RESUMEN
To assess the pre-operative indicators of incudal necrosis in tubo-tympanic CSOM. A total of 80 patients with tubo-tympanic type of CSOM attending the SMGS Hospital ENT OPD/IPD of both genders were enrolled for the study. Pre-operative findings on oto-microscopic examination, pure-tone audiometry, x-ray mastoid and intra-operative microscopy was recorded. It was found that patients with age > 30 years and more than 10 years of CSOM had had higher incidence of ossicular necrosis as compared to patients age < 30 years and less than 10 years of CSOM (P < 0.05). Patients who had granulation tissue and moderate to moderately severe hearing loss had higher incidence of ossicular necrosis as compared to other patients. The difference was seen significant (P < 0.05). In this study, it was observed that the presence of granulations over the perforation margins, disease persisting for more than 10 years, moderate to moderately severe hearing loss appear to be significant reliable indicators of incudal necrosis in tubo-tympanic type of CSOM. All patients of tubo-tympanic type of CSOM should be assessed in detail so as to reach early diagnosis of ossicular erosion that helps in surgical decision making and preparedness regarding ossiculoplasty and patient consent.
RESUMEN
Background: Elevated lactate levels in neurosurgical patients are seen in brain tumors, traumatic brain-injury, brain infarction, and subarachnoid hemorrhage. Hyperlactatemia during craniotomy may be caused by hypotension due to multiple factors. Recently, intraoperative hyperlactatemia has been associated with fresh-onset neurodeficits. Aims: We studied the prevalence of hyperlactatemia in patients undergoing craniotomy and relationship between intraoperative hyperlactatemia and development of new postoperative neurodeficit. Study Design: Eighty-six patients, American Society of Anesthesiologists Classes I,II and III, undergoing elective craniotomy for neurosurgical indications were included in this prospective, observational study in a tertiary care center. Materials and Methods: Baseline, intraoperative, and postoperative (upto 12 h) lactate levels were noted. Neurological examination to detect new-onset neurodeficits was done at intervals up to 72 h postoperatively. Lactate levels were compared between patients who developed neurodeficits and those who did not develop neurodeficits postoperatively. Statistical Analysis: Statistical analysis of the correlation between intraoperative hyperlactatemia and fresh postoperative neurodeficit was done using the Chi-square test. Results: The prevalence of intraoperative hyperlactatemia was found to be 52.3% and that of fresh-onset postoperative neurodeficits was 31.4%. The relationship between the two was statistically insignificant (P > 0.05). Conclusion: The intraoperative hyperlactatemia is not correlated with the development of fresh-onset postoperative neurodeficit. Implications: There may be no relationship between the intraoperative lactate levels and fresh-onset postoperative neurodeficits. Multifactorial reasons may be responsible for increased lactate levels which need to be identified by further research.
RESUMEN
INTRODUCTION: Dexamethasone is commonly administered in intracranial tumors to reduce the cerebral edema. Its administration may be associated with hyperglycemia. The primary objective of this study was to study the magnitude of rise in blood sugar levels following the administration of a single 10 mg dose of dexamethasone. METHODS: Seventy patients who underwent various neurosurgical procedures were enrolled in the study. Group D (n = 35 undergoing surgery for intracranial tumors) were administered injection dexamethasone 10 mg while as Group P (n = 35 undergoing surgery for subarachnoid hemorrhage) received placebo. Blood samples were obtained through the arterial line at baseline (before dexamethasone administration), 60, 120, 180, and 240 min after the dexamethasone administration and blood glucose concentrations noted. RESULTS: Glucose concentrations were significantly increased in patients who received dexamethasone compared with those who received placebo (P < 0.05). Blood glucose concentrations at different time intervals were greater when compared with the baseline blood sugar levels in both the placebo and dexamethasone group (P < 0.05). The arterial blood glucose concentration in those who received 10 mg dexamethasone (n = 35) increased from 95.29 ± 13.69 mg.dl-1 to 139.97 ± 10.34 mg.dl-1 over 4 h, compared with a change from 94.74 ± 10.05 mg.dl-1 to 122.34 ± 10.68 mg.dl-1 in those who received placebo (n = 35) (P < 0.05). CONCLUSION: The administration of a single intravenous dose of 10-mg dose dexamethasone caused a significant increase in the blood glucose concentrations at different point intervals when compared with the placebo over a 4-h period. We recommend intensive monitoring of the blood sugar levels during the intraoperative period to prevent the development of severe hyperglycemia and its associated complications.
