, cough and noisy breathing that progressed further in hospital with the development of stridor and severe respiratory compromise requiring mechanical ventilatory support. Investigations were consistent with a diagnosis of endotracheal tuberculosis with tracheal and bronchial stenosis. Despite adequate anti-tuberculous therapy and ventilation the patient had high airway pressures, low tidal volumes and hypercapnia, which prevented weaning from mechanical ventilation. Balloon dilatation and stenting of the 4.5cm long, 2.3mm diameter stenotic tracheal segment was performed under radiological guidance. The patient was weaned successfully from the ventilator post-procedure. This report illustrates the successful management of an uncommon presentation of a common disease with modern endoscopic therapy.

Drug interaction: rifampicin and glibenclamide.

BACKGROUND: Rifampicin is a potent inducer of the hepatic microsomal enzyme system. However, the drug has been shown to cause clinically important interactions with many drugs. This study was designed to test the interaction of rifampicin with the oral hypoglycaemic agent glibenclamide. METHODS: Twenty-nine well-controlled diabetic patients on a combination therapy of diet and glibenclamide, and willing to participate in the trial, received a daily dose of 450 mg (body weight < 50 kg) or 600 mg (body-weight > 50kg) of rifampicin for 10 days. RESULTS: There was a significant (p < 0.001) worsening of fasting and post-prandial blood sugar after administration of rifampicin. Dose modification of glibenclamide was required in 15 of the 17 patients in whom the diabetes became uncontrolled. Blood sugar normalized by day 6 after stopping rifampicin in all patients. CONCLUSION: Rifampicin and glibenclamide interact. Therefore, necessary dose modifications should be made in order to achieve euglycaemia if these two drugs are given together.