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Objective: To study the prevalence of 25-hydroxyvitamin D deficiency pattern during three year (2017-2020) and severity correlation among individuals with acute traumatic brain injury (TBI). Methodology: Subjects with acute TBI admitted from June 1st, 2017 through June 30th, 2020 were recruited. 280 out of 445 met inclusion criteria. The demographic injury related details, assessment of 25 OH vitamin D and Glasgow Comma (GCS) score were done at the time of admission. Results: The year wise enrolled subjects were young with mean age of 28.39±0.86 years with males (73.3%) and female (23.7%), in first year, 27.77±5.35 years with males (81.67%) and female (18.33%), in second year and 23.04±7.10 years with males (88.57%) and female (11.42%), in third years. Mean value of 25(OH) vitamin D in subjects during three years were 23.78±11.79ng/mL, 21.65±12.53 ng/mL and 25.18±18.58ng/mL. The vitamin D deficiency levels in this study were tabulated as: deficient (level <20 ng/mL), insufficient (level 20–29.9ng/mL), and sufficient (level ≥30ng/mL). Which were found during three years as: In First year, Deficient (64.44%), Sufficient (11.11%), insufficient (24.44%), in second years, Deficient (88.33%), Sufficient (2.66%), insufficient (10.00%) and in third year Deficient (88.57%), Sufficient (1.42%), insufficient (10.00%). In which sufficient level were found to be decreased statistically significant with years with P value= 0.0001. The severity assessment through GCS score were found to be statistically increased with deficient levels with P values=0.0447, but found no significance, when comparison were done between years wise GCS score and levels of vitamin D. Conclusion: The study found decreased prevalence of vitamin D deficiency levels with increased severity. Therefore it should be routinely screened and treated as indicated.
Objective: To study the prevalence of 25-hydroxyvitamin D deficiency pattern during three year (2017-2020) and severity correlation among individuals with acute traumatic brain injury (TBI). Methodology: Subjects with acute TBI admitted from June 1st, 2017 through June 30th, 2020 were recruited. 280 out of 445 met inclusion criteria. The demographic injury related details, assessment of 25 OH vitamin D and Glasgow Comma (GCS) score were done at the time of admission. Results: The year wise enrolled subjects were young with mean age of 28.39±0.86 years with males (73.3%) and female (23.7%), in first year, 27.77±5.35 years with males (81.67%) and female (18.33%), in second year and 23.04±7.10 years with males (88.57%) and female (11.42%), in third years. Mean value of 25(OH) vitamin D in subjects during three years were 23.78±11.79ng/mL, 21.65±12.53 ng/mL and 25.18±18.58ng/mL. The vitamin D deficiency levels in this study were tabulated as: deficient (level <20 ng/mL), insufficient (level 20–29.9ng/mL), and sufficient (level ≥30ng/mL). Which were found during three years as: In First year, Deficient (64.44%), Sufficient (11.11%), insufficient (24.44%), in second years, Deficient (88.33%), Sufficient (2.66%), insufficient (10.00%) and in third year Deficient (88.57%), Sufficient (1.42%), insufficient (10.00%). In which sufficient level were found to be decreased statistically significant with years with P value= 0.0001. The severity assessment through GCS score were found to be statistically increased with deficient levels with P values=0.0447, but found no significance, when comparison were done between years wise GCS score and levels of vitamin D. Conclusion: The study found decreased prevalence of vitamin D deficiency levels with increased severity. Therefore it should be routinely screened and treated as indicated.
Children with coagulopathy had a greater mortality rate after moderate to severe traumatic brain injury (TBI). The purpose of the current study was to examine the most recent relevant literature in relation to the therapy of TIC in pediatric isolated severe TBI patients. A 5 years old boy presented to emergency department with decrease of consciousness after hit by a motorcycle. He was referred from the district hospital without proper stabilization within 3 hours after the injury. From the blood examination, hemoglobin level was 8.1 g/dl, base deficit -9.9mEq/L with PTT and aPTT no coagulation suggesting coagulopathy. Emergency non-contrast head computed tomography was performed and showed anterior skull base fracture with discontinuity in left squamous suture suggesting a diastases fracture with an air hypodensity lesion in left frontal area suggesting a pneumocephalus. There was also a hyperdense lesion with crescent shape in frontal and interhemispheric region suggesting subdural hematoma. Delayed operation for almost 6 hours was advocated due to transfusion of whole blood and fresh frozen plasma to correct coagulopathy. The operation was successful, the patient was survived but upon 2 years follow up, the patient still wasn’t able to perform normal daily activity. Localized injury at the brain manifesting in systemic coagulopathy requires special care. Several steps need to be evaluated before surgery but it should not delay the attempt of controlling the source of coagulopathy by it means lesion in the brain. Our case demonstrates the important of recognizing and managing coagulopathy in severe traumatic brain injury.
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