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1.
Article | IMSEAR | ID: sea-202689

ABSTRACT

Introduction: Transient intraocular pressure rise is acommonly observed phenomenon following Nd:YAGcapsulotomy. However, IOP change is considered to bedependent on multiple factors. Study aimed to assess factorsdetermining the IOP change following Nd:YAG capsulotomy.Material and Methods:A total of 150 adult patients, scheduledto undergo Nd:YAG laser capsulotomy for management ofposterior chamber opacification (PCO) were enrolled. Age,gender, time since cataract surgery, PCO grade, IOP, topicalhypotensive use was noted in all the cases. Amount of energyused in Nd:YAG procedure was recorded. Postoperative IOPchange was noted immediately, 1 hr and 3 hr postoperativeintervals. Rise >5 mm was considered clinically significant.Independent samples ‘t’-test, Chi-square test and binarylogistic regression were used. Data analysis was performedusing SPSS 15.0 software.Results: Mean age of patients was 60±11.3 years. Majoritywere females (59.3%). Majority of patients had Grade I andII of PCO (64%), 5-10 years duration since cataract surgery(79.3%) and topical hypotensive use was done(58%).Preoperative mean IOP was 15.99±2.72 mmHg. Energyused was 55.7±52.7 mJ. A total of 19 (12.7%) patients hadIOP rise >5 mm. On univariate analysis, Grade III or abovePCO, higher level of total energy use and low hypotensive usewere found to be significantly associated with IOP rise. Onmultivariate assessment, low hypotensive use and high energyuse were found to be significantly associated with clinicallysignificant IOP rise (p<0.05).Conclusions: Low energy and prophylactic topicalhypotensives were protective against IOP rise.

2.
Article | IMSEAR | ID: sea-202688

ABSTRACT

Introduction: Use of LED based devices is increasingsubstantially in recent years, however, these devices couldhave an adverse effect on ocular health. Study aimed toevaluate the relationship between direct exposure to LED andocular symptoms.Material and Methods: The data was collected from secondaryschool students studying in a girls’ college at Bareilly duringan eye camp organized by Muskaan Foundation. Only girlshaving known intact vision (BCVA 6-6/6-9) were enrolledin the study. A total of 536 girls were enrolled in the study.Average daily direct exposure <3-4 hours was categorized asunexposed while those having >3-4 hours daytime or 1-2 hrsor more night time exposure were categorized as exposed. Theexposed girls were divided into day exposed and night exposedrespectively. Ocular symptoms were noted. Chi-square testand ANOVA were calculated using SPSS 21.0 software.Results: Mean age of girls was 17.02±1.42 (Range 15-19)years. A total of 298 (55.5%) had direct exposure to LED.Prevalence of ocular symptoms like headache, pain in eyes,blurring, floaters, burning sensation and eye fatigue was34.3%, 34.1%, 26.3%, 24.3%, 41.6% and 39% respectively.Total No. of symptomatic girls was 387 (72.2%) A significantincrease in ocular symptoms was observed from unexposed todaytime and to night exposed girls (p<0.001). Mean numberof total symptoms also showed a significant increasing trendfrom unexposed to nighttime exposure (p<0.001).Conclusion: Direct LED light exposure for a substantialperiod, particularly during night time is detrimental to ocularhealth.

3.
Article in English | IMSEAR | ID: sea-166715

ABSTRACT

Abstracts: Background: Nasogastric aspiration is bedside procedure in surgical wards. Amount and type of nasogastic drainage is helpful in establishing conditions such as intestinal obstruction and its level. Knotted nasogastric tube is rarely reported in literature. In our case of intestinal obstruction this rare condition led to a diagnostic dilemma. Through this we want to highlight that in patients with intestinal obstruction and inadequate nasogastric tube drainage, possibility of this rare complication should be thought of.

4.
Br J Med Med Res ; 2013 Oct-Dec; 3(4): 1398-1406
Article in English | IMSEAR | ID: sea-163013

ABSTRACT

We report the 1st case of severe, symptomatic hypocalcemia after denosumab (RANKL inhibitor) treatment in a peritoneal dialysis patient with secondary hyperparathyroidism and osteoporosis. A 58-year-old Caucasian female has been receiving chronic ambulatory peritoneal dialysis for four years secondary to polycystic kidney disease. Laboratory studies revealed: albumin-corrected calcium 9.0 mg/dL, phosphorus 5 mg/dL, alkaline phosphatase (ALP) 58 U/L [normal, 40-105], albumin 3.4 gm/dL [normal, 3.6-5.4] and intact parathyroid hormone (PTH) 315 pg/mL [normal, 40-72]. Marked osteoporosis was noted on the DXA scan, preventing her from renal transplantation considerations. She had failed conventional medical treatment, including per os calcium, monthly ergocalciferol (50,000 units/month), activated vitamin-D analog (doxercalciferol) and renal-failure adjusted alendronate (70 mg twice a month). She was started on subcutaneous denosumab 60 mg every 6 months. After her first dose, she developed a progressive drop of calcium, phosphorus, bicarbonate and magnesium, in spite of massive escalation of doxercalciferol and calcium supplementation. Hypocalcemia nadired at 6.3 mg/dL with symptomatic tetany, requiring a brief hospitalization approximately 7 weeks after denosumab treatment. Her elevated PTH rose further transiently (647 pg/mL), along with ALP (123 U/L). Bone-mineral parameters normalized approximately 3 months after denosumab administration. The observed phenomenon resembled the phenotype of “hungry bone syndrome” observed after surgical parathyroidectomy. Conclusion: Treatment decisions based on bone densitometry results alone are not transposable between patients with or without end-stage renal disease. Denosumab may lead to critical hypocalcemia in dialysis patients and further aggravate existing secondary hyperparathyroidism.

5.
Article in English | IMSEAR | ID: sea-182279

ABSTRACT

Horner’s syndrome (Bernard-Horner’s syndrome or oculosympathetic palsy) is a clinical syndrome caused by paralysis of the cervical sympathetic trunk. It is characterized by miosis, ptosis, enophthalmos and anhidrosis. Most of the cases are due to vascular causes, trauma or cancer. Occasionally, Horner’s syndrome is encountered in a patient where no cause can be ascertained. Here, we describe one such case.

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